subject:(canine herpes virus CHV 1 )

University of Helsinki

1. Johnsson, Mia. Brucella canis ja Canine Herpes Virus -1, seroprevalenssi Suomen koirapopulaatiossa ja merkitys lisääntymisongelmissa.

Degree: Department of Clinical Veterinary Sciences; Helsingin yliopisto, Eläinlääketieteellinen tiedekunta, Kliinisen eläinlääketieteen laitos; Helsingfors universitet, Veterinärmedicinska fakulteten, Institutionen för klinisk veterinärmedicin, 2006, University of Helsinki

URL: http://hdl.handle.net/1975/1168

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Koirilla esiintyvistä lisääntymisongelmia aiheuttavista infektiivisistä mikrobeista tyypillisimmät ovat Brucella canis ja canine herpes virus-1 (CHV-1). Näiden aiheuttamat ongelmat saattavat muodostua hyvinkin merkittäviksi yksittäisessä kennelissä alentaen… (more)

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Koirilla esiintyvistä lisääntymisongelmia aiheuttavista infektiivisistä mikrobeista tyypillisimmät ovat Brucella canis ja canine herpes virus-1 (CHV-1). Näiden aiheuttamat ongelmat saattavat muodostua hyvinkin merkittäviksi yksittäisessä kennelissä alentaen syntyvien pentujen määrää huomattavasti vuositasolla. Useissa maissa tehtyjen tutkimusten perusteella on todettu herpeksen olevan enzoottinen virus koirapopulaatioissa. Brucella canista esiintyy harvemmin, mutta sen aiheuttamien vakavien lisääntymisongelmien takia vähäinenkin esiintyvyys on merkittävää. Suomessa ei ole aiemmin tutkittu Brucella canis –bakteerin tai CHV-1:n esiintyvyyttä paikallisessa koirapopulaatiossa. Tutkimuksen tarkoituksena oli kartoittaa näiden mikrobien esiintyvyys Suomessa ja niiden merkitys suomalaisten koirien lisääntymisongelmissa. Tutkimukseen pyydettiin lehti-ilmoituksella mukaan jalostuskoiria, joilla oli ollut lisääntymisongelmia. Näytteitä otettiin myös täysin terveistä koirista verrokkiryhmäksi. Näytteeksi otettiin verta lasiseen seerumiputkeen noin 8 ml. Näytteet kerättiin pääsääntöisesti kenneleissä paikan päällä. Yhteensä näytteitä saatiin 388 kpl. Brucella canis –vasta-aineet tutkittiin kaikista näytteistä EELA:ssa. Yhdestäkään näytteestä ei löytynyt positiiviseksi tulkittavia vasta-ainemääriä. Herpesvasta-ainetutkimusta varten valittiin 40 lisääntymisongelmista kärsivien kenneleiden näytettä sekä 41 näytettä verrokkiryhmäksi ongelmattomista kenneleistä. Herpesvasta-aineet tutkittiin Ruotsissa SVA:n laboratoriossa. Herpesvasta-aineita tutkimuksessa todettiin usealla koiralla. Seroprevalenssi ongelmakenneleiden ryhmässä oli 90%. Verrokkiryhmän kenneleissä seroprevalenssi oli selvästi matalampi, 24%. Vasta-ainetiitterin korkeus todettiin tilastollisesti merkitsevästi riippuvaksi kennelin ongelmastatuksesta ja koiran käytöstä jalostuksessa. Herpesvasta-aineita todettiin enemmän ongelmakennelien koirilla kuin ongelmattomien kenneleiden koirilla. Tutkimuksen johtopäätöksenä voidaan todeta herpeksen olevan yksi tärkeimmistä aiheuttajista kennelin lisääntymisongelmissa. Kennelin herpestilanteen selvittäminen tulisikin sisällyttää tutkimuksiin kartoitettaessa syitä kennelin lisääntymisongelmiin.

Vain tiivistelmä. Koko työ lainattavissa Viikin tiedekirjastosta.

Subjects/Keywords: abortointi; lisääntymisongelmat; neonataalikuolema; Brucella canis; canine herpes virus (CHV-1); Kotieläinten lisääntymistiede; Husdjurens reproduktion; Reproduction of Domestic Animals; abortointi; lisääntymisongelmat; neonataalikuolema; Brucella canis; canine herpes virus (CHV-1)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Johnsson, M. (2006). Brucella canis ja Canine Herpes Virus -1, seroprevalenssi Suomen koirapopulaatiossa ja merkitys lisääntymisongelmissa. (Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/1975/1168

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Johnsson, Mia. “Brucella canis ja Canine Herpes Virus -1, seroprevalenssi Suomen koirapopulaatiossa ja merkitys lisääntymisongelmissa.” 2006. Thesis, University of Helsinki. Accessed January 24, 2021. http://hdl.handle.net/1975/1168.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Johnsson, Mia. “Brucella canis ja Canine Herpes Virus -1, seroprevalenssi Suomen koirapopulaatiossa ja merkitys lisääntymisongelmissa.” 2006. Web. 24 Jan 2021.

Vancouver:

Johnsson M. Brucella canis ja Canine Herpes Virus -1, seroprevalenssi Suomen koirapopulaatiossa ja merkitys lisääntymisongelmissa. [Internet] [Thesis]. University of Helsinki; 2006. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1975/1168.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Johnsson M. Brucella canis ja Canine Herpes Virus -1, seroprevalenssi Suomen koirapopulaatiossa ja merkitys lisääntymisongelmissa. [Thesis]. University of Helsinki; 2006. Available from: http://hdl.handle.net/1975/1168

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Technical University of Lisbon

2. Dias, Mariana Anjo. Análise molecular e serológica de herpesvírus canino, CHV-1, em canideos de canis da Região de Lisboa e Vale do Tejo e do Distrito de Coimbra.

Degree: 2018, Technical University of Lisbon

URL: https://www.rcaap.pt/detail.jsp?id=oai:www.repository.utl.pt:10400.5/15005

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Dissertação de Mestrado Integrado em Medicina Veterinária

O herpesvírus canino tipo I (CHV-1) é um vírus, monotípico, pertencente à família Herpesviridae, subfamília Alphaherpesvirinae, género Varicellovirus,… (more)

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Dissertação de Mestrado Integrado em Medicina Veterinária

O herpesvírus canino tipo I (CHV-1) é um vírus, monotípico, pertencente à família Herpesviridae, subfamília Alphaherpesvirinae, género Varicellovirus, e que tem como hospedeiros, canídeos domésticos e selvagens. É responsável por induzir uma necrose hemorrágica sistémica fatal em cachorros com menos de três semanas de vida e por provocar sinais clínicos respiratórios, oculares e reprodutivos em cães adultos, sobretudo jovens e imunodeprimidos. Após o contacto com o vírus, este permanece latente nos tecidos linfoides e nervosos dos animais infetados, podendo haver períodos de reativação viral, geralmente associados a períodos de stress, tais como gestação, introdução de novos animais, doenças, entre outros. O objetivo deste estudo foi a deteção molecular do ácido nucleico do CHV-1 (por qPCR) e deteção de anticorpos específicos contra o vírus (por imunofluorescência indireta) em cadelas de canis da Grande Lisboa e do distrito de Coimbra, e avaliar se existe uma associação entre a infeção por CHV-1 e a dimensão do canil (nº de animais), número de gestações, idade, historial de problemas reprodutivos, presença de traqueobronquite infeciosa no efetivo e a fase do ciclo éstrico. As cadelas com potencial reprodutivo são um grupo de particular interesse, uma vez que cadelas gestantes sem títulos protetores de anticorpos (o que acontece geralmente no primeiro contacto destas com o vírus) podem sofrer abortos e infertilidade. Se estes títulos se mantiverem baixos ao longo da gestação o colostro ingerido pelos cachorros não lhes irá conferir proteção contra o CHV-1. A amostra deste estudo incluiu 49 cadelas de 11 criadores nacionais e de 2 associações de animais, às quais foi colhido sangue para análise serológica e 3 amostras por zaragatoa de secreções nasal, vaginal e ocular, para análise molecular por qPCR. Todas as amostras foram negativas na análise por qPCR, não sendo possível detetar qualquer ADN viral nas secreções analisadas, pelo que foi concluído que nenhuma das cadelas em estudo estava a excretar o vírus. A análise serológica revelou uma proporção de 75,5% de seropositivos e observou-se uma associação significativa (p=0.006), entre a seropositividade e a idade dos animais, concluindo-se que, com o aumento da idade é maior a probabilidade de encontrar animais seropositivos. Dos seropositivos, 32,45% (12/37) foram positivos a IgG, 35,1% (13/37) foram positivos a IgM e 32,45% (12/37) foram positivos a IgG e IgM. Este estudo revelou que o herpesvírus canino é, como se suspeitava, um agente bastante prevalente, nos canis nacionais.

ABSTRACT - Canine herpesvirus type I (CHV-1) is a monotypic virus included in the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus, whose hosts are domestic and wild canids. It is responsible for a fatal systemic hemorrhagic disease in puppies less than three weeks old. It also induces respiratory, ocular and reproductive clinical signs in adult dogs, especially in young and immunocompromised animals. After…

Advisors/Committee Members: Silva, Francisco Machado da, Duarte, Ana Isabel Simões Pereira.

Subjects/Keywords: Herpesvírus canino; cadelas; CHV-1; serologia; qPCR; imunofluorescência; Canine herpesvirus; bitches; indirect imunofluorescence

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dias, M. A. (2018). Análise molecular e serológica de herpesvírus canino, CHV-1, em canideos de canis da Região de Lisboa e Vale do Tejo e do Distrito de Coimbra. (Thesis). Technical University of Lisbon. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:www.repository.utl.pt:10400.5/15005

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dias, Mariana Anjo. “Análise molecular e serológica de herpesvírus canino, CHV-1, em canideos de canis da Região de Lisboa e Vale do Tejo e do Distrito de Coimbra.” 2018. Thesis, Technical University of Lisbon. Accessed January 24, 2021. https://www.rcaap.pt/detail.jsp?id=oai:www.repository.utl.pt:10400.5/15005.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dias, Mariana Anjo. “Análise molecular e serológica de herpesvírus canino, CHV-1, em canideos de canis da Região de Lisboa e Vale do Tejo e do Distrito de Coimbra.” 2018. Web. 24 Jan 2021.

Vancouver:

Dias MA. Análise molecular e serológica de herpesvírus canino, CHV-1, em canideos de canis da Região de Lisboa e Vale do Tejo e do Distrito de Coimbra. [Internet] [Thesis]. Technical University of Lisbon; 2018. [cited 2021 Jan 24]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:www.repository.utl.pt:10400.5/15005.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dias MA. Análise molecular e serológica de herpesvírus canino, CHV-1, em canideos de canis da Região de Lisboa e Vale do Tejo e do Distrito de Coimbra. [Thesis]. Technical University of Lisbon; 2018. Available from: https://www.rcaap.pt/detail.jsp?id=oai:www.repository.utl.pt:10400.5/15005

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

3. Muenzner, Julia. Viral subversion of host cell membrane trafficking.

Degree: PhD, 2017, University of Cambridge

URL: https://doi.org/10.17863/CAM.13818 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725575

► Enveloped viruses acquire their membrane coat from the plasma membrane or intracellular organelles and rely on cellular machinery to facilitate envelopment and egress of virus… (more)

▼ Enveloped viruses acquire their membrane coat from the plasma membrane or intracellular organelles and rely on cellular machinery to facilitate envelopment and egress of virus progeny. This thesis examines egress-related interactions between host cell factors and proteins of two different enveloped viruses: hepatitis D virus (HDV) and herpes simplex virus 1 (HSV-1). HDV is a small RNA virus causing fulminant hepatitis or severely aggravating cirrhosis and hepatocellular carcinoma. HSV-1 is a large DNA virus infecting epithelial and neuronal cells. Infection with HSV-1 not only triggers the development of recurring sores on oral or genital mucosa, but can also cause severe disease in neonates and immunocompromised patients. The interaction between the large antigen of HDV (HDAg-L) and the N-terminal domain (NTD) of clathrin, a protein crucial for endocytosis and intracellular vesicular trafficking, was examined by structural, biochemical and biophysical techniques. Co-crystal structures of NTD bound to HDAg-L peptides derived from different HDV genotypes revealed that HDV interacts with multiple binding sites on NTD promiscuously, prompting re-evaluation of the binding between cellular peptides and NTD. Surprisingly, co-crystal structures and pull-down capture assays showed that cellular peptides containing clathrin-binding motifs can also bind multiple sites on the surface of NTD simultaneously. In addition, the structures of viral and cellular peptides bound to NTD enabled the molecular characterization of the fourth peptide binding site on NTD, the “Royle box”, and led to the identification of a novel binding mode at the “arrestin box” peptide binding site on NTD. The work in this thesis therefore not only identifies the molecular basis of HDV:clathrin interactions, but also furthers our understanding of basic clathrin biology. Even though many HSV-1 proteins have been implicated in the envelopment and egress of viral particles, only few interactions between HSV-1 and cellular proteins promoting these processes have been described. Therefore, the HSV-1 proteins gE, UL21 and UL56 were selected and characterized bioinformatically and/or biochemically. Cellular proteins interacting with UL56 were identified by yeast two-hybrid screening and quantitative mass spectrometry. Co-immunoprecipitation and pull-down experiments confirmed the Golgi-trafficking protein GOPC, components of the mammalian trafficking protein particle complex, and the ubiquitin ligase NEDD4 as novel binding partners of UL56, thereby suggesting exciting new avenues for the investigation of cellular mechanisms contributing to HSV-1 envelopment and egress.

Subjects/Keywords: 616.9; clathrin; membrane trafficking; herpes simplex virus 1; hepatitis D virus

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Muenzner, J. (2017). Viral subversion of host cell membrane trafficking. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.13818 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725575

Chicago Manual of Style (16^th Edition):

Muenzner, Julia. “Viral subversion of host cell membrane trafficking.” 2017. Doctoral Dissertation, University of Cambridge. Accessed January 24, 2021. https://doi.org/10.17863/CAM.13818 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725575.

MLA Handbook (7^th Edition):

Muenzner, Julia. “Viral subversion of host cell membrane trafficking.” 2017. Web. 24 Jan 2021.

Vancouver:

Muenzner J. Viral subversion of host cell membrane trafficking. [Internet] [Doctoral dissertation]. University of Cambridge; 2017. [cited 2021 Jan 24]. Available from: https://doi.org/10.17863/CAM.13818 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725575.

Council of Science Editors:

Muenzner J. Viral subversion of host cell membrane trafficking. [Doctoral Dissertation]. University of Cambridge; 2017. Available from: https://doi.org/10.17863/CAM.13818 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725575

Louisiana State University

4. Liu, Shiliang Anthony. Development and Characterization of a Live-attenuated Vaccine to Combat Equine Herpesvirus Type-1 infections.

Degree: PhD, Veterinary Pathology and Pathobiology, 2015, Louisiana State University

URL: etd-11162015-102110 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3816

► Equine Herpesvirus 1 (EHV-1) is an important ubiquitous enzootic equine pathogen and one of the most common pathogens of the horse, causing, respiratory disease, epidemic… (more)

▼ Equine Herpesvirus 1 (EHV-1) is an important ubiquitous enzootic equine pathogen and one of the most common pathogens of the horse, causing, respiratory disease, epidemic abortion, occasionally neurological disease in horses, which leads to significant economic losses to the horse industry. EHV-1 induces several clinical signs of disease ranging in severity, from mild respiratory disease to abortion in pregnant mares, neonatal foal death and neuropathogenic disorders. Natural EHV-1 infection stimulated short lived protective immunity and had both humoral and cellular immune responses. Currently vaccination remains the best option to prevent EHV-1 infection and different applications of vaccination have been investigated and developed over the past decades. The objective of this research was the design of a safe and effective virus-vectored vaccine to prevent EHV-1 infections. In this research, EHV-1 glycoprotein D (gD) gene was cloned into the Herpes Simplex Virus Type-1 (HSV-1) VC2 vector, which contains the gK∆31-68 deletion and UL20∆2-22 deletion. The VC2 strain cannot infect axonal neurons of mice and rats and has been shown to produce protective immune responses against both HSV-1 and HSV-2 viruses in mice and guinea pigs. Vaccination of mice with the HSV-VC2-EHV-gD increased virus neutralizing activities against EHV-1 (33.6%) in mice after three vaccinations, which was similar to commercial whole virus vaccine group (32.6%) and significantly higher than VC2 and Unvaccinated control groups (p<0.01 or p<0.001). Mice vaccinated with the VC2-EHV-gD group exhibited significantly higher humoral and cellular immune responses as detected by polychromatic flow cytometry when compared to the other groups (p<0.01 or p<0.001). Induction of IgG1 and IgG2a antibodies were significantly higher in the VC2-EHV-gD group than other groups after three vaccinations (p<0.001). It’s interesting that induction of IgM antibody in the Vetera group was significantly higher than other groups before and after challenge (p<0.01 or P<0.05). Vaccination with the VC2-EHV-gD also stimulated strong cellular immune response (IFN-γ and TNF). Additional studies are needed to assess the VC2-EHV-gD vaccine efficacy in generating protective humoral and cellular immune responses in horses.

Subjects/Keywords: live-attenuated vaccine; Equine Herpersvirus 1; infection; Herpes simplex virus 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Liu, S. A. (2015). Development and Characterization of a Live-attenuated Vaccine to Combat Equine Herpesvirus Type-1 infections. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-11162015-102110 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3816

Chicago Manual of Style (16^th Edition):

Liu, Shiliang Anthony. “Development and Characterization of a Live-attenuated Vaccine to Combat Equine Herpesvirus Type-1 infections.” 2015. Doctoral Dissertation, Louisiana State University. Accessed January 24, 2021. etd-11162015-102110 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3816.

MLA Handbook (7^th Edition):

Liu, Shiliang Anthony. “Development and Characterization of a Live-attenuated Vaccine to Combat Equine Herpesvirus Type-1 infections.” 2015. Web. 24 Jan 2021.

Vancouver:

Liu SA. Development and Characterization of a Live-attenuated Vaccine to Combat Equine Herpesvirus Type-1 infections. [Internet] [Doctoral dissertation]. Louisiana State University; 2015. [cited 2021 Jan 24]. Available from: etd-11162015-102110 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3816.

Council of Science Editors:

Liu SA. Development and Characterization of a Live-attenuated Vaccine to Combat Equine Herpesvirus Type-1 infections. [Doctoral Dissertation]. Louisiana State University; 2015. Available from: etd-11162015-102110 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3816

University of Manitoba

5. Caligiuri, Kyle. Investigation of the deregulated miRNome identified during acute viral infections in a murine model of HSV-1 encephalitis.

Degree: Medical Microbiology, 2013, University of Manitoba

URL: http://hdl.handle.net/1993/23926

► Herpes simplex virus type 1 (HSV-1) is a double stranded DNA virus that causes epithelial skin infections and persists through the life of the host… (more)

▼ Herpes simplex virus type 1 (HSV-1) is a double stranded DNA virus that causes epithelial skin infections and persists through the life of the host by infecting neurons, where it can switch to a latent state to evade an immune response. In rare cases during primary infection or after reactivation, instead of undergoing lytic infection at the epithelial surface, it instead travels to the brain and causes herpes simplex virus encephalitis (HSVE) which can have a ≥70% mortality rate if untreated. As the virus takes over its host cell, it gains control of the host cell machinery and manipulates host gene expression in order to evade the immune system and to pool its resources into the replication of the virus. One aspect of the dysregulated gene expression involves microRNAs (miRNAs). MiRNAs are short, non-coding RNAs that bind to the 3' untranslated region (3'UTR) of messenger RNAs (mRNAs), leading to translational repression of the target. Dysregulated miRNAs are often down-regulated during infection as the virus takes over, but many miRNAs have also been found to be up-regulated as well1–5. The aim of this study is to observe the full cellular miRNA changes in the context of an acute viral encephalitic infection using HSV-1, and to further characterize selected up-regulated miRNAs to determine their function in the context of the disease state. Of particular note were miR-141 and miR-200c which showed anti-apoptotic effects on neuronal cell culture and did not impact cell viability during an over-expression of the miRNAs. MiR-141, miR-183 and miR-200a expression was enriched within specific areas of the brain during infection. In addition, the potential for miR-150 to bind to a bioinformatically predicted target site within the shared 3'UTR of the HSV-1 UL18, UL19 and UL20 genes was explored. Examining the changes in expression of this class of regulatory RNAs and investigating their potential functions may yield new insight into the relationship between host and virus during infection. Advisors/Committee Members: Booth, Stephanie (Medical Microbiology) (supervisor), Yao, Xiaojian (Medical Microbiology) Hombach-Klonisch, Sabine (Human Anatomy & Cell Science) (examiningcommittee).

Subjects/Keywords: herpes simplex virus type 1; microRNA; HSV-1; miRNA; next generation sequencing; NGS; deep sequencing; miRNome; herpes simplex virus encephalitis; HSVE

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Caligiuri, K. (2013). Investigation of the deregulated miRNome identified during acute viral infections in a murine model of HSV-1 encephalitis. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/23926

Chicago Manual of Style (16^th Edition):

Caligiuri, Kyle. “Investigation of the deregulated miRNome identified during acute viral infections in a murine model of HSV-1 encephalitis.” 2013. Masters Thesis, University of Manitoba. Accessed January 24, 2021. http://hdl.handle.net/1993/23926.

MLA Handbook (7^th Edition):

Caligiuri, Kyle. “Investigation of the deregulated miRNome identified during acute viral infections in a murine model of HSV-1 encephalitis.” 2013. Web. 24 Jan 2021.

Vancouver:

Caligiuri K. Investigation of the deregulated miRNome identified during acute viral infections in a murine model of HSV-1 encephalitis. [Internet] [Masters thesis]. University of Manitoba; 2013. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1993/23926.

Council of Science Editors:

Caligiuri K. Investigation of the deregulated miRNome identified during acute viral infections in a murine model of HSV-1 encephalitis. [Masters Thesis]. University of Manitoba; 2013. Available from: http://hdl.handle.net/1993/23926

Universidad de Chile

6. González Troncoso, María Paz. Implementación de CRISPR-Cas9 para el desarrollo de virus herpes simple de tipo 2 mutantes con expresión interrumpida de las proteínas virales gG (US4), gD (US6) y gK (UL53).

Degree: 2019, Universidad de Chile

URL: http://repositorio.uchile.cl/handle/2250/171076

► Diversos mecanismos de edición génica se han implementado a lo largo de los años para mutar el genoma del virus herpes simple tipo 2 (VHS-2).… (more)

▼ Diversos mecanismos de edición génica se han implementado a lo largo de los años para mutar el genoma del virus herpes simple tipo 2 (VHS-2). Éstos se han basado principalmente en el uso de procesos de recombinación homóloga. Un mecanismo comúnmente utilizado consiste en la realización de recombinación homóloga con un sustrato de intercambio alélico (AES) directamente sobre células transfectadas con genoma viral. Otra aproximación comúnmente utilizada es el desarrollo de recombinación homóloga en bacterias transformadas con un cromosoma artificial bacteriano (BAC) que contiene el genoma completo del virus herpes simple. La progenie viral mutante es luego obtenida mediante transfección de células con este material genético modificado. Si bien se han desarrollado diversas cepas mutantes de VHS-2 utilizando estas metodologías, ambas metodologías son laboriosas y presentan problemas técnicos tanto previos como posteriores a la generación de la mutación en el genoma. Dadas estas dificultades, se ha buscado desarrollar otros mecanismos más convenientes los cuales faciliten este proceso. Una metodología relativamente reciente que permite realizar modificaciones genéticas de manera más simple es aquella conocida como la tecnología de CRISPR-Cas9. Dada la mayor facilidad y especificidad de esta técnica, comparada a las más antiguas, nos propusimos mutar mediante el sistema CRISPR-Cas9, los genes virales US6, US4 y UL53 del VHS-2 para interrumpir la síntesis de las proteínas virales gD, gG y gK, respectivamente. Si bien se lograron desarrrollar los reactivos para realizar estas mutaciones, lamentablemente no se obtuvieron los aislados mutantes deseados. Se discuten los eventuales problemas que no permitieron lograr el objetivo; Several mechanisms of genetic edition have been implemented over the year to mutate the genome of herpes simplex virus type 2 (HSV-2). These have been based mainly on homologous recombination process. A mechanism commonly used consist in homologous recombination with an allelic exchange substrate (AES) directly on transfected cells with HSV genome. Another approach normally used is the development of homologous recombination in bacteria transformed with a Bacterial Artificial Chromosome (BAC) that contains the complete genome of HSV. The mutant viral progeny is then obtained by transfecting cells with this modified genetic material. Even though several mutant strains of HSV-2 have been developed with these methodologies, both are laborious and present technical problems before and after the generation of the genome mutation. Due to this difficulties, it has been sought to develop other more convenient mechanisms to facilitate this process. A relatively recent methodology that allows genetic modifications to be made in a simpler way is that known as CRISPR/Cas9 technology. Due to the greater facility and specificity of this technique, compare to the other ones, we decided to mutate with CRISPR/Cas9 system, the viral genes US6, US4 y UL53 of HSV-2 to interrupt the synthesis of gD, gG and gK…

Subjects/Keywords: Virus herpes

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APA (6^th Edition):

González Troncoso, M. P. (2019). Implementación de CRISPR-Cas9 para el desarrollo de virus herpes simple de tipo 2 mutantes con expresión interrumpida de las proteínas virales gG (US4), gD (US6) y gK (UL53). (Thesis). Universidad de Chile. Retrieved from http://repositorio.uchile.cl/handle/2250/171076

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

González Troncoso, María Paz. “Implementación de CRISPR-Cas9 para el desarrollo de virus herpes simple de tipo 2 mutantes con expresión interrumpida de las proteínas virales gG (US4), gD (US6) y gK (UL53).” 2019. Thesis, Universidad de Chile. Accessed January 24, 2021. http://repositorio.uchile.cl/handle/2250/171076.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

González Troncoso, María Paz. “Implementación de CRISPR-Cas9 para el desarrollo de virus herpes simple de tipo 2 mutantes con expresión interrumpida de las proteínas virales gG (US4), gD (US6) y gK (UL53).” 2019. Web. 24 Jan 2021.

Vancouver:

González Troncoso MP. Implementación de CRISPR-Cas9 para el desarrollo de virus herpes simple de tipo 2 mutantes con expresión interrumpida de las proteínas virales gG (US4), gD (US6) y gK (UL53). [Internet] [Thesis]. Universidad de Chile; 2019. [cited 2021 Jan 24]. Available from: http://repositorio.uchile.cl/handle/2250/171076.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

González Troncoso MP. Implementación de CRISPR-Cas9 para el desarrollo de virus herpes simple de tipo 2 mutantes con expresión interrumpida de las proteínas virales gG (US4), gD (US6) y gK (UL53). [Thesis]. Universidad de Chile; 2019. Available from: http://repositorio.uchile.cl/handle/2250/171076

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universiteit Utrecht

7. Driel, B.J. van. evasion of interferon responses by herpes viruses.

Degree: 2010, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/188849

► Mammalian hosts have developed a highly effective anti-viral strategy that uses interferons (signaling molecules). The recognition of a virus by the wide arsenal of detection… (more)

Subjects/Keywords: herpes; virus; innate; immune; evasion; pattern recognition receptor; interferon type 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Driel, B. J. v. (2010). evasion of interferon responses by herpes viruses. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/188849

Chicago Manual of Style (16^th Edition):

Driel, B J van. “evasion of interferon responses by herpes viruses.” 2010. Masters Thesis, Universiteit Utrecht. Accessed January 24, 2021. http://dspace.library.uu.nl:8080/handle/1874/188849.

MLA Handbook (7^th Edition):

Driel, B J van. “evasion of interferon responses by herpes viruses.” 2010. Web. 24 Jan 2021.

Vancouver:

Driel BJv. evasion of interferon responses by herpes viruses. [Internet] [Masters thesis]. Universiteit Utrecht; 2010. [cited 2021 Jan 24]. Available from: http://dspace.library.uu.nl:8080/handle/1874/188849.

Council of Science Editors:

Driel BJv. evasion of interferon responses by herpes viruses. [Masters Thesis]. Universiteit Utrecht; 2010. Available from: http://dspace.library.uu.nl:8080/handle/1874/188849

University of Gothenburg / Göteborgs Universitet

8. Tang, Ka-Wei. Herpes Simplex Virus 1 DNA replication and its role in recombination and transcription.

Degree: 2015, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/40883

► Herpes simplex virus 1 (HSV-1) is one of nine different herpesvirus infecting man. They are all capable of establishing a life-long latent state following the… (more)

▼ Herpes simplex virus 1 (HSV-1) is one of nine different herpesvirus infecting man. They are all capable of establishing a life-long latent state following the primary infection. HSV-1 as well as other herpesviruses may reactivate from the latent state and give rise to a productive infection with clinical symptoms or asymptomatic shedding. HSV-1 infections are primarily treated by targeting the viral DNA replication carried out by a molecular machinery, a replisome, encoded by the virus. Here we examine the mechanism of initiation of viral DNA replication and also how viral DNA replication interacts with DNA recombination and gene expression. In our first study we examined the initiation-step of HSV-1 replication. The origin binding protein (OBP) initiates replication by binding to the origin of replication (oriS and/or oriL). We showed, using phylogenetics and biochemical experiments, that there was a step-wise evolutionary development of herpesvirus DNA replication initiation. The initial divergence was seen in herpesviruses acquiring an amino-acid motif RVKNL in OBP which binds the sequence TTCGCAC in the oriS. The next step was the development of an ICP8 binding motif at the C-terminus of OBP and finally the arrangement of the binding-sites for OBP in the oriS-sequence and the ability to form a stable hairpin. We presented molecular in vitro data to support the phylogenetic analysis and thereby defining essential motifs in OBP for protein-protein and protein-DNA interactions. The next study was focused on genetic recombination between different HSV-1 strains. We followed the propagation of HSV-1 in cells infected with one to three genotypes of HSV-1 and calculated the number of recombination events. We found evidence for Rad51 and Rad52 involvement in recombination of the unique long and unique short gene segments of HSV-1. We also observed an increased recombination rate in cells with retarded ligation of Okazaki-fragments. The fidelity of recombination in virus propagated through mixed infections appears to be high since expansion or shortening of repeated sequences in the US7 gene was not detected. In the third study we examined the replication-coupled transcription of HSV-1 late genes, which are known to depend on DNA replication for efficient expression. Using chromatin immuno-precipitation we could determine that recruitment of RNA polymerase II to late gene promoters occur even in the absence of replication. Recruitment was dependent on ICP4, but delayed in comparison with early gene promoters. These observations suggested the involvement of transcription elongation and/or maturation in the expression of gamma genes. By using the drug DRB, which inhibits the kinase CDK9, a component of the positive transcription elongation factor B, and siRNA against Spt5, a transcription processivity factor, we could show a specific impairment of late gene expression, with only minimal effect on early gene expression and DNA synthesis. We suggest that CDK9 and Spt5 are specifically recruited to replicated late genes and…

Subjects/Keywords: Herpes Simplex Virus 1; DNA replication; DNA recombination; Transcription

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tang, K. (2015). Herpes Simplex Virus 1 DNA replication and its role in recombination and transcription. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/40883

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tang, Ka-Wei. “Herpes Simplex Virus 1 DNA replication and its role in recombination and transcription.” 2015. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 24, 2021. http://hdl.handle.net/2077/40883.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tang, Ka-Wei. “Herpes Simplex Virus 1 DNA replication and its role in recombination and transcription.” 2015. Web. 24 Jan 2021.

Vancouver:

Tang K. Herpes Simplex Virus 1 DNA replication and its role in recombination and transcription. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2015. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2077/40883.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tang K. Herpes Simplex Virus 1 DNA replication and its role in recombination and transcription. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2015. Available from: http://hdl.handle.net/2077/40883

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

9. Zhao, Zhiyuan. Molecular aspects on Herpes simplex virus type 1 DNA replication and gene expression.

Degree: 2017, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/53912

► Herpesviruses infect a variety of animals from molluscs to humans and they have evolved in a close relationship with their hosts. In humans, we find… (more)

▼ Herpesviruses infect a variety of animals from molluscs to humans and they have evolved in a close relationship with their hosts. In humans, we find nine herpesviruses, representing all three subfamilies of the family Herpesviridae and they can cause a variety of symptoms. The viruses have evolved independently, but they have all kept a conserved molecular machinery for the replication of their genomes. We have been studying the protein interactions within the molecular machinery of herpes simplex virus I (HSV-1), to gain further insight into the molecular mechanism of how the virus replicates and maintains its genome. In addition, we have been investigating the molecular requirements for the expression of the HSV-1 DNA replication-dependent late genes. We expect that detailed knowledge of these molecular events will help the development of new antiviral therapies, and perhaps also promote the understanding of related events in our own cells. In this thesis, we have shown that the interactions between the seven viral proteins, which are essential for the HSV-1 DNA replication, are species-specific. The proteins cannot be substituted with homologs from a closely related virus, Equine herpesvirus 1. This observation suggests that the seven replication proteins function as a molecular machinery unit, a replisome, which is characterized by numerous protein-protein interactions. Additionally, we have identified important amino acids in an enzymatically inactive protein, UL8, in the HSV-1 helicase-primase complex, which is required for its interaction with the primase component, UL52, in the complex. Mutations of these amino acids in UL8 impaired their interaction and reduced or abolished the DNA replication capacity of the HSV-1 replisome at the non-permissive temperature. Next, we examined the interactions between UL52 of the HSV-1 helicase-primase complex and other replication proteins. We found that UL52 consisted of different domains, and that the domains had different interaction partners. Stable interactions were detected between the N-terminal domain of UL52 and the helicase component, UL5, while the middle domain showed stable interactions with UL8. We could only detect a relative weak association between UL5 and the C-terminal domain of UL52, which may suggest the existence of a transient interaction. Furthermore, a new group of drugs against HSV infection targets the helicase-primase complex, but their inhibitory action was unknown. We have now demonstrated that these drugs inhibit HSV-1 DNA replication by affecting the interaction between UL5 and UL52. We suggest that the drugs lock these proteins in a certain conformation, preventing them from assisting in viral DNA replication. In addition to its interaction within the helicase-primase complex, the middle domain of UL52 also exhibited stable interaction with HSV-1 single-strand DNA binding protein, UL29/ICP8. The interaction between these two proteins may indicate how the helicase-primase complex is loaded onto the activated origins of replication in…

Subjects/Keywords: Herpes simplex virus type 1; DNA replication; gene expression

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhao, Z. (2017). Molecular aspects on Herpes simplex virus type 1 DNA replication and gene expression. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/53912

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhao, Zhiyuan. “Molecular aspects on Herpes simplex virus type 1 DNA replication and gene expression.” 2017. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 24, 2021. http://hdl.handle.net/2077/53912.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhao, Zhiyuan. “Molecular aspects on Herpes simplex virus type 1 DNA replication and gene expression.” 2017. Web. 24 Jan 2021.

Vancouver:

Zhao Z. Molecular aspects on Herpes simplex virus type 1 DNA replication and gene expression. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2017. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2077/53912.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhao Z. Molecular aspects on Herpes simplex virus type 1 DNA replication and gene expression. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2017. Available from: http://hdl.handle.net/2077/53912

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

10. Sanders, Leon. A Cell-type Dependent Growth Defect in HSV-1 ICP27 Mutants.

Degree: MS, Microbiology, Immunology and Cancer Biology, 2015, University of Minnesota

URL: http://hdl.handle.net/11299/174836

► Herpes simplex virus type 1 (HSV-1) is a common human herpesvirus that has a sero-prevalence between 70-80% in the adult population and can lead to… (more)

Subjects/Keywords: Growth Defect; Herpes Simplex Virus; HSV-1; ICP27; Replication Deficient; Vero

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sanders, L. (2015). A Cell-type Dependent Growth Defect in HSV-1 ICP27 Mutants. (Masters Thesis). University of Minnesota. Retrieved from http://hdl.handle.net/11299/174836

Chicago Manual of Style (16^th Edition):

Sanders, Leon. “A Cell-type Dependent Growth Defect in HSV-1 ICP27 Mutants.” 2015. Masters Thesis, University of Minnesota. Accessed January 24, 2021. http://hdl.handle.net/11299/174836.

MLA Handbook (7^th Edition):

Sanders, Leon. “A Cell-type Dependent Growth Defect in HSV-1 ICP27 Mutants.” 2015. Web. 24 Jan 2021.

Vancouver:

Sanders L. A Cell-type Dependent Growth Defect in HSV-1 ICP27 Mutants. [Internet] [Masters thesis]. University of Minnesota; 2015. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/11299/174836.

Council of Science Editors:

Sanders L. A Cell-type Dependent Growth Defect in HSV-1 ICP27 Mutants. [Masters Thesis]. University of Minnesota; 2015. Available from: http://hdl.handle.net/11299/174836

11. Gross, Sylvain. Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1 : Study of the protein and chromatin structures destabilization of centromeres by the herpes simplex virus type 1 protein ICP0.

Degree: Docteur es, Biologie moléculaire et cellulaire, virologie, 2011, Université Claude Bernard – Lyon I

URL: http://www.theses.fr/2011LYO10238

►

Le virus Herpes Simplex de type 1 (HSV-1) possède un mode d’infection particulier dit bimodal. Il peut soit se répliquer de manière active lors d’une… (more)

▼

Le virus Herpes Simplex de type 1 (HSV-1) possède un mode d’infection particulier dit bimodal. Il peut soit se répliquer de manière active lors d’une phase dite lytique soit migrer dans les neurones et rester en latence. Il peut réactiver pour rétablir une infection lytique. Une protéine virale majeure dans la réactivation de HSV-1 est ICP0. C’est une protéine nucléaire à activité E3 ubiquitine ligase, qui possède la particularité d’induire la dégradation par le protéasome de plusieurs protéines centromériques constitutives, ce qui provoque une déstabilisation du centromère interphasique. Mon équipe a découvert une réponse cellulaire à l’instabilité centromérique, induite par la protéine ICP0, et nommée iCDR (pour interphase Centromere Damage Response.). L’objectif général de ma thèse est de déterminer les modifications structurales que subissent les centromères endommagés par ICP0 à l’origine de l’iCDR et probablement de la réactivation. J’ai pu démontrer qu’ICP0 affectait toute la structure protéique étroitement associée aux centromères durant l’interphase. Suite à ces résultats, j’ai pu démontrer, par des analyses de digestion de chromatine à la nucléase microccocale (MNAse), que l’occupation nucléosomique de la chromatine centromérique suite à l’activité d’ICP0 était affectée de façon significative. Une étude in vivo effectuée à partir de tissus nerveux provenant de souris infectées de manière latente, a permis de démontrer une co-localisation entre les génomes HSV-1 latents et les centromères. Cette co-localisation est associée à une répression transcriptionnelle du virus. Les résultats de ma thèse montrent donc que les effets d’ICP0 sur la déstabilisation des centromères sont en relation avec un rôle de ces centromères durant la latence. Ceci suggère fortement une implication de la déstabilisation des centromères dans le processus de réactivation contrôlé par ICP0.

The Herpes Simplex type 1 (HSV-1) virus possesses a bimodal mode of infection. It can either replicates in an active way during the lytic cycle, or it can infect neurons and stay in latency. HSV-1 reactivates from latently infected neurons for re-establishing a lytic infection. A major viral protein implicated in reactivation is ICP0. It is a nuclear E3 ubiquitin-ligase, which has the particularity to induce the proteasome-mediated degradation of several constitutive centromeric proteins. This activity severely destabilizes the interphase centromere. My team has discovered a novel cellular response triggered by the estabilization of centromeres by ICP0, called iCDR (interphase Centromere Damage Response). The general aim of my thesis is to determine the centromere structural modifications induced by ICP0 that can trigger the iCDR and probably the reactivation. I was able to demonstrate that ICP0 affected the entire proteinacious structure of interphase centromeres. Following this, I showed by micrococcal nuclease (MNase) digestion approach that the nucleosomal organization of centromeric chromatin was significantly affected by ICP0. An in vivo…

Advisors/Committee Members: Lomonte, Patrick (thesis director).

Subjects/Keywords: Virus Herpes Simplex de type 1 (HSV-1); ICP0; Protéines centromériques; Centromère; Chromatine; Herpes Simplex Type 1 (HSV-1)virus; ICP0; Centromeric proteins; Centromere; Chromatin; 571.6

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gross, S. (2011). Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1 : Study of the protein and chromatin structures destabilization of centromeres by the herpes simplex virus type 1 protein ICP0. (Doctoral Dissertation). Université Claude Bernard – Lyon I. Retrieved from http://www.theses.fr/2011LYO10238

Chicago Manual of Style (16^th Edition):

Gross, Sylvain. “Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1 : Study of the protein and chromatin structures destabilization of centromeres by the herpes simplex virus type 1 protein ICP0.” 2011. Doctoral Dissertation, Université Claude Bernard – Lyon I. Accessed January 24, 2021. http://www.theses.fr/2011LYO10238.

MLA Handbook (7^th Edition):

Gross, Sylvain. “Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1 : Study of the protein and chromatin structures destabilization of centromeres by the herpes simplex virus type 1 protein ICP0.” 2011. Web. 24 Jan 2021.

Vancouver:

Gross S. Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1 : Study of the protein and chromatin structures destabilization of centromeres by the herpes simplex virus type 1 protein ICP0. [Internet] [Doctoral dissertation]. Université Claude Bernard – Lyon I; 2011. [cited 2021 Jan 24]. Available from: http://www.theses.fr/2011LYO10238.

Council of Science Editors:

Gross S. Etude de la déstabilisation des structures protéique et chromatinienne des centromères par la protéine ICP0 du virus Herpes Simplex de Type 1 : Study of the protein and chromatin structures destabilization of centromeres by the herpes simplex virus type 1 protein ICP0. [Doctoral Dissertation]. Université Claude Bernard – Lyon I; 2011. Available from: http://www.theses.fr/2011LYO10238

12. Okuda, Osmar Shizuo. Detecção do herpes simples vírus, citomegalovírus, Epstein-Barr vírus e bactérias periodontopatogênicas em bolsas periodontais de pacientes com periodontite crônica e gengivite.

Degree: Mestrado, Periodontia, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/23/23146/tde-02022010-085806/ ;

►

Recentemente, estudos têm associado a presença de vírus da família herpesviridae à doença periodontal, os quais poderiam estar envolvidos na ocorrência e progressão de diferentes… (more)

▼

Recentemente, estudos têm associado a presença de vírus da família herpesviridae à doença periodontal, os quais poderiam estar envolvidos na ocorrência e progressão de diferentes formas da doença periodontal, através da supressão do sistema imune do periodonto, liberação de citotoxinas, mediadores pró-inflamatórios, o que poderia favorecer o crescimento subgengival de microrganismos. Neste estudo, testamos a hipótese de que a prevalência do herpes vírus na placa subgengival de pacientes com gengivite é igual a de pacientes portadores de periodontite crônica. Desse modo, o presente estudo teve como objetivo determinar a presença dos vírus Herpes simples vírus tipo 1 (HSV-1), Citomegalovírus (HCMV) e Epstein-Barr vírus tipo 1 (EBV-1), relacionando-os com a presença de bactérias periodontopatogênicas como: Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Tannerella forsythia (Tf) e Dialister pneumosintes (Dp) em amostras de placa subgengival, coletadas de 30 pacientes portadores de periodontite crônica (grupo PC), 30 pacientes com gengivite (grupo G) e 30 indivíduos periodontalmente saudáveis (grupo C). Foram coletadas quatro amostras de placa subgengival do sítio mais profundo de cada quadrante nos pacientes do grupo PC e nos pacientes do grupo G e C, um sítio aleatório de cada quadrante foi examinado. A detecção de espécies bacterianas e de herpes vírus na placa subgengival dos grupos foi realizada por PCR e Nested PCR, respectivamente. A análise estatística mostrou que o HCMV foi detectado com freqüência similar nos três grupos estudados e que houve uma maior prevalência do HSV-1, EBV-1 e P. intermedia nos pacientes com periodonite crônica e gengivite em relação ao grupo controle. Houve associação da periodontite crônica com o EBV-1 e as cinco bactérias estudadas, além da associação entre os vírus (EBV-1+ HCMV; EBV-1 + HSV-1; HSV-1 + HCMV) e entre vírus e bactérias (EBV-1+ P.intermedia, EBV-1 + P. gingivalis; HCMV + T. forsythia; HCMV + A. actinomycetemcomitans; HSV-1 + T. forsythia; HSV-1 + P. gingivalis).

Recently, studies have linked the presence of the virus family herpesviridae and periodontal disease, which may be involved in the occurrence and progression of different forms of periodontal disease through the suppression of the immune system of the periodontium, release of cytotoxins, pro-inflammatory mediators and immunopathological events, may promote growth of subgingival microorganisms. In this study, we tested the hypothesis that the prevalence of herpes virus in sub-gingival plaque of patients with gingivitis is equal to patients with chronic periodontitis. Thus, this study aimed to determine the presence of the virus Herpes simplex virus type 1 (HSV-1), Cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1), relating to the presence of bacteria as periodontopathogens: Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Tannerella forsythia (Tf) and Dialister pneumosintes (Dp) in subgingival…

Advisors/Committee Members: Lima, Luiz Antonio Pugliesi Alves de.

Subjects/Keywords: Chronic periodontitis; EBV-1; EBV-1; HCMV; HCMV; Herpes virus; Herpes vírus; HSV-1; HSV-1; PCR; PCR; Periodontite crônica; Periodontopathogens; Periodontopatógenos

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Okuda, O. S. (2009). Detecção do herpes simples vírus, citomegalovírus, Epstein-Barr vírus e bactérias periodontopatogênicas em bolsas periodontais de pacientes com periodontite crônica e gengivite. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/23/23146/tde-02022010-085806/ ;

Chicago Manual of Style (16^th Edition):

Okuda, Osmar Shizuo. “Detecção do herpes simples vírus, citomegalovírus, Epstein-Barr vírus e bactérias periodontopatogênicas em bolsas periodontais de pacientes com periodontite crônica e gengivite.” 2009. Masters Thesis, University of São Paulo. Accessed January 24, 2021. http://www.teses.usp.br/teses/disponiveis/23/23146/tde-02022010-085806/ ;.

MLA Handbook (7^th Edition):

Okuda, Osmar Shizuo. “Detecção do herpes simples vírus, citomegalovírus, Epstein-Barr vírus e bactérias periodontopatogênicas em bolsas periodontais de pacientes com periodontite crônica e gengivite.” 2009. Web. 24 Jan 2021.

Vancouver:

Okuda OS. Detecção do herpes simples vírus, citomegalovírus, Epstein-Barr vírus e bactérias periodontopatogênicas em bolsas periodontais de pacientes com periodontite crônica e gengivite. [Internet] [Masters thesis]. University of São Paulo; 2009. [cited 2021 Jan 24]. Available from: http://www.teses.usp.br/teses/disponiveis/23/23146/tde-02022010-085806/ ;.

Council of Science Editors:

Okuda OS. Detecção do herpes simples vírus, citomegalovírus, Epstein-Barr vírus e bactérias periodontopatogênicas em bolsas periodontais de pacientes com periodontite crônica e gengivite. [Masters Thesis]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/23/23146/tde-02022010-085806/ ;

Wright State University

13. Alhazmi, Amani Mohammed. The Response of M0, M1, and M2 RAW246.7 Macrophage Cell Line to HSV-1 Infection in vitro.

Degree: MS, Microbiology and Immunology, 2019, Wright State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=wright1557759403892368

► Herpes Simplex Virus Type 1 (HSV-1) infection occurs through the epithelial cells of the skin or mucous membranes. The beginning of the primary infection is… (more)

▼ Herpes Simplex Virus Type 1 (HSV-1) infection occurs through the epithelial cells of the skin or mucous membranes. The beginning of the primary infection is rapid and is characterized by pain in the mouth, salivation, and submandibular lymphadenitis. The infected mucosa produces numerous, small and red lesions known as cold sores, however, many cases are asymptomatic. After the primary infection HSV-1 moves through the nerve to stay in trigeminal ganglia and to cause a recurrent infection from time to time. In the early hours of the HSV-1 infection, the cytokines produced by infected cells are critical in the stimulation of the innate immune response to the infection. One of the innate immune cells responded to the infected cells is macrophages. So, macrophage recruitment and differentiation are essential for effective control and clearance of viral infections.To mimic the in vivo role of three types of macrophages against HSV-1 infected epithelial cells (PAM 212), M0, M1, or M2 RAW246.7 macrophages were added at 2 and 4 hours after an initial established infection. These times were selected to represent the influx of macrophages to the infection site within the first few hours of exposure to HSV-1 virus. In all experiments, we performed cell viabilities and virus titers at 24, 48, and 72 hours after the initial infection. After the HSV-1 infection, a morphological change was observed among all types of macrophages where most of it appeared round and granulated. This change makes it challenging to differentiate M1 from M0 or M2. Importantly, all phenotype of macrophages showed an essential role against the HSV-1 replication in PAM-212 keratinocytes. However, the addition of M1 Macrophages to HSV-1 infected PAM212 keratinocytes significantly decreased the percentage of the viable cells by more than 80% and restricted the HSV-1 replication more effectively than M0 and M2 macrophages. The virus replication pattern was similar in a different type of M2 macrophages (M2 a and M2 c) which was low at 24 h, then increased significantly 48 hpi then decreased significantly 72 hpi. Advisors/Committee Members: Bigley, Nancy J. (Advisor).

Subjects/Keywords: Immunology; Herpes Simplex Virus Type 1; HSV-1; HSV-1 infection; macrophage; macrophage recruitment; macrophage differentiation

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APA (6^th Edition):

Alhazmi, A. M. (2019). The Response of M0, M1, and M2 RAW246.7 Macrophage Cell Line to HSV-1 Infection in vitro. (Masters Thesis). Wright State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=wright1557759403892368

Chicago Manual of Style (16^th Edition):

Alhazmi, Amani Mohammed. “The Response of M0, M1, and M2 RAW246.7 Macrophage Cell Line to HSV-1 Infection in vitro.” 2019. Masters Thesis, Wright State University. Accessed January 24, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1557759403892368.

MLA Handbook (7^th Edition):

Alhazmi, Amani Mohammed. “The Response of M0, M1, and M2 RAW246.7 Macrophage Cell Line to HSV-1 Infection in vitro.” 2019. Web. 24 Jan 2021.

Vancouver:

Alhazmi AM. The Response of M0, M1, and M2 RAW246.7 Macrophage Cell Line to HSV-1 Infection in vitro. [Internet] [Masters thesis]. Wright State University; 2019. [cited 2021 Jan 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1557759403892368.

Council of Science Editors:

Alhazmi AM. The Response of M0, M1, and M2 RAW246.7 Macrophage Cell Line to HSV-1 Infection in vitro. [Masters Thesis]. Wright State University; 2019. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1557759403892368

University of Manitoba

14. Berard, Alicia. Global quantitative host proteomic assay of infected cells highlight virus specific protein changes and identify a novel role for secretogranin ii protein in virus infections.

Degree: Medical Microbiology, 2012, University of Manitoba

URL: http://hdl.handle.net/1993/30717

► Viruses are obligate parasites that use the host cellular machinery to produce progeny virions. The host responds to this invading pathogen by induction of the… (more)

▼ Viruses are obligate parasites that use the host cellular machinery to produce progeny virions. The host responds to this invading pathogen by induction of the immune system; however, the virus employs a variety of strategies to overcome these attacks. The complexity of the virus-host interaction is of great interest to researchers with aims to both characterize the relationship and target steps of the viral life cycle to hinder infection. Many targeted tactics employ single protein analysis; however, approaches that examine the whole set of virus/host interactions are available. Transcriptional alterations within host cells have been determined for many virus- host interactions by micro-array techniques; however little is known about the effects on cellular proteins. This study uses a quantitative mass spectrometric-based method, SILAC, to study differences in a host cell's proteome with infection by a virus. Mammalian reoviruses and herpes simplex viruses are prototypical viruses commonly studied to determine virus life cycle and interactions with hosts. Using three strains of reoviruses and one HSV1 strain, cells were infected to identify differentially regulated proteins at different times. Thousands of proteins were identified for each virus type, some up or down regulated after infection. Biological functions and network analyses were performed using online networking tools. These pathway analyses indicated numerous processes including cell death and inflammatory response are affected by T1L reovirus infection. Comparing reovirus strains revealed a greater overall proteomic change in host function when infected with the more pathogenic T3DC strain. For the HSV infection, host proteins altered during the different immediate early, earlyand late phases of infection helped characterize the host-virus interaction parallel to the virus life cycle. Overall, my study has characterized proteomic changes in different virus infection systems, identifying numerous novel cellular functional pathways and specific proteins altered during virus infections, specifically the secretogranin II protein that had opposite types of regulation in reoviruses and HSV and was examined for its effects on virus replication. Further studies on the novel proteomic characteristics may provide greater understanding to the complex virus-host interactome, leading to possible antiviral targets. Advisors/Committee Members: Severini, Alberto (Medical Microbiology) Coombs, Kevin (Medical Microbiology) (supervisor), Wilkins, John (Biochemistry & Medical Genetics) Feldmann, Heinz (Medical Microbiology).

Subjects/Keywords: SILAC; Reovirus; Herpes simplex virus 1; Proteomics; Host-virus relationship; Cell biology; Mass spectrometry; Systems biology

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APA (6^th Edition):

Berard, A. (2012). Global quantitative host proteomic assay of infected cells highlight virus specific protein changes and identify a novel role for secretogranin ii protein in virus infections. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/30717

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Berard, Alicia. “Global quantitative host proteomic assay of infected cells highlight virus specific protein changes and identify a novel role for secretogranin ii protein in virus infections.” 2012. Thesis, University of Manitoba. Accessed January 24, 2021. http://hdl.handle.net/1993/30717.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Berard, Alicia. “Global quantitative host proteomic assay of infected cells highlight virus specific protein changes and identify a novel role for secretogranin ii protein in virus infections.” 2012. Web. 24 Jan 2021.

Vancouver:

Berard A. Global quantitative host proteomic assay of infected cells highlight virus specific protein changes and identify a novel role for secretogranin ii protein in virus infections. [Internet] [Thesis]. University of Manitoba; 2012. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1993/30717.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Berard A. Global quantitative host proteomic assay of infected cells highlight virus specific protein changes and identify a novel role for secretogranin ii protein in virus infections. [Thesis]. University of Manitoba; 2012. Available from: http://hdl.handle.net/1993/30717

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

15. Ren, Yudan. Glycoprotein M and ESCRT in herpes simplex virus type 1 assembly.

Degree: PhD, 2012, University of Cambridge

URL: http://www.dspace.cam.ac.uk/handle/1810/241516https://www.repository.cam.ac.uk/bitstream/1810/241516/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/3/license_url ; https://www.repository.cam.ac.uk/bitstream/1810/241516/4/license_text ; https://www.repository.cam.ac.uk/bitstream/1810/241516/5/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/241516/8/PhD_Ren2011.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/9/PhD_Ren2011.pdf.jpg

► Herpes simplex virus type 1 (HSV-1) has a large linear double-stranded DNA genome in an icosahedral capsid shell, a cell-derived lipid envelope and a proteinaceous… (more)

▼ Herpes simplex virus type 1 (HSV-1) has a large linear double-stranded DNA genome in an icosahedral capsid shell, a cell-derived lipid envelope and a proteinaceous tegument layer. There are over fifty viral proteins and many host proteins identified in HSV-1 virions. The final formation of mature virus particles requires the membrane wrapping of tegumented capsids in the cytoplasm, a process termed secondary envelopment. This process involves the coordination of numerous viral and cellular proteins and results in double-membrane structures with enveloped virions contained within cellular vesicles. Mature viruses are then released through the fusion of these virion-containing vesicles and plasma membranes. This thesis describes investigation into the functions of viral glycoprotein M (gM) and the cellular Endosomal Sorting Complexes Required for Transport (ESCRT) in secondary envelopment. Firstly, it has been reported that gH/L can be efficiently internalised and targeted to the TGN by the co-expression of gM in transfection assays. In order to examine the role of gM in guiding the localisation of viral proteins in infected cells, a HSV-1 gM deletion virus (∆gM), and its revertant virus were constructed. The major phenotype demonstrated was that the absence of gM caused the internalisation of cell surface gH/L to be inhibited and higher levels of gH/L to be observed on the cell surface. Further, lower levels of gH/L were detected in purified ∆gM virions, which was in agreement with the delayed entry kinetics, smaller plaque sizes and greater replication deficits at low multiplicity of infection observed in ∆gM infected cells. Over all the results presented in this thesis demonstrate that in infected cells the efficient incorporation of gH/L into virions relies on the function of gM in HSV-1. Secondly, during HSV-1 secondary envelopment the budding and scission of the viral envelope from the host membrane share topological similarities with the formation of intraluminal vesicle in multivesicular bodies, retrovirus budding, and abscission at the end of cytokinesis, processes that require the cellular ESCRT machinery. There are four multiprotein ESCRT complexes and many associated proteins involved in their regulation. It has been previously shown that the ESCRT-III complex and a functional ATPase VPS4 are required for HSV-1 secondary envelopment, but different from the strategy utilised by HIV-1, the recruitment of ESCRT during HSV-1 infection is independent of TSG101 and/or ALIX. Data presented in this thesis demonstrate that CHMP4A/B/C proteins of the ESCRT-III complex are specifically crucial for HSV-1 secondary envelopment. Simultaneous depletion of CHMP4A/B/C proteins significantly inhibited HSV-1 replication. Ultrastructure analysis revealed that there were virtually no extracellular virions in CHMP4A/B/C depleted samples while more free capsids were observed in the cytoplasm, although the nuclear capsids and primary envelopment events appeared to be normal. In order to identify interactions between HSV-1 and…

Subjects/Keywords: Herpes simplex virus type 1 (HSV-1); Tegument; Assembly; Glycoprotein M; Endosomal sorting complexes required for transport (ESCRT); Viral-host interaction

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APA (6^th Edition):

Ren, Y. (2012). Glycoprotein M and ESCRT in herpes simplex virus type 1 assembly. (Doctoral Dissertation). University of Cambridge. Retrieved from http://www.dspace.cam.ac.uk/handle/1810/241516https://www.repository.cam.ac.uk/bitstream/1810/241516/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/3/license_url ; https://www.repository.cam.ac.uk/bitstream/1810/241516/4/license_text ; https://www.repository.cam.ac.uk/bitstream/1810/241516/5/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/241516/8/PhD_Ren2011.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/9/PhD_Ren2011.pdf.jpg

Chicago Manual of Style (16^th Edition):

Ren, Yudan. “Glycoprotein M and ESCRT in herpes simplex virus type 1 assembly.” 2012. Doctoral Dissertation, University of Cambridge. Accessed January 24, 2021. http://www.dspace.cam.ac.uk/handle/1810/241516https://www.repository.cam.ac.uk/bitstream/1810/241516/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/3/license_url ; https://www.repository.cam.ac.uk/bitstream/1810/241516/4/license_text ; https://www.repository.cam.ac.uk/bitstream/1810/241516/5/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/241516/8/PhD_Ren2011.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/9/PhD_Ren2011.pdf.jpg.

MLA Handbook (7^th Edition):

Ren, Yudan. “Glycoprotein M and ESCRT in herpes simplex virus type 1 assembly.” 2012. Web. 24 Jan 2021.

Vancouver:

Ren Y. Glycoprotein M and ESCRT in herpes simplex virus type 1 assembly. [Internet] [Doctoral dissertation]. University of Cambridge; 2012. [cited 2021 Jan 24]. Available from: http://www.dspace.cam.ac.uk/handle/1810/241516https://www.repository.cam.ac.uk/bitstream/1810/241516/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/3/license_url ; https://www.repository.cam.ac.uk/bitstream/1810/241516/4/license_text ; https://www.repository.cam.ac.uk/bitstream/1810/241516/5/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/241516/8/PhD_Ren2011.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/9/PhD_Ren2011.pdf.jpg.

Council of Science Editors:

Ren Y. Glycoprotein M and ESCRT in herpes simplex virus type 1 assembly. [Doctoral Dissertation]. University of Cambridge; 2012. Available from: http://www.dspace.cam.ac.uk/handle/1810/241516https://www.repository.cam.ac.uk/bitstream/1810/241516/2/license.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/3/license_url ; https://www.repository.cam.ac.uk/bitstream/1810/241516/4/license_text ; https://www.repository.cam.ac.uk/bitstream/1810/241516/5/license_rdf ; https://www.repository.cam.ac.uk/bitstream/1810/241516/8/PhD_Ren2011.pdf.txt ; https://www.repository.cam.ac.uk/bitstream/1810/241516/9/PhD_Ren2011.pdf.jpg

Georgia State University

16. Brock, Nicole. Host-specific Plasmacytoid Dendritic Cell Defenses In The Presence of Human and Macaque Skin Cells Infected with B virus.

Degree: PhD, Biology, 2014, Georgia State University

URL: https://scholarworks.gsu.edu/biology_diss/139

► Plasmacytoid dendritic cells (pDC) are a specialized group of circulating dendritic cells that respond to viral nucleic acids with Type I IFN production as… (more)

▼ Plasmacytoid dendritic cells (pDC) are a specialized group of circulating dendritic cells that respond to viral nucleic acids with Type I IFN production as well as other cytokine and chemokines. These pDC responses lead to the production of antiviral molecules and recruitment of defense cells. During zoonotic B virus infection, a simplex virus of the subfamily Alphaherpesviridae, our lab has observed that infected individuals who succumb to infection have little-to-no-antibody or cell-mediated defenses. To identify whether this was partly due to failure of pDCs to produce antiviral interferon responses or produce chemokine and cytokines, we tested the hypothesis that B virus modulates the IFN response during zoonotic infection by blocking pDC activation and subsequent IFN signaling pathways to circumvent host defenses, while these pathways remain intact in the macaque hosts. We showed that human pDCs respond to B virus through the production of IFN-a, IL-1a, IL-6, TNF-a, MIP-1a/b and IP-10. Human pDCs co-cultured with B virus infected fibroblasts produced fewer cytokines and at lower levels. The macaque response to B virus was measured using PBMCs, as there are no specific reagents available to enrich macaque pDCs. Human and macaque PBMCs produced IFN-a when exposed directly to B virus infected lysates. Co-cultures of PBMCs with B virus infected fibroblasts from both hosts failed to produce any significant amounts of IFN-a. To quantify the antiviral effects of PBMC induced IFN-a, we measured B virus titers after exposure to supernatants from B virus exposed PBMCs, PBMC co-cultures with infected fibroblasts and exogenous recombinant Type I IFN. Our data further suggest that B virus resistance was not due to virus specific blockade of the Type I IFN signaling pathway because STAT-1 was activated in infected fibroblasts when treated with Type I IFNs. These data demonstrate for the first time that B virus replication is unimpeded in the presence of any source of IFN-a in either host cell type. In conclusion, this dissertation shows that the IFN-a production by both hosts in response to B virus is similar and that IFN-a treatment of B virus infected fibroblasts did not reduce B virus replication. Advisors/Committee Members: Julia Hilliard, Richard Dix, Yuan Liu.

Subjects/Keywords: Plasmacytoid dendritic cells; Interferon; Fibroblasts; Macaque; Herpes B virus; Macacine herpesvirus 1; STAT-1; Innate immunity

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APA (6^th Edition):

Brock, N. (2014). Host-specific Plasmacytoid Dendritic Cell Defenses In The Presence of Human and Macaque Skin Cells Infected with B virus. (Doctoral Dissertation). Georgia State University. Retrieved from https://scholarworks.gsu.edu/biology_diss/139

Chicago Manual of Style (16^th Edition):

Brock, Nicole. “Host-specific Plasmacytoid Dendritic Cell Defenses In The Presence of Human and Macaque Skin Cells Infected with B virus.” 2014. Doctoral Dissertation, Georgia State University. Accessed January 24, 2021. https://scholarworks.gsu.edu/biology_diss/139.

MLA Handbook (7^th Edition):

Brock, Nicole. “Host-specific Plasmacytoid Dendritic Cell Defenses In The Presence of Human and Macaque Skin Cells Infected with B virus.” 2014. Web. 24 Jan 2021.

Vancouver:

Brock N. Host-specific Plasmacytoid Dendritic Cell Defenses In The Presence of Human and Macaque Skin Cells Infected with B virus. [Internet] [Doctoral dissertation]. Georgia State University; 2014. [cited 2021 Jan 24]. Available from: https://scholarworks.gsu.edu/biology_diss/139.

Council of Science Editors:

Brock N. Host-specific Plasmacytoid Dendritic Cell Defenses In The Presence of Human and Macaque Skin Cells Infected with B virus. [Doctoral Dissertation]. Georgia State University; 2014. Available from: https://scholarworks.gsu.edu/biology_diss/139

University of Zambia

17. Tembo, Rabecca. Detection of Human Herpes Virus-8 in Kaposi's Sarcoma tissues at the University Teaching Hospital, Lusaka .

Degree: 2015, University of Zambia

URL: http://hdl.handle.net/123456789/4195

► Background: Human herpes virus-8, a 2-herpesvirus, is the aetiological agent of Kaposi‘s sarcoma. Recently, there has been an increase in kaposi‘s sarcoma cases in Zambia… (more)

Subjects/Keywords: Herpes virus-8; Kaposi's Sarcoma

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APA (6^th Edition):

Tembo, R. (2015). Detection of Human Herpes Virus-8 in Kaposi's Sarcoma tissues at the University Teaching Hospital, Lusaka . (Thesis). University of Zambia. Retrieved from http://hdl.handle.net/123456789/4195

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tembo, Rabecca. “Detection of Human Herpes Virus-8 in Kaposi's Sarcoma tissues at the University Teaching Hospital, Lusaka .” 2015. Thesis, University of Zambia. Accessed January 24, 2021. http://hdl.handle.net/123456789/4195.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tembo, Rabecca. “Detection of Human Herpes Virus-8 in Kaposi's Sarcoma tissues at the University Teaching Hospital, Lusaka .” 2015. Web. 24 Jan 2021.

Vancouver:

Tembo R. Detection of Human Herpes Virus-8 in Kaposi's Sarcoma tissues at the University Teaching Hospital, Lusaka . [Internet] [Thesis]. University of Zambia; 2015. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/123456789/4195.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tembo R. Detection of Human Herpes Virus-8 in Kaposi's Sarcoma tissues at the University Teaching Hospital, Lusaka . [Thesis]. University of Zambia; 2015. Available from: http://hdl.handle.net/123456789/4195

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Alberta

18. Conn, Kristen Lea. Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection.

Degree: PhD, Department of Biochemistry, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/6t053g31z

► Herpes simplex virus type 1 (HSV-1) genomes associate with histones in unstable nucleosomes during lytic infections. Nucleosome core particles are 146 base pairs of DNA… (more)

▼ Herpes simplex virus type 1 (HSV-1) genomes associate with histones in unstable nucleosomes during lytic infections. Nucleosome core particles are 146 base pairs of DNA wrapped around a histone octamer of two molecules of each H2A, H2B, H3, and H4. Histone H1 binds to nucleosomes at DNA entry and exit points. Association with histones is proposed to regulate HSV-1 gene expression. Consistently, HSV-1 transcription transactivators disrupt chromatin and HSV-1 strains mutant in these transactivators are replication impaired or transcriptionally inactive. HSV-1 genomes have dynamic associations with histones. The genomes are not associated with histones in capsids, and input genomes are delivered to nuclear domains depleted of histones. Later during infection, HSV-1 genomes again occupy nuclear domains depleted of histones. Histone synthesis is inhibited during infection and the total level of nuclear histones remains relatively constant. It is therefore unlikely that the histones that first bind to HSV-1 genomes are newly synthesized. The source of the histones that associate with HSV-1 genomes has yet to be addressed. Histones in cellular chromatin normally disassociate, diffuse through the nucleus, and re-associate at different sites. I propose that histones are mobilized from domains of cellular chromatin to those domains containing HSV-1 genomes in cellular attempts to silence HSV-1 gene expression. I additionally propose that HSV-1 further mobilizes histones to counteract such silencing attempts. My hypothesis is that histones are mobilized during HSV-1 infection. In this thesis, I show that linker and core histones are mobilized during HSV-1 infection. Such mobilization results in increases to their “free” (not bound to chromatin) pools. Linker and core histones were mobilized even when HSV-1 proteins were not expressed, mobilization that likely reflects cellular responses to infection. Histone mobilization was enhanced when HSV-1 IE or E proteins were expressed. This enhanced mobilization was independent of HSV-1 DNA replication and late proteins. Core histones H2B and H3.3 were differentially mobilized, suggesting that different mechanisms may mobilize histones during HSV-1 infection. My discovery of histone mobilization reveals a novel consequence of cell-virus interactions that addresses a previously unexplained aspect of HSV-1 infection.

Subjects/Keywords: histones; herpes simplex virus

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Conn, K. L. (2010). Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/6t053g31z

Chicago Manual of Style (16^th Edition):

Conn, Kristen Lea. “Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection.” 2010. Doctoral Dissertation, University of Alberta. Accessed January 24, 2021. https://era.library.ualberta.ca/files/6t053g31z.

MLA Handbook (7^th Edition):

Conn, Kristen Lea. “Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection.” 2010. Web. 24 Jan 2021.

Vancouver:

Conn KL. Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection. [Internet] [Doctoral dissertation]. University of Alberta; 2010. [cited 2021 Jan 24]. Available from: https://era.library.ualberta.ca/files/6t053g31z.

Council of Science Editors:

Conn KL. Discovery and characterization of the mobilization of linker and core histones during herpes simplex virus type 1 (HSV-1) infection. [Doctoral Dissertation]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/6t053g31z

Univerzitet u Beogradu

19. Martić, Jelena M., 1971-. Kliničke i laboratorijske osobenosti infekcije izazvane Herpes simpleks virusom kod novorođene dece.

Degree: Medicinski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:14002/bdef:Content/get

►

Medicina / Medicine

Cilj rada: analiza kliničkih i laboratorijskih karakteristika novorođenčadi sa infekcijom izazvanom Herpes simpleks virusom (HSV). Procena učestalosti neonatalnog herpesa (NH) u našoj… (more)

Subjects/Keywords: herpes simplex virus; infection; newborn

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APA (6^th Edition):

Martić, Jelena M., 1. (2016). Kliničke i laboratorijske osobenosti infekcije izazvane Herpes simpleks virusom kod novorođene dece. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:14002/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Martić, Jelena M., 1971-. “Kliničke i laboratorijske osobenosti infekcije izazvane Herpes simpleks virusom kod novorođene dece.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 24, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:14002/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Martić, Jelena M., 1971-. “Kliničke i laboratorijske osobenosti infekcije izazvane Herpes simpleks virusom kod novorođene dece.” 2016. Web. 24 Jan 2021.

Vancouver:

Martić, Jelena M. 1. Kliničke i laboratorijske osobenosti infekcije izazvane Herpes simpleks virusom kod novorođene dece. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 24]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:14002/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Martić, Jelena M. 1. Kliničke i laboratorijske osobenosti infekcije izazvane Herpes simpleks virusom kod novorođene dece. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:14002/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Chandranaik, B M. Molecular epidemiology of Bovine Herpes Virus 1 and development of real time PCR based antigen detection kit for diagnosis of Bovine Herpes Virus 1;.

Degree: Veterinary Microbiology, 2012, Karnataka Veterinary, Animal and Fisheries Sciences University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/6958

Included

Summary p. 163-166, Bibliography p. 167-195

Advisors/Committee Members: Rathnamma D.

Subjects/Keywords: Veterinary Sciences; Veterinary Microbiology; Bovine Herpes Virus-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chandranaik, B. M. (2012). Molecular epidemiology of Bovine Herpes Virus 1 and development of real time PCR based antigen detection kit for diagnosis of Bovine Herpes Virus 1;. (Thesis). Karnataka Veterinary, Animal and Fisheries Sciences University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/6958

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chandranaik, B M. “Molecular epidemiology of Bovine Herpes Virus 1 and development of real time PCR based antigen detection kit for diagnosis of Bovine Herpes Virus 1;.” 2012. Thesis, Karnataka Veterinary, Animal and Fisheries Sciences University. Accessed January 24, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/6958.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chandranaik, B M. “Molecular epidemiology of Bovine Herpes Virus 1 and development of real time PCR based antigen detection kit for diagnosis of Bovine Herpes Virus 1;.” 2012. Web. 24 Jan 2021.

Vancouver:

Chandranaik BM. Molecular epidemiology of Bovine Herpes Virus 1 and development of real time PCR based antigen detection kit for diagnosis of Bovine Herpes Virus 1;. [Internet] [Thesis]. Karnataka Veterinary, Animal and Fisheries Sciences University; 2012. [cited 2021 Jan 24]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/6958.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chandranaik BM. Molecular epidemiology of Bovine Herpes Virus 1 and development of real time PCR based antigen detection kit for diagnosis of Bovine Herpes Virus 1;. [Thesis]. Karnataka Veterinary, Animal and Fisheries Sciences University; 2012. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/6958

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Glasgow

21. Kathoria, Meeta. An investigation of the properties and functions of the Herpes Associated Ubiquitin-Specific Protease, HAUSP.

Degree: PhD, 1999, University of Glasgow

URL: http://theses.gla.ac.uk/75383/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284737

► Herpes simplex virus type 1 (HSV-1) is a common human pathogen best known as the causative agent of 'cold sores' around the mouth. It initially… (more)

▼ Herpes simplex virus type 1 (HSV-1) is a common human pathogen best known as the causative agent of 'cold sores' around the mouth. It initially infects cells at the periphery, however it often spreads to the sensory neurones where it establishes life-long latent infection and from which it can be reactivated periodically to cause recurrent episodes of disease. The immediate early (IE) protein Vmw110 of HSV-1 stimulates the onset of lytic infection as well as increases the efficiency of reactivation from latency. As such, it has been proposed that Vmw110 plays an important role in the balance between lytic and latent states of infection. The mechanisms by which Vmw110 functions are poorly defined. However, earlier work in which Vmw110 was shown to migrate to discrete nuclear structures called NDIO, suggested that it exerts much of its effects through interactions with cellular proteins (Everett & Maul, 1994, Gelman & Silverstein, 1985, Maul et al, 1993). Investigations searching for such interactions resulted in the identification of a novel member of the ubiquitin-specific protease (USP) family named HAUSP (herpes- associated-ubiquitin specific protease) which both strongly and specifically interacted with Vmwl 10 (Everett et al., 1997, Meredith et al, 1995, Meredith et al, 1994). Studies described herein were initiated to improve the understanding of the role of HAUSP, both within the cell and for HSV-1 infection. In particular, experiments using a model USP enzyme assay confirmed that HAUSP was an enzymatically active member of the USP family. Furthermore, the presence of specific cysteine and histidine residues were shown to be essential for this activity. Investigations into the effect of transient expression of HAUSP in eukaryotic cells were also carried out. These studies suggested firstly that levels of intracellular HAUSP may be tightly controlled and secondly that increases in HAUSP expression might be toxic for cells. They also implied localisation of HAUSP to the NDIO domains was limited by protein-protein interactions. Work was also initiated to search for cellular proteins that interact with HAUSP. This resulted in the identification of strong and specific interactions between: the N-terminal region of HAUSP with cellular proteins of approximately 100kD and 105kD; and sequences in the C-terminal half of HAUSP with a cellular protein of approximately 40kD. Immunoprecipitation analysis supported the interaction of wild type HAUSP with cellular proteins of approximately 40kD and 105kD. It was also revealed that of these cellular proteins only the approximately 40kD cellular protein (which interacted with the C-terminus of HAUSP) was a substrate for proteasome-dependent degradation. More direct investigations were also carried out to improve our understanding of the mechanics and functioning of the Vmw110/HAUSP interaction. In particular, a variety of GST 'pull-down' assays were designed and tested to define the region of HAUSP required for this interaction. Results of this work implied that regions of HAUSP…

Subjects/Keywords: 579; Herpes simplex virus type 1; Herpesviridae

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kathoria, M. (1999). An investigation of the properties and functions of the Herpes Associated Ubiquitin-Specific Protease, HAUSP. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/75383/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284737

Chicago Manual of Style (16^th Edition):

Kathoria, Meeta. “An investigation of the properties and functions of the Herpes Associated Ubiquitin-Specific Protease, HAUSP.” 1999. Doctoral Dissertation, University of Glasgow. Accessed January 24, 2021. http://theses.gla.ac.uk/75383/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284737.

MLA Handbook (7^th Edition):

Kathoria, Meeta. “An investigation of the properties and functions of the Herpes Associated Ubiquitin-Specific Protease, HAUSP.” 1999. Web. 24 Jan 2021.

Vancouver:

Kathoria M. An investigation of the properties and functions of the Herpes Associated Ubiquitin-Specific Protease, HAUSP. [Internet] [Doctoral dissertation]. University of Glasgow; 1999. [cited 2021 Jan 24]. Available from: http://theses.gla.ac.uk/75383/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284737.

Council of Science Editors:

Kathoria M. An investigation of the properties and functions of the Herpes Associated Ubiquitin-Specific Protease, HAUSP. [Doctoral Dissertation]. University of Glasgow; 1999. Available from: http://theses.gla.ac.uk/75383/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284737

University of Washington

22. Agyemang, Elfriede Ampong. Performance of commercial enzyme-linked immunosorbent assays (ELISA) for diagnosis of HSV-1 and HSV-2 infection in a clinical setting.

Degree: 2016, University of Washington

URL: http://hdl.handle.net/1773/36668

► Background FDA-approved ELISA assays for determining type-specific herpes simplex virus (HSV) serostatus are widely used in clinics. We compared the performance of such assays with… (more)

Subjects/Keywords: ELISA; enzyme-linked immunosorbent assays; herpes simplex virus; HSV-1; HSV-2; western blot; Medicine; Virology; epidemiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Agyemang, E. A. (2016). Performance of commercial enzyme-linked immunosorbent assays (ELISA) for diagnosis of HSV-1 and HSV-2 infection in a clinical setting. (Thesis). University of Washington. Retrieved from http://hdl.handle.net/1773/36668

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Agyemang, Elfriede Ampong. “Performance of commercial enzyme-linked immunosorbent assays (ELISA) for diagnosis of HSV-1 and HSV-2 infection in a clinical setting.” 2016. Thesis, University of Washington. Accessed January 24, 2021. http://hdl.handle.net/1773/36668.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Agyemang, Elfriede Ampong. “Performance of commercial enzyme-linked immunosorbent assays (ELISA) for diagnosis of HSV-1 and HSV-2 infection in a clinical setting.” 2016. Web. 24 Jan 2021.

Vancouver:

Agyemang EA. Performance of commercial enzyme-linked immunosorbent assays (ELISA) for diagnosis of HSV-1 and HSV-2 infection in a clinical setting. [Internet] [Thesis]. University of Washington; 2016. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1773/36668.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Agyemang EA. Performance of commercial enzyme-linked immunosorbent assays (ELISA) for diagnosis of HSV-1 and HSV-2 infection in a clinical setting. [Thesis]. University of Washington; 2016. Available from: http://hdl.handle.net/1773/36668

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

East Tennessee State University

23. Slade, Jessica A. In Vitro and In Vivo Characterization of Chlamydia and HSV Co-infection.

Degree: PhD, Biomedical Sciences, 2016, East Tennessee State University

URL: https://dc.etsu.edu/etd/3026

► The obligate intracellular bacterium, Chlamydia trachomatis, and Herpes Simplex Virus Type-2 (HSV-2) are the leading sexually transmitted pathogens in the world. These infections are… (more)

▼ The obligate intracellular bacterium, Chlamydia trachomatis, and Herpes Simplex Virus Type-2 (HSV-2) are the leading sexually transmitted pathogens in the world. These infections are usually asymptomatic and clinically mild, but complications can be severe. Reports of dual detection of Chlamydia and HSV within the genital tracts of humans led our laboratory to develop an in vitro Chlamydia/HSV co-infection model. Little is known regarding the specific pathogenesis of Chlamydia and HSV co-infections, but HSV-super-infection of Chlamydia-infected cells caused the chlamydiae to deviate from their normal developmental cycle into a non-replicative state termed persistence, or the chlamydial stress response. Interactions between HSV envelope protein, gD with host cell junction protein, nectin-1, were enough to stimulate the departure from normal chlamydial development. Additional data also suggested that there might be differences between single infection and co-infection outcomes in vivo. Thus, two diverging hypotheses were investigated here: i) that host nectin-1 is required for normal chlamydial development; and ii) that pathogen shedding and/or disease progression in Chlamydia and HSV-2 co-infected animals will differ from that observed in singly-infected animals. Chlamydial infection of nectin-1 knockdown cell lines revealed no inhibition of chlamydial entry, but significant reductions in inclusion size and production of infectious chlamydiae. Additionally, nectin-1 knockout mice shed fewer Chlamydia compared to wild type mice. In other studies, we developed a novel in vivo Chlamydia and HSV-2 intravaginal super-infection model in BALB/c mice. Infection with Chlamydia muridarum, followed up to 9 days later by HSV-2 super-infection, both reduced HSV shedding and protected mice from HSV-induced fatal neurologic disease compared to HSV singly-infected animals. Protection is lost when: i) infected animals are no longer shedding C. muridarum; ii) when mice are inoculated with UV-inactivated C. muridarum; or iii) when viable chlamydiae are eliminated from the genital tract using antibiotics prior to HSV-2 super-infection. Altogether, we have determined that host nectin-1 is required for chlamydial development both in vitro and in vivo, and that chlamydial pre-infection protects mice from subsequent HSV infection. We predict that these observations may lead to novel approaches to prevent human infection by these two common sexually transmitted pathogens.

Subjects/Keywords: Chlamydia; Herpes Simplex Virus; Co-infection; Nectin-1; Chlamydia trachomatis; Chlamydia muridarum; Bacteriology; Microbiology; Pathogenic Microbiology; Virology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Slade, J. A. (2016). In Vitro and In Vivo Characterization of Chlamydia and HSV Co-infection. (Doctoral Dissertation). East Tennessee State University. Retrieved from https://dc.etsu.edu/etd/3026

Chicago Manual of Style (16^th Edition):

Slade, Jessica A. “In Vitro and In Vivo Characterization of Chlamydia and HSV Co-infection.” 2016. Doctoral Dissertation, East Tennessee State University. Accessed January 24, 2021. https://dc.etsu.edu/etd/3026.

MLA Handbook (7^th Edition):

Slade, Jessica A. “In Vitro and In Vivo Characterization of Chlamydia and HSV Co-infection.” 2016. Web. 24 Jan 2021.

Vancouver:

Slade JA. In Vitro and In Vivo Characterization of Chlamydia and HSV Co-infection. [Internet] [Doctoral dissertation]. East Tennessee State University; 2016. [cited 2021 Jan 24]. Available from: https://dc.etsu.edu/etd/3026.

Council of Science Editors:

Slade JA. In Vitro and In Vivo Characterization of Chlamydia and HSV Co-infection. [Doctoral Dissertation]. East Tennessee State University; 2016. Available from: https://dc.etsu.edu/etd/3026

24. Vlahava, Virginia-Maria. Study of the cellular signaling pathways during latent infection and reactivation by HSV-1 (Herpes Simplex Virus type 1).

Degree: 2015, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/36015

►

HSV-1 is a DNA virus of the herpesviruses family (Herpesviridae) and specifically belongs to the Alpha subfamily (Alphaherpesvirinae). It is a neurotropic virus that alternates… (more)

▼

HSV-1 is a DNA virus of the herpesviruses family (Herpesviridae) and specifically belongs to the Alpha subfamily (Alphaherpesvirinae). It is a neurotropic virus that alternates from a lytic cycle in epithelial cells to a latent cycle in neurons. Its lytic cycle takes place in three phases, the immediate early (IE), the early (E) and the late (L). In the present thesis, we studied the mechanisms that govern infection by Herpes Simplex virus type-1 investigating two directions; the effect of CD40L on the outcome of infection and the methylation profile of host genes during the course of infection.In the first part, the effect of CD40L on HSV-1 infection was studied and it was found that CD40L directly inhibits infection by HSV-1 following entry of the virus in the host cell. Different stages of viral infection were analyzed as well as antiviral mechanisms with a particular emphasis on autophagy. Collectively, it was demonstrated that HSV-1 is directly inhibited by the activation of the CD40L pathway by a mechanism that is PI3K-dependent and autophagy-independent.At the second part of the study, the methylation profile of the host cell genome was analyzed during lytic and latent infection by HSV-1 with particular interest on the enzymes associated to epigenetic phenomena. PCR-array analysis showed that there is a great variation in the methylation profile during the immediate early (IE) and early (E) phase of infection while in the late (L) phase of infection and in latently infected cells the methylation profile remains stable, however, different from the steady state methylation of the host. Several histone deacetylase genes were identified as targets for alterations in DNA methylation and an effort was made to correlate the changes in DNA methylation to gene expression and their impact on the progeny virus.

Ο HSV-1 είναι ένας DNA ιός που ανήκει στην οικογένεια των ερπητοϊών (Herpesviridae) και συγκεκριμένα στην οικογένεια των α-ερπητοϊών (Alphaherpesvirinae). Είναι νευροτρόπος ιός ο οποίος πραγματοποιεί λυτικό κύκλο στα επιθηλιακά κύτταρα ενώ στα νευρικά κύτταρα βρίσκεται σε λανθάνουσα φάση. Ο λυτικός κύκλος του HSV-1 λαμβάνει χώρα σε τρεις φάσεις, την άμεσα πρώιμη (α), την πρώιμη (β) και την όψιμη(γ) και αποτελεί χαρακτηριστικό τρόπο έκφρασης των γονιδίων των ερπητοϊών. Στα πλαίσια της παρούσας διδακτορικής διατριβής διερευνήθηκαν μηχανισμοί που διέπουν την μόλυνση από τον ιό του απλού έρπητα τύπου Ι (HSV-1). Συγκεκριμένα, διερευνήθηκε η δράση του CD40L και ο ρόλος του στην έκβαση της μόλυνσης από τον HSV-1. Επιπλέον, διερευνήθηκε το πρότυπο μεθυλίωσης κυτταρικών γονιδίων σε διάφορα στάδια της μόλυνσης από τον ιό.Ως προς το πρώτο σκέλος της εργασίας, κατά την οποία διερευνήθηκε η δράση του CD40L στην μόλυνση από τον HSV-1, βρέθηκε ότι ο CD40L παρεμποδίζει την εξέλιξη της μόλυνσης άμεσα, μετά την είσοδο του ιού στο κύτταρο. Μελετήθηκαν διάφορα στάδια της μόλυνσης καθώς κ αντιϊκοί μηχανισμοί ενώ έμφαση δόθηκε στον μηχανισμό της αυτοφαγίας. Συνολικά, ο ιός παρεμποδίζεται από την ενεργοποίηση του μονοπατιού του CD40L…

Subjects/Keywords: Απλός έρπητας; Αυτοφαγία; Επιγενετική ρύθμιση; Υποδοχέας CD40; HDAC; Herpes Simplex Virus type 1; Autophagy; Epigenetics; CD40 receptor; HDAC

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vlahava, V. (2015). Study of the cellular signaling pathways during latent infection and reactivation by HSV-1 (Herpes Simplex Virus type 1). (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/36015

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Vlahava, Virginia-Maria. “Study of the cellular signaling pathways during latent infection and reactivation by HSV-1 (Herpes Simplex Virus type 1).” 2015. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 24, 2021. http://hdl.handle.net/10442/hedi/36015.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Vlahava, Virginia-Maria. “Study of the cellular signaling pathways during latent infection and reactivation by HSV-1 (Herpes Simplex Virus type 1).” 2015. Web. 24 Jan 2021.

Vancouver:

Vlahava V. Study of the cellular signaling pathways during latent infection and reactivation by HSV-1 (Herpes Simplex Virus type 1). [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2015. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10442/hedi/36015.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Vlahava V. Study of the cellular signaling pathways during latent infection and reactivation by HSV-1 (Herpes Simplex Virus type 1). [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2015. Available from: http://hdl.handle.net/10442/hedi/36015

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Sydney

25. Wu, Jiadai. Haliotis rubra hemocyanin: sequencing, recombinant expression and investigation of the binding activities of expressed function units with HSV-1 .

Degree: 2017, University of Sydney

URL: http://hdl.handle.net/2123/17792

► Hemocyanin (HrH) has been shown to possess antiviral activity against HSV-1 by selectively binding to viral glycoproteins (gB, gC, gD). Its large size however precluded… (more)

Subjects/Keywords: Haliotis rubra hemocyanin; Herpes Simplex Virus type 1; Gene Clone; Protein recombinant expression; Protein purification; Protein-protein interaction

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wu, J. (2017). Haliotis rubra hemocyanin: sequencing, recombinant expression and investigation of the binding activities of expressed function units with HSV-1 . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17792

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wu, Jiadai. “Haliotis rubra hemocyanin: sequencing, recombinant expression and investigation of the binding activities of expressed function units with HSV-1 .” 2017. Thesis, University of Sydney. Accessed January 24, 2021. http://hdl.handle.net/2123/17792.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wu, Jiadai. “Haliotis rubra hemocyanin: sequencing, recombinant expression and investigation of the binding activities of expressed function units with HSV-1 .” 2017. Web. 24 Jan 2021.

Vancouver:

Wu J. Haliotis rubra hemocyanin: sequencing, recombinant expression and investigation of the binding activities of expressed function units with HSV-1 . [Internet] [Thesis]. University of Sydney; 2017. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2123/17792.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wu J. Haliotis rubra hemocyanin: sequencing, recombinant expression and investigation of the binding activities of expressed function units with HSV-1 . [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/17792

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

The Ohio State University

26. Trego, Kelly S. Functional significance of the physical interaction between the herpes simplex virus type 1 origin-binding protein, UL9, and the DNA polymerase processivity factor, UL42.

Degree: PhD, Molecular Genetics, 2003, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1061240569

► The origin (ori)-binding protein of herpes simplex virus type 1 (HSV-1), encoded by the UL9 open-reading frame, has been shown to physically interact with a… (more)

▼ The origin (ori)-binding protein of herpes simplex virus type 1 (HSV-1), encoded by the UL9 open-reading frame, has been shown to physically interact with a number of cellular and viral proteins, including three HSV-1 proteins (ICP8, UL42, and UL8) essential for ori-dependent DNA replication. In this report, it is demonstrated for the first time that the DNA polymerase processivity factor, UL42 protein, provides accessory function to the UL9 protein, by enhancing the 3' to 5' helicase activity of UL9 on partially duplex non-specific DNA substrates. UL42 fails to enhance the unwinding activity of a non-cognate helicase, suggesting enhancement of unwinding requires the physical interaction between UL42 and UL9. UL42 increases the steady-state rate for unwinding a 23/38-mer by UL9, but only at limiting UL9 concentrations, consistent with a role in increasing the affinity of UL9 for DNA. Optimum enhancement of unwinding was observed at UL42:UL9 molecular ratios of 4:1, although enhancement was reduced when high ratios of UL42:DNA were present. Under the assay conditions employed, UL42 did not alter the rate of dissociation of UL9 from the DNA substrate. UL42 also did not alter the requirement or time for an assembly/conformational change step, regardless of whether it was added to DNA prior to or at the same time as UL9, or after steady-state unwinding by UL9 alone had been achieved. Thus, the increased affinity of UL9 for DNA most likely is the result of an increase in the association rate constant for binding of UL9 to DNA, and explains why helicase enhancement is observed only at subsaturating concentrations of UL9 with respect to DNA. Consistent with this interpretation are results which demonstrate that UL42 also enhances the ATPase activity of UL9 on single-strand and partially duplex DNA substrates when UL9 is limiting. In contrast, ICP8 enhances unwinding at both saturating and subsaturating UL9 concentrations, and reduces or eliminates the lag period. The different means by which ICP8 and UL42 enhance activities of UL9 suggest that these two members of the presumed functional replisome may act synergistically on UL9 to effect initiation of HSV-1 DNA replication in vivo. Advisors/Committee Members: Parris, Deborah (Advisor).

Subjects/Keywords: UL9; UL42; herpes simplex virus type 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Trego, K. S. (2003). Functional significance of the physical interaction between the herpes simplex virus type 1 origin-binding protein, UL9, and the DNA polymerase processivity factor, UL42. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1061240569

Chicago Manual of Style (16^th Edition):

Trego, Kelly S. “Functional significance of the physical interaction between the herpes simplex virus type 1 origin-binding protein, UL9, and the DNA polymerase processivity factor, UL42.” 2003. Doctoral Dissertation, The Ohio State University. Accessed January 24, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1061240569.

MLA Handbook (7^th Edition):

Trego, Kelly S. “Functional significance of the physical interaction between the herpes simplex virus type 1 origin-binding protein, UL9, and the DNA polymerase processivity factor, UL42.” 2003. Web. 24 Jan 2021.

Vancouver:

Trego KS. Functional significance of the physical interaction between the herpes simplex virus type 1 origin-binding protein, UL9, and the DNA polymerase processivity factor, UL42. [Internet] [Doctoral dissertation]. The Ohio State University; 2003. [cited 2021 Jan 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1061240569.

Council of Science Editors:

Trego KS. Functional significance of the physical interaction between the herpes simplex virus type 1 origin-binding protein, UL9, and the DNA polymerase processivity factor, UL42. [Doctoral Dissertation]. The Ohio State University; 2003. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1061240569

University of Cambridge

27. Ahmed, Md Firoz. Studies of viral and cellular proteins involved in herpes simplex virus type-1 egress.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.35587 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763877

► The egress pathway of herpes simplex virus-1 (HSV-1) is a complicated process mediated by co-ordinated activity of several virus glycoproteins. The virions are first assembled… (more)

▼ The egress pathway of herpes simplex virus-1 (HSV-1) is a complicated process mediated by co-ordinated activity of several virus glycoproteins. The virions are first assembled and enveloped at trans-Golgi-network (TGN) or endosome membranes and then travel through a guided pathway that is directed towards the cell adherent points for secretion. Once secreted the vast majority of virions remain associated with the extracellular membrane of cells and very few free virions are released into the culture medium (< 1%). The mechanisms that mediate both the targeted secretion of newly assembled virions at cell contact points and post-secretion attachment of virions with the extracellular surface of cells are poorly understood, and were the topics of this research. In this thesis, an HSV-1 passage mutant of increased virion secretion phenotype had been studied. Genome sequencing of the mutant virus identified mutations in three viral envelope proteins. Study of recombinant viruses that were constructed based on those three mutations revealed that a single amino acid change in glycoprotein I (gI) of glycine to arginine at residue 39 is responsible for the increased release of virus. The result suggests the principal effect of this mutation is to modify the secretory pathway used by virions during their release from infected cells. Data also suggests a role of gC in the attachment of virions to the extracellular surface of cells after egress. In the context of HSV-1 envelopment and egress glycoprotein E (gE), which forms a heterodimeric complex with gI (gE/gI), is known to be important. The gE/gI complex has been shown to interact with many tegument proteins and have a redundant role in secondary envelopment. The gE/gI complex has been also proposed to colocalise with various cellular components and sort the nascent virions to cell contact points. However, there is little understanding of the cellular proteins that gE/gI interact with, or the mechanisms that mediate targeted secretion of virions. This research has identified a novel interactome of gE/gI by mass-spectrometric analysis utilising stable isotope labelling with amino acids in cell culture (SILAC) medium. Among the cellular interactome obtained, Nipsnap1 was validated by co-precipitation assays from both infected and transfected cells, and furthermore using cell free systems, suggesting gE and Nipsnap1 directly interact. Nipsnap1 and its homologue Nipsnap2 have been proposed to contribute in vesicle transport and membrane fusion in cells. Using CRISPR-Cas9 technology these proteins were knocked out in a keratinocyte cell line (HaCaT) to investigate their role in HSV-1 egress. However, little or no effect on HSV-1 egress could be observed upon loss of either or both of these proteins suggesting the biological significance of gE-Nipsnap1 interaction may not be directly linked to any egress function of gE/gI. Two further interesting 'hits' from the gE/gI interactome were interferon-induced transmembrane protein type-2 (IFITM2), a virus restriction factor, and Myoferlin…

Subjects/Keywords: 616.9; Virology; HSV-1; Herpes simplex virus 1; HSV-1 egress; HSV-1 gE/gI; gE/gI; glycoprotin E; glycoprotein I; Nipsnap; IFITM; Myoferlin; MYOF; virus egress; SILAC; Host virus interaction; gIG39R; HSV-1 KOS; CRISPR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ahmed, M. F. (2019). Studies of viral and cellular proteins involved in herpes simplex virus type-1 egress. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.35587 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763877

Chicago Manual of Style (16^th Edition):

Ahmed, Md Firoz. “Studies of viral and cellular proteins involved in herpes simplex virus type-1 egress.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 24, 2021. https://doi.org/10.17863/CAM.35587 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763877.

MLA Handbook (7^th Edition):

Ahmed, Md Firoz. “Studies of viral and cellular proteins involved in herpes simplex virus type-1 egress.” 2019. Web. 24 Jan 2021.

Vancouver:

Ahmed MF. Studies of viral and cellular proteins involved in herpes simplex virus type-1 egress. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 24]. Available from: https://doi.org/10.17863/CAM.35587 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763877.

Council of Science Editors:

Ahmed MF. Studies of viral and cellular proteins involved in herpes simplex virus type-1 egress. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.35587 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763877

Wright State University

28. Van Buren, Lauren Kay. HSV-1 Infection of C3H Central Nervous System Cell Lines.

Degree: MS, Microbiology and Immunology, 2007, Wright State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=wright1189746668

► Herpes Simplex Virus Type 1 (HSV-1) can infect the nervous system, resulting in a disease known as herpes encephalitis (HSE). Herpes encephalitis affects thousands of… (more)

▼ Herpes Simplex Virus Type 1 (HSV-1) can infect the nervous system, resulting in a disease known as herpes encephalitis (HSE). Herpes encephalitis affects thousands of people each year; many cases are fatal or permanently debilitating. Approximately two thousand known cases occur in the United States each year alone (Neuroland online source). Acyclovir has been the drug of choice used to treat herpes encephalitis. Even after the administration of acyclovir, permanent neurological damage and/or death often results. Thousands of individuals would benefit by the discovery of drugs that are more effective at preventing lasting HSE damage and death. Knowledge concerning HSE infection of the brain could be advanced with the development of co-culture systems that allow for the study of one specific cell type or a subpopulation of cells during an active infection. Additional models are needed to test therapies against HSE. The majority of models that currently exist are in-vivo or primary cell line models. Even though many of these models can be used to mimic what actually occurs during herpes encephalitis infection in humans, these systems have several weaknesses. The usage of in-vivo models requires a great deal of time, preparation, funding, and care by a veterinarian staff. Primary cell lines can be difficult to isolate and maintain for long lengths of time in cell culture. Unlike primary cell lines, continuous cell lines are able to be used for longer periods of time. Many can be easily purchased from cell banks such as the American Type Culture Collection (ATCC) for a reasonable price. Continuous cell lines are easy to culture and can be used in many different types of experiments. The use of a continuous cell lines prevents animal suffering and death. The purpose of this thesis was to determine if cell lines from a C3H murine strain can accurately mimic viral production that occurs during an actual HSV-1 infection in the central nervous system. One cell line is a pure microglial cell line. Three other cell lines, derived from P19 cells, were also tested. One cell culture tested was a system composed of mixed brain cells such as neurons, astrocyte-like cells, and fibroblast-like cells. Another culture evaluated contained only neuronal cells. P19 cells were evaluated as well. The results indicate that only the microglial and mixed cell cultures supported viral production that mirrors what occurs in animal models. The neuronal cells not only failed to produce virus, but the neurons survived for less than twenty-four hours in culture after in infection with HSV-1. Advisors/Committee Members: Bigley, Nancy (Advisor).

Subjects/Keywords: Biology, Microbiology; HSV-1 (Herpes Simplex Virus) Type 1; herpes; neurons; astrocytes; fibroblast-like cells; herpes encephalitis; HSE; microglia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Van Buren, L. K. (2007). HSV-1 Infection of C3H Central Nervous System Cell Lines. (Masters Thesis). Wright State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=wright1189746668

Chicago Manual of Style (16^th Edition):

Van Buren, Lauren Kay. “HSV-1 Infection of C3H Central Nervous System Cell Lines.” 2007. Masters Thesis, Wright State University. Accessed January 24, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1189746668.

MLA Handbook (7^th Edition):

Van Buren, Lauren Kay. “HSV-1 Infection of C3H Central Nervous System Cell Lines.” 2007. Web. 24 Jan 2021.

Vancouver:

Van Buren LK. HSV-1 Infection of C3H Central Nervous System Cell Lines. [Internet] [Masters thesis]. Wright State University; 2007. [cited 2021 Jan 24]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1189746668.

Council of Science Editors:

Van Buren LK. HSV-1 Infection of C3H Central Nervous System Cell Lines. [Masters Thesis]. Wright State University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1189746668

University of Oulu

29. Mattila, R. (Riikka). The roles of virulence factors Us3 and γ₁34.5 during different phases of HSV-1 life cycle.

Degree: 2015, University of Oulu

URL: http://urn.fi/urn:isbn:9789526210469

►

Abstract Herpes simplex virus type 1 (HSV-1) is a common pathogen with an age-standardized seroprevalence of 52% in Finland. The most common manifestation of HSV-1… (more)

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Abstract Herpes simplex virus type 1 (HSV-1) is a common pathogen with an age-standardized seroprevalence of 52% in Finland. The most common manifestation of HSV-1 infection is labial herpes, but recently HSV-1 has emerged as the most common cause of primary genital herpes in Finnish women. HSV-1 can also lead to severe conditions such as encephalitis. After the primary lytic HSV-1 infection at the epithelia, the progeny viruses infect the innervating sensory neurons. The neuronal infection may lead to a quiescent infection form, called latency. Periodically, the virus may reactivate, which can lead to recurrent infection at the epithelia. During different phases of the viral life cycle the host cells try to restrict the infection. This study set out to investigate the roles of two HSV-1 proteins, γ134.5 and Us3 during different phases of the HSV-1 life cycle. The aim of the first study was to investigate how the deletion of Us3 affected host responses, especially Toll-like Receptor (TLR) signaling, in monocytic U937 cells. TLR3 expression was increased during Us3 deletion virus infections. This also led to increased activation of IRF-3 and increased expression of type I interferons (IFN) and an interferon stimulated protein. This study shows that TLR3 is involved in controlling the HSV-1 infection and that Us3 regulates IRF-3 activation. The second study focused on the role of the γ134.5 protein in HSV-1 latency. Embryonic mouse dorsal root ganglion (DRG) cultures were used as a cell culture model for HSV-1 latency and reactivation. In this model γ134.5 deletion viruses did not reactivate as efficiently as wild-type viruses, even though they replicated well and established latency in the neurons. Stress granules are part of the host response. In the third study, the roles of the innate immunity effectors HSV-1 Us3 and human Z-DNA binding protein 1 (ZBP1) in stress granule formation (SG) were studied. Wild-type HSV-1 efficiently prevented the formation of SGs. The overexpression of ZBP1 resulted in accumulation of smaller but more abundant SGs during oxidative stress. Overexpression of Us3 did not significantly affect the size or number of SGs, but during Us3 deletion virus infection, SG proteins localized to cis-Golgi. This work shows that HSV-1 uses Us3 to evade and modulate host responses and that the γ134.5 protein is required for reactivation in mouse DRG cultures.

Tiivistelmä Herpes simplex virus tyyppi 1 (HSV-1) on yleinen taudinaiheuttaja, jonka ikävakioitu seroprevalenssi Suomessa on 52 %. HSV-1 tunnetaan yleisimmin huuliherpeksen aiheuttajana, mutta myös kasvava osuus genitaaliherpeksistä on HSV-1:n aiheuttamia. HSV-1 voi johtaa myös vakaviin ilmentymiin, kuten aivotulehdukseen. Epiteelisolujen infektion tuottamia viruksia siirtyy aluetta hermottaviin tuntohermosoluihin, mikä voi johtaa piilevään infektiomuotoon eli latenssiin. Latentti virus voi ajoittain reaktivoitua, mistä voi seurata uusintainfektio. Isäntäsolu pyrkii rajoittamaan infektiota sen eri vaiheissa. Tämän tutkimuksen tarkoituksena oli…

Advisors/Committee Members: Hukkanen, V. (Veijo), Harila, K. (Kirsi).

Subjects/Keywords: Us3 protein kinase; ganglion culture; herpes simplex virus type 1; immune evasion; innate immunity; latency; neurovirulence; stress granule; viral culture; γ₁34.5 protein; Us3-proteiinikinaasi; ganglioviljely; herpes simplex virus tyyppi 1; immuunivasteiden välttely; latenssi; luontainen immuniteetti; neurovirulenssi; virusviljely; γ₁34.5 proteiini

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mattila, R. (. (2015). The roles of virulence factors Us3 and γ₁34.5 during different phases of HSV-1 life cycle. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789526210469

Chicago Manual of Style (16^th Edition):

Mattila, R (Riikka). “The roles of virulence factors Us3 and γ₁34.5 during different phases of HSV-1 life cycle.” 2015. Doctoral Dissertation, University of Oulu. Accessed January 24, 2021. http://urn.fi/urn:isbn:9789526210469.

MLA Handbook (7^th Edition):

Mattila, R (Riikka). “The roles of virulence factors Us3 and γ₁34.5 during different phases of HSV-1 life cycle.” 2015. Web. 24 Jan 2021.

Vancouver:

Mattila R(. The roles of virulence factors Us3 and γ₁34.5 during different phases of HSV-1 life cycle. [Internet] [Doctoral dissertation]. University of Oulu; 2015. [cited 2021 Jan 24]. Available from: http://urn.fi/urn:isbn:9789526210469.

Council of Science Editors:

Mattila R(. The roles of virulence factors Us3 and γ₁34.5 during different phases of HSV-1 life cycle. [Doctoral Dissertation]. University of Oulu; 2015. Available from: http://urn.fi/urn:isbn:9789526210469

30. Muenzner, Julia. Viral subversion of host cell membrane trafficking.

Degree: PhD, 2017, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/267890

► Enveloped viruses acquire their membrane coat from the plasma membrane or intracellular organelles and rely on cellular machinery to facilitate envelopment and egress of virus… (more)

▼ Enveloped viruses acquire their membrane coat from the plasma membrane or intracellular organelles and rely on cellular machinery to facilitate envelopment and egress of virus progeny. This thesis examines egress-related interactions between host cell factors and proteins of two different enveloped viruses: hepatitis D virus (HDV) and herpes simplex virus 1 (HSV-1). HDV is a small RNA virus causing fulminant hepatitis or severely aggravating cirrhosis and hepatocellular carcinoma. HSV-1 is a large DNA virus infecting epithelial and neuronal cells. Infection with HSV-1 not only triggers the development of recurring sores on oral or genital mucosa, but can also cause severe disease in neonates and immunocompromised patients. The interaction between the large antigen of HDV (HDAg-L) and the N-terminal domain (NTD) of clathrin, a protein crucial for endocytosis and intracellular vesicular trafficking, was examined by structural, biochemical and biophysical techniques. Co-crystal structures of NTD bound to HDAg-L peptides derived from different HDV genotypes revealed that HDV interacts with multiple binding sites on NTD promiscuously, prompting re-evaluation of the binding between cellular peptides and NTD. Surprisingly, co-crystal structures and pull-down capture assays showed that cellular peptides containing clathrin-binding motifs can also bind multiple sites on the surface of NTD simultaneously. In addition, the structures of viral and cellular peptides bound to NTD enabled the molecular characterization of the fourth peptide binding site on NTD, the “Royle box”, and led to the identification of a novel binding mode at the “arrestin box” peptide binding site on NTD. The work in this thesis therefore not only identifies the molecular basis of HDV:clathrin interactions, but also furthers our understanding of basic clathrin biology. Even though many HSV-1 proteins have been implicated in the envelopment and egress of viral particles, only few interactions between HSV-1 and cellular proteins promoting these processes have been described. Therefore, the HSV-1 proteins gE, UL21 and UL56 were selected and characterized bioinformatically and/or biochemically. Cellular proteins interacting with UL56 were identified by yeast two-hybrid screening and quantitative mass spectrometry. Co-immunoprecipitation and pull-down experiments confirmed the Golgi-trafficking protein GOPC, components of the mammalian trafficking protein particle complex, and the ubiquitin ligase NEDD4 as novel binding partners of UL56, thereby suggesting exciting new avenues for the investigation of cellular mechanisms contributing to HSV-1 envelopment and egress.

Subjects/Keywords: clathrin; membrane trafficking; herpes simplex virus 1; hepatitis D virus

…1 INTRODUCTION 1.1 Overview 1.2 The cellular endomembrane system 1.2.1 Organelles and… …virus 1.4.1 Transmission, infection scenarios and disease burden …

11 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Muenzner, J. (2017). Viral subversion of host cell membrane trafficking. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/267890

Chicago Manual of Style (16^th Edition):

Muenzner, Julia. “Viral subversion of host cell membrane trafficking.” 2017. Doctoral Dissertation, University of Cambridge. Accessed January 24, 2021. https://www.repository.cam.ac.uk/handle/1810/267890.

MLA Handbook (7^th Edition):

Muenzner, Julia. “Viral subversion of host cell membrane trafficking.” 2017. Web. 24 Jan 2021.

Vancouver:

Muenzner J. Viral subversion of host cell membrane trafficking. [Internet] [Doctoral dissertation]. University of Cambridge; 2017. [cited 2021 Jan 24]. Available from: https://www.repository.cam.ac.uk/handle/1810/267890.

Council of Science Editors:

Muenzner J. Viral subversion of host cell membrane trafficking. [Doctoral Dissertation]. University of Cambridge; 2017. Available from: https://www.repository.cam.ac.uk/handle/1810/267890

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