subject:(HCV)

1. Simeon, Rudo Lyndon. Selecting a path against Hepatitis C Virus.

Degree: 2013, Texas Digital Library

URL: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66834

► Hepatitis C virus (HCV) currently affects ~5% of the world???s population and has relatively limited treatment options for infected patients. Genetic suppressor elements (GSE) derived… (more)

▼ Hepatitis C virus (HCV) currently affects ~5% of the world???s population and has relatively limited treatment options for infected patients. Genetic suppressor elements (GSE) derived from a gene or genome of interest can act as transdominant inhibitors of a particular biology function presumably by binding to and blocking an essential interaction surface for protein activity. Taking advantage of hepatoma cell line n4mBid, that supports all stages of the HCV life cycle and strongly report HCV infection by a cell-death phenotype, we developed an iterative selection/enrichment strategy for the identification of GSE against HCV. Using this strategy, a library expressing random fragments of the HCV genome was screened for sequences able to suppress HCV infection. A 244 amino acid gene fragment, B1, was strongly enriched after 5 rounds of selection. B1 has a very high net positive charge of 43 at neutral pH and a high charge-to-mass (kDa) ratio of 1.5. We show that B1 expression specifically inhibits HCV replication, apparently due to its high positive charge. We also show that recombinant positively charged proteins can inhibit HCV infection, when supplied in vitro.In addition, eGFP-fused B1 potently penetrates both adherent and suspension cells with >80% of cells taking up the protein. Importantly, we show that B1 not only facilitates cellular uptake, but allows protein cargo to reach sites of biological relevance. B1 also delivers non-covalently conjugated RNA and DNA across the cell membrane to cytosolic and nuclear sites, with efficiency comparable to commercially available cationic lipid reagents. Our data suggest that B1 utilizes cell-surface glycans and multiple competing endocytic pathways to enter and traffic through cells.During a separate screening carried out in our lab, we identified a TACR3 inhibitor SB 222200 that had significant HCV activity. We go on to show that both TACR1 and TACR3 receptors are expressed in the HCV-permissive Huh 7.5 cell line. We also show that both TACR1 and TACR3 inhibitors significantly inhibit HCV infection. These results point to the potential for TACR1 antagonists in treating patients infected with both HCV and HIV. Advisors/Committee Members: Chen, Zhilei (advisor).

Subjects/Keywords: HCV

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APA (6^th Edition):

Simeon, R. L. (2013). Selecting a path against Hepatitis C Virus. (Thesis). Texas Digital Library. Retrieved from http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66834

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):

Simeon, Rudo Lyndon. “Selecting a path against Hepatitis C Virus.” 2013. Thesis, Texas Digital Library. Accessed February 16, 2020. http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66834.

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

MLA Handbook (7^th Edition):

Simeon, Rudo Lyndon. “Selecting a path against Hepatitis C Virus.” 2013. Web. 16 Feb 2020.

Vancouver:

Simeon RL. Selecting a path against Hepatitis C Virus. [Internet] [Thesis]. Texas Digital Library; 2013. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66834.

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

Council of Science Editors:

Simeon RL. Selecting a path against Hepatitis C Virus. [Thesis]. Texas Digital Library; 2013. Available from: http://hdl.handle.net/1969; http://hdl.handle.net/2249.1/66834

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

University of Saskatchewan

2. Li, Zhubing. Interactions Between Hepatitis C Virus and Proprotein Convertase Subtilisin/Kexin Type 9.

Degree: 2018, University of Saskatchewan

URL: http://hdl.handle.net/10388/10449

► Hepatitis C virus (HCV) is a small enveloped positive-sense single-stranded RNA virus that infects 2-3% of the world population. The majority of infected people develop… (more)

▼ Hepatitis C virus (HCV) is a small enveloped positive-sense single-stranded RNA virus that infects 2-3% of the world population. The majority of infected people develop chronic hepatitis, which results in severe liver damages. No HCV vaccine has been developed and the current antiviral regimens have some limitations such as high costs and not being effective in some difficult-to-treat patients. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease primarily produced in the liver. Its gene expression can be regulated by several transcription factors, such as sterol-regulatory element binding proteins (SREBPs), hepatocyte nuclear factor (HNF)-1, forkhead box O3 (FoxO3) and specificity protein 1 (Sp1). PCSK9 plays an important role in lipid homeostasis through facilitating the degradation of the low-density lipoprotein receptor (LDLR). It also exerts an antiviral effect on HCV. It can suppress HCV entry by reducing HCV receptors LDLR and cluster of differentiation 81. Although PCSK9 has been shown to inhibit HCV replication, the underlying mechanism has not been thoroughly characterized. Besides, the effects of PCSK9 on HCV translation and virion assembly/secretion have not been studied. Since PCSK9 can regulate lipid levels and the HCV life cycle is closely connected with lipid metabolism, I hypothesized that PCSK9 has an inhibitory effect on the HCV life cycle. I first showed that PCSK9 does not affect HCV translation or virion assembly/secretion. However, an inhibitory effect of PCSK9 on HCV replication is shown by overexpressing or knocking down PCSK9 in HCV replicon cells. Then I demonstrated that PCSK9-induced LDLR degradation is not involved in HCV replication regulation using gain-of-function (D374Y) or loss-of-function (Δaa. 31-52) PCSK9 mutants for LDLR degradation. Moreover, the auto-cleavage of PCSK9 affects HCV replication since only uncleaved proPCSK9 suppresses HCV replication and cleaved PCSK9 does not have effect on HCV replication. Next, I found that PCSK9 can interact with several HCV proteins including NS5A. The PCSK9 interacting region of NS5A is aa. 95-215 in domain I. The interaction between PCSK9 and NS5A inhibits NS5A dimerization and HCV RNA binding to NS5A. Considering that NS5A dimerization and RNA binding activity of NS5A are required for HCV replication, the interaction between PCSK9 and NS5A could be a mechanism of the inhibitory effect of PCSK9 on HCV replication. Since interferon (IFN) produced by innate immune system is important to clear viral infection and PCSK9 can inhibit HCV infection, I further hypothesized that PCSK9 affects HCV infection through regulating IFN production. I showed that PCSK9 suppresses IFNβ expression at the transcription and protein levels. The inhibitory effect of PCSK9 on IFNβ promoter/enhancer activity is mediated by positive regulatory domain IV in the IFNβ enhancer region where the activating transcription factor-2 (ATF-2)/c-Jun complex can bind. I demonstrated an interaction between PCSK9 and ATF-2. This interaction reduces… Advisors/Committee Members: Liu, Qiang, Tikoo, Suresh, Chelico, Linda, Mousseau, Darrell, Yang, Jian.

Subjects/Keywords: HCV; PCSK9

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APA (6^th Edition):

Li, Z. (2018). Interactions Between Hepatitis C Virus and Proprotein Convertase Subtilisin/Kexin Type 9. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/10449

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):

Li, Zhubing. “Interactions Between Hepatitis C Virus and Proprotein Convertase Subtilisin/Kexin Type 9.” 2018. Thesis, University of Saskatchewan. Accessed February 16, 2020. http://hdl.handle.net/10388/10449.

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

MLA Handbook (7^th Edition):

Li, Zhubing. “Interactions Between Hepatitis C Virus and Proprotein Convertase Subtilisin/Kexin Type 9.” 2018. Web. 16 Feb 2020.

Vancouver:

Li Z. Interactions Between Hepatitis C Virus and Proprotein Convertase Subtilisin/Kexin Type 9. [Internet] [Thesis]. University of Saskatchewan; 2018. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/10388/10449.

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

Council of Science Editors:

Li Z. Interactions Between Hepatitis C Virus and Proprotein Convertase Subtilisin/Kexin Type 9. [Thesis]. University of Saskatchewan; 2018. Available from: http://hdl.handle.net/10388/10449

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

Boston University

3. Freiman, J. Morgan. Evidence toward a novel approach to hepatitis C virus testing in resource-limited settings.

Degree: MS, Epidemiology, 2018, Boston University

URL: http://hdl.handle.net/2144/27854

► RATIONALE: A low cost point of care test (POCT) to diagnose hepatitis C virus (HCV) viremia could be a critical step toward HCV elimination. The… (more)

Subjects/Keywords: Epidemiology; HCV

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APA (6^th Edition):

Freiman, J. M. (2018). Evidence toward a novel approach to hepatitis C virus testing in resource-limited settings. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/27854

Chicago Manual of Style (16^th Edition):

Freiman, J Morgan. “Evidence toward a novel approach to hepatitis C virus testing in resource-limited settings.” 2018. Masters Thesis, Boston University. Accessed February 16, 2020. http://hdl.handle.net/2144/27854.

MLA Handbook (7^th Edition):

Freiman, J Morgan. “Evidence toward a novel approach to hepatitis C virus testing in resource-limited settings.” 2018. Web. 16 Feb 2020.

Vancouver:

Freiman JM. Evidence toward a novel approach to hepatitis C virus testing in resource-limited settings. [Internet] [Masters thesis]. Boston University; 2018. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/2144/27854.

Council of Science Editors:

Freiman JM. Evidence toward a novel approach to hepatitis C virus testing in resource-limited settings. [Masters Thesis]. Boston University; 2018. Available from: http://hdl.handle.net/2144/27854

University of New South Wales

4. Sugden, Peter Burnet. Determinants of protection against hepatitis C virus infection in highly exposed, uninfected individuals.

Degree: Medical Sciences, 2014, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/53638 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12333/SOURCE02?view=true

► Introduction: Individuals infected with hepatitis C virus (HCV) have two recognised outcomes of infection, clearance or persistence. Individuals who clear remain susceptible to re-infection. Some… (more)

▼ Introduction: Individuals infected with hepatitis C virus (HCV) have two recognised outcomes of infection, clearance or persistence. Individuals who clear remain susceptible to re-infection. Some high-risk individuals have been found to have HCV-specific immune responses in the absence of apparent infection, possibly indicating an exposed-but-uninfected (EU) phenotype, with protective immunity. This thesis sought to better understand this phenotype by examining: occult infection (with low level virus undetected by standard assays), the characteristics of potentially protective cellular immunity, and identification of potential genetic factors associated with EU status. Subjects and Methods: For occult infection, a two centre, masked, case-control study (n=35) and a longitudinal study (n=32) were undertaken using ultrasensitive nested PCR. For the protective immunity study, a nested case-control series with incident cases (n=28) and matched EU subjects (n=28) was analysed for natural killer cell (NK) phenotypes and HCV-specific CD4 and CD8 T cell responses. For the genetics study, DNA (n=210 subjects designated by varied risk of HCV infection) were genotyped for polymorphisms associated with clearance. To quantify risk, a composite index was derived from longitudinally collected risk behaviour data predicting incident infection in a prospective cohort of injecting drug user, prison inmates. Results: Two EU subjects in the first study (10%) and one in the second study (3%) were found to have consistently detectable HCV RNA. The numbers of activated (CD69+) NK cells in the mature CD56LowCD16+ subset, and cytotoxic (NKp30+) cells in the CD56HighCD16+ subset were higher in the EU subjects (p=0.040, p=0.038 respectively). EU subjects had higher frequencies of interferon (IFN)-γ producing NK cells, and lower frequencies of CD107a expression (p=0.003, p=0.015 respectively). No other factor differed. The risk index was strongly associated with incident HCV infection (p<0.0001). There were no significant differences in frequencies of the genetic markers. Conclusion: Occult infection occurs rarely in apparently uninfected subjects. NK cell activation is associated with likely protection against HCV infection. Genetic determinants of resistance to HCV infection remain to be identified. Further studies to confirm NK cell-mediated protection and to understand the mechanisms are needed. Advisors/Committee Members: Lloyd, Andrew, Medical Sciences, Faculty of Medicine, UNSW, Cameron, Barbara, Medical Sciences, Faculty of Medicine, UNSW.

Subjects/Keywords: HCV; Immunology

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APA (6^th Edition):

Sugden, P. B. (2014). Determinants of protection against hepatitis C virus infection in highly exposed, uninfected individuals. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53638 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12333/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Sugden, Peter Burnet. “Determinants of protection against hepatitis C virus infection in highly exposed, uninfected individuals.” 2014. Doctoral Dissertation, University of New South Wales. Accessed February 16, 2020. http://handle.unsw.edu.au/1959.4/53638 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12333/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Sugden, Peter Burnet. “Determinants of protection against hepatitis C virus infection in highly exposed, uninfected individuals.” 2014. Web. 16 Feb 2020.

Vancouver:

Sugden PB. Determinants of protection against hepatitis C virus infection in highly exposed, uninfected individuals. [Internet] [Doctoral dissertation]. University of New South Wales; 2014. [cited 2020 Feb 16]. Available from: http://handle.unsw.edu.au/1959.4/53638 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12333/SOURCE02?view=true.

Council of Science Editors:

Sugden PB. Determinants of protection against hepatitis C virus infection in highly exposed, uninfected individuals. [Doctoral Dissertation]. University of New South Wales; 2014. Available from: http://handle.unsw.edu.au/1959.4/53638 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12333/SOURCE02?view=true

Queens University

5. Huang, George. Modeling the Impact of Needle Exchange Programs Accounting for both HIV and HCV Infections and HIV/CV Co-Infections .

Degree: Community Health and Epidemiology, 2014, Queens University

URL: http://hdl.handle.net/1974/12155

► Purpose: The aim of this study is to model the impact of needle exchange interventions on human immunodeficiency virus (HIV) and hepatitis C virus (HCV).… (more)

Subjects/Keywords: HCV; HIV

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APA (6^th Edition):

Huang, G. (2014). Modeling the Impact of Needle Exchange Programs Accounting for both HIV and HCV Infections and HIV/CV Co-Infections . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12155

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):

Huang, George. “Modeling the Impact of Needle Exchange Programs Accounting for both HIV and HCV Infections and HIV/CV Co-Infections .” 2014. Thesis, Queens University. Accessed February 16, 2020. http://hdl.handle.net/1974/12155.

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

MLA Handbook (7^th Edition):

Huang, George. “Modeling the Impact of Needle Exchange Programs Accounting for both HIV and HCV Infections and HIV/CV Co-Infections .” 2014. Web. 16 Feb 2020.

Vancouver:

Huang G. Modeling the Impact of Needle Exchange Programs Accounting for both HIV and HCV Infections and HIV/CV Co-Infections . [Internet] [Thesis]. Queens University; 2014. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/1974/12155.

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

Council of Science Editors:

Huang G. Modeling the Impact of Needle Exchange Programs Accounting for both HIV and HCV Infections and HIV/CV Co-Infections . [Thesis]. Queens University; 2014. Available from: http://hdl.handle.net/1974/12155

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

University of Saskatchewan

6. Wu, Qi. MOLECULAR PATHOGENESIS OF HEPATITIS B VIRUS AND HEPATITIS C VIRUS INFECTIONS.

Degree: 2017, University of Saskatchewan

URL: http://hdl.handle.net/10388/7984

► Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections cause a wide range of liver diseases including hepatocellular carcinoma (HCC) worldwide. Because these two… (more)

▼ Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections cause a wide range of liver diseases including hepatocellular carcinoma (HCC) worldwide. Because these two viruses have the same modes of transmission, HBV HCV co-infections are found in approximately 7 to 20 million people globally. HBV HCV co-infections are associated with more severe liver diseases and higher risk of HCC. Previous studies have established that HBV and HCV mono-infection can cause hepatic steatosis, and steatosis is a confirmed risk factor for HCC. However, whether and how HBV HCV co-infections synergistically increase the risk of HCC development through modulating lipid metabolism is not well understood. PTEN is a phosphatase which contains both lipid and protein phosphatase activities. PTEN acts as a tumor suppressor by down-regulating the phosphoinositide-3-kinase (PI3K)/Akt/ sterol regulatory element-binding protein (SREBP) signaling pathway. It has been reported that PTEN is frequently mutated or deleted in tumors including HCC. PTEN-Long, a longer isoform of PTEN, which is able to be exported into the extracellular compartments, enter neighboring cells, and induce signaling events in recipient cells. Both HBV and HCV infections can inhibit PTEN and activate SREBP. However, how regulation of PTEN/SREBP pathway affects HBV and HCV infections is not fully understood. Therefore, the effect of the PTEN/SREBP pathway on HBV and/or HCV infections is worthy to study. In this study, we showed that both HBV X protein (HBx) and HCV core protein regulate PTEN/SREBP pathway. We established that HBx activates SREBP-1a and SREBP-1c through different mechanisms. This process is involved in up-regulating of HBV enhancer I or HBV enhancer II. We demonstrated multiple mechanisms of how HBx regulates HBV replication. We also showed that HCV core interacts with PTEN and PTEN-Long which is involved in regulating of HCV life cycle. In an HBV HCV co-infection cellular model, HBx and HCV core have similar regulatory effects on the PTEN/SREBP pathway as in mono-infections. However, PTEN and SREBP differentially regulate HBV and HCV replication in HBV HCV co-infection. Advisors/Committee Members: Liu, Qiang, Hill, Janet, Chelico, Linda, Liu, Lixin, Anderson, Deborah.

Subjects/Keywords: HBV; HCV; HBx; HCV core; PTEN; SREBP

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APA (6^th Edition):

Wu, Q. (2017). MOLECULAR PATHOGENESIS OF HEPATITIS B VIRUS AND HEPATITIS C VIRUS INFECTIONS. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/7984

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, Qi. “MOLECULAR PATHOGENESIS OF HEPATITIS B VIRUS AND HEPATITIS C VIRUS INFECTIONS.” 2017. Thesis, University of Saskatchewan. Accessed February 16, 2020. http://hdl.handle.net/10388/7984.

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, Qi. “MOLECULAR PATHOGENESIS OF HEPATITIS B VIRUS AND HEPATITIS C VIRUS INFECTIONS.” 2017. Web. 16 Feb 2020.

Vancouver:

Wu Q. MOLECULAR PATHOGENESIS OF HEPATITIS B VIRUS AND HEPATITIS C VIRUS INFECTIONS. [Internet] [Thesis]. University of Saskatchewan; 2017. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/10388/7984.

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

Council of Science Editors:

Wu Q. MOLECULAR PATHOGENESIS OF HEPATITIS B VIRUS AND HEPATITIS C VIRUS INFECTIONS. [Thesis]. University of Saskatchewan; 2017. Available from: http://hdl.handle.net/10388/7984

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

University of Saskatchewan

7. Kandangwa, Mangyung Limbu 1993-. Investigating the Hepatitis C Virus (HCV) RNA Translation Modulation by Non-Structural Protein 5A (NS5A).

Degree: 2016, University of Saskatchewan

URL: http://hdl.handle.net/10388/12539

► Hepatitis C virus (HCV) non-structural protein NS5A is a multifunctional protein and despite lacking enzymatic activity has critical roles in viral replication and assembly. The… (more)

▼ Hepatitis C virus (HCV) non-structural protein NS5A is a multifunctional protein and despite lacking enzymatic activity has critical roles in viral replication and assembly. The role of NS5A in HCV RNA translation has not been well studied. In an attempt to better understand the role of HCV NS5A in RNA translation, our previous work showed that HCV-1b NS5A downregulates viral RNA translation by binding to the poly(U/UC) region in the 3’UTR. All three domains are capable of individually downregulating translation, albeit with a lesser effect than the full-length wild-type NS5A. There are multiple HCV genotypes and NS5A from different genotypes may or may not carry out the same function. Therefore, to determine whether the role of NS5A is conserved in other genotypes, we studied the effect of HCV-2a NS5A on monocistronic HCV-2a RNA reporters and replication defective genomic RNA with or without poly(U/UC) region at the 3’UTR. We found that although HCV-2a NS5A also downregulates viral translation, it does not require the poly(U/UC) region in 3’UTR. The translation downregulation by HCV-2a NS5A was predominantly mediated by domain I. Our results elucidated that HCV-2a NS5A modulates viral translation through a mechanism different from HCV-1b NS5A. NS5A is a phospho-protein and exists as hypo- and hyper-phosphorylated NS5A. The hyperphosphorylation of NS5A is mediated through the phosphorylation of the conserved serine residues cluster in the low complexity sequence LCS I. The serine residues are S222, S225, S229, S232, S235 and S238. Phosphorylation on these serine residues has been found to be important for HCV replication and viral assembly. To further understand the significance of NS5A hyperphosphorylation on HCV life cycle, we investigated the role of HCV-1b NS5A hyperphosphorylation on translation by analyzing the effects of phospho-ablative and phospho-mimetic mutants of the six serine residues on HCV-1b genomic RNA translation. We showed that phosphorylation of S222, S225, S235 is not involved in translation downregulation by NS5A. In contrast, alanine mutations at S229 or S238 can no longer downregulate translation, whereas S229D or S238D mutations have no effect. Interestingly, S232D, but not S232A, abrogates translation downregulation by NS5A. NS5A exists as a dimer and its dimerization is important for regulating its function. Therefore, we studied the effect of phospho-mutants of S229, S232, and S238 on dimerization in a protein-protein interaction assay and showed that phospho-mimetic S229D or S238D mutations enhance NS5A dimerization, whereas the phospho-ablative mutations of them have no effect. In contrast, neither phospho-ablative nor phospho-mimetic mutations of S232 affect dimerization. In conclusion, these results indicated that phosphorylation of NS5A at S229, S232, and S238 is involved in viral translation regulation and NS5A dimerization. In summary, these findings suggest that NS5A downregulates the translation of HCV RNA however, the mechanism may differ within the genotypes. In addition,… Advisors/Committee Members: Liu, Qiang, Tikoo, Suresh, Falzarano, Darryl, Luo , Yu.

Subjects/Keywords: HCV NS5A; HCV RNA translation; NS5A hyperphophorylation

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APA (6^th Edition):

Kandangwa, M. L. 1. (2016). Investigating the Hepatitis C Virus (HCV) RNA Translation Modulation by Non-Structural Protein 5A (NS5A). (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/12539

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):

Kandangwa, Mangyung Limbu 1993-. “Investigating the Hepatitis C Virus (HCV) RNA Translation Modulation by Non-Structural Protein 5A (NS5A).” 2016. Thesis, University of Saskatchewan. Accessed February 16, 2020. http://hdl.handle.net/10388/12539.

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

MLA Handbook (7^th Edition):

Kandangwa, Mangyung Limbu 1993-. “Investigating the Hepatitis C Virus (HCV) RNA Translation Modulation by Non-Structural Protein 5A (NS5A).” 2016. Web. 16 Feb 2020.

Vancouver:

Kandangwa ML1. Investigating the Hepatitis C Virus (HCV) RNA Translation Modulation by Non-Structural Protein 5A (NS5A). [Internet] [Thesis]. University of Saskatchewan; 2016. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/10388/12539.

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

Council of Science Editors:

Kandangwa ML1. Investigating the Hepatitis C Virus (HCV) RNA Translation Modulation by Non-Structural Protein 5A (NS5A). [Thesis]. University of Saskatchewan; 2016. Available from: http://hdl.handle.net/10388/12539

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

University of New South Wales

8. Alavi, Maryam. Barriers to the assessment and treatment of Hepatitis C virus infection in people who inject drugs.

Degree: Kirby Institute, 2014, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/54298 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:34697/SOURCE02?view=true

► Background: Hepatitis C virus (HCV)-related morbidity and mortality are rising. Despite recent therapeutic advances, HCV assessment and treatment uptake remains suboptimal, particularly among people who… (more)

▼ Background: Hepatitis C virus (HCV)-related morbidity and mortality are rising. Despite recent therapeutic advances, HCV assessment and treatment uptake remains suboptimal, particularly among people who inject drugs (PWID). Aims: The broad aim of this research was to inform barriers to the assessment and treatment of HCV infection among PWID. Specific aims included evaluation of mortality and life expectancy among people with chronic HCV infection; evaluation of HCV treatment uptake and associated factors among inner city residents; evaluation of HCV assessment and treatment uptake among PWID in opioid substitution setting; evaluation of willingness to receive HCV treatment among PWID; and evaluation of the impact of treatment for HCV infection on depression and mental health parameters.Methods: In Chapter Two, data from a population-based linkage study were analysed, using a competing risk methodology for calculation of mortality rates and life expectancy. In Chapter Three, data from the Community Health and Safety Evaluation (CHASE) cohort were analysed, using person-time and logistic regression methods. In Chapters Four and Five, data from the Enhancing Treatment for Hepatitis C in Opioid Substitution Settings (ETHOS) study were analysed, using logistic regression. In Chapter Six, data from the Australian Trial in Acute Hepatitis C (ATAHC) study were analysed, using logistic regression. Key Findings: Among people with an HCV notification, liver-related mortality is increasing. Life expectancy in this population is considerably lower, compared to the general population. Over the last decade, HCV treatment uptake has slightly increased yet remained suboptimal. Integration of HCV care within existing infrastructures for addiction care is successful in increasing HCV assessment and treatment uptake among PWID. Despite low HCV treatment uptake, treatment willingness is high among PWID and predicts subsequent assessment and treatment. PWID with poor social functioning may be most at risk of developing depression during HCV therapy. However, depression prior to or during treatment does not have an impact on sustained virological response.Conclusion: Strategic public health planning is needed to lower the rising HCV disease burden. Barriers to HCV assessment and treatment among PWID are complex and require a multidimensional approach. Multidisciplinary partnerships are needed to expand access to HCV services. Advisors/Committee Members: Dore, Gregory, Faculty of Medicine, UNSW, Grebely, Jason, Faculty of Medicine, UNSW.

Subjects/Keywords: Treatment; PWID; HCV

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APA (6^th Edition):

Alavi, M. (2014). Barriers to the assessment and treatment of Hepatitis C virus infection in people who inject drugs. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/54298 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:34697/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Alavi, Maryam. “Barriers to the assessment and treatment of Hepatitis C virus infection in people who inject drugs.” 2014. Doctoral Dissertation, University of New South Wales. Accessed February 16, 2020. http://handle.unsw.edu.au/1959.4/54298 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:34697/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Alavi, Maryam. “Barriers to the assessment and treatment of Hepatitis C virus infection in people who inject drugs.” 2014. Web. 16 Feb 2020.

Vancouver:

Alavi M. Barriers to the assessment and treatment of Hepatitis C virus infection in people who inject drugs. [Internet] [Doctoral dissertation]. University of New South Wales; 2014. [cited 2020 Feb 16]. Available from: http://handle.unsw.edu.au/1959.4/54298 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:34697/SOURCE02?view=true.

Council of Science Editors:

Alavi M. Barriers to the assessment and treatment of Hepatitis C virus infection in people who inject drugs. [Doctoral Dissertation]. University of New South Wales; 2014. Available from: http://handle.unsw.edu.au/1959.4/54298 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:34697/SOURCE02?view=true

9. COSTA, Joanne Elizabeth Ferraz da. Ocorrência de marcadores dos vírus da hepatite B e C e de infecção oculta pelo vírus da hepatite B em pacientes com hanseníase na Paraíba .

Degree: 2017, Universidade Federal de Pernambuco

URL: https://repositorio.ufpe.br/handle/123456789/24984

► Estudos têm reportado maiores prevalências de marcadores sorológicos do vírus da hepatite B (HBV) e da hepatite C (HCV) em pacientes hansênicos e sua associação… (more)

▼ Estudos têm reportado maiores prevalências de marcadores sorológicos do vírus da hepatite B (HBV) e da hepatite C (HCV) em pacientes hansênicos e sua associação com os episódios reacionais. Por outro lado, a deficiência imune apresentada por esses pacientes pode predispor à ocorrência de infecção oculta pelo HBV. O objetivo desta pesquisa foi determinar a prevalência e fatores de risco para os marcadores sorológicos do HBV e do HCV e para a infecção oculta pelo HBV em pacientes com hanseníase. Foi realizado estudo transversal no período de fevereiro de 2015 a janeiro de 2016 em pacientes de Centro de Referência em hanseníase na Paraíba, que após assinatura de termo de consentimento livre e esclarecido foram submetidos à entrevista e coleta de amostras sanguíneas. Os testes sorológicos (ELISA) foram realizados no Setor de Virologia do Laboratório de Imunopatologia Keizo Asami (LIKA) da Universidade Federal de Pernambuco (UFPE). Amostras de plasma foram encaminhadas ao Laboratório Central de Saúde Pública do Estado da Paraíba para estudo molecular (HBV DNA; HCV RNA) por PCR em tempo real. Foram incluídos 403 pacientes no estudo sorológico e 114 pacientes na pesquisa da infecção oculta (HBV DNA). Foi observada frequência de anti-HBc de 14,1% (57/403), de HBsAg 0% (0/403), de anti-HBs isolado 14,1% (57/403), de anti-HCV 0,5% (2/403) e de infecção oculta por HBV 5,3% (6/114). Quanto aos fatores de risco, identificou-se associação do anti-HBc com ter trabalhado na área de saúde e com um menor número de anos de estudo (até nove anos). Não foi observada associação do anti-HBc ou anti-HCV com episódios reacionais, porém identificou-se associação da infecção oculta pelo HBV com história de episódio reacional tipo 2. Assim, as prevalências dos marcadores do HBV e do HCV em hansênicos de Centro de Referência na região Nordeste foram semelhantes às da população geral da mesma região, sugerindo que estes pacientes não apresentam propensão para a infecção crônica por esses vírus. Este foi o primeiro estudo no Brasil sobre a infecção oculta pelo HBV em hansênicos, demonstrando que a pesquisa do HBV DNA deve ser considerada durante o acompanhamento do paciente com hanseníase, tendo em vista a possibilidade de ocorrência de infecção oculta nesses indivíduos. Estudos prospectivos que incluam maior número de pacientes poderão contribuir para uma melhor compreensão da influência da infecção oculta na evolução da hanseníase e em seu tratamento. Advisors/Committee Members: COÊLHO, Maria Rosângela Cunha Duarte (advisor), http://lattes.cnpq.br/7133083621997139 (advisor).

Subjects/Keywords: HBV; HCV; Hanseníase

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

APA (6^th Edition):

COSTA, J. E. F. d. (2017). Ocorrência de marcadores dos vírus da hepatite B e C e de infecção oculta pelo vírus da hepatite B em pacientes com hanseníase na Paraíba . (Doctoral Dissertation). Universidade Federal de Pernambuco. Retrieved from https://repositorio.ufpe.br/handle/123456789/24984

Chicago Manual of Style (16^th Edition):

COSTA, Joanne Elizabeth Ferraz da. “Ocorrência de marcadores dos vírus da hepatite B e C e de infecção oculta pelo vírus da hepatite B em pacientes com hanseníase na Paraíba .” 2017. Doctoral Dissertation, Universidade Federal de Pernambuco. Accessed February 16, 2020. https://repositorio.ufpe.br/handle/123456789/24984.

MLA Handbook (7^th Edition):

COSTA, Joanne Elizabeth Ferraz da. “Ocorrência de marcadores dos vírus da hepatite B e C e de infecção oculta pelo vírus da hepatite B em pacientes com hanseníase na Paraíba .” 2017. Web. 16 Feb 2020.

Vancouver:

COSTA JEFd. Ocorrência de marcadores dos vírus da hepatite B e C e de infecção oculta pelo vírus da hepatite B em pacientes com hanseníase na Paraíba . [Internet] [Doctoral dissertation]. Universidade Federal de Pernambuco; 2017. [cited 2020 Feb 16]. Available from: https://repositorio.ufpe.br/handle/123456789/24984.

Council of Science Editors:

COSTA JEFd. Ocorrência de marcadores dos vírus da hepatite B e C e de infecção oculta pelo vírus da hepatite B em pacientes com hanseníase na Paraíba . [Doctoral Dissertation]. Universidade Federal de Pernambuco; 2017. Available from: https://repositorio.ufpe.br/handle/123456789/24984

10. Vounatsou, Myrsini. Επιδημιολογία της λοίμωξης από τον ιό της ηπατίτιδας C σε ασθενείς κλινικής σεξουαλικών μεταδιδόμενων νοσημάτων και AIDS.

Degree: 2014, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/41110

►

In the present doctoral thesis we try to record epidemiology of Hepatitis C virus (HCV) in Greece, since there are no sufficient relative scientific studies… (more)

▼

In the present doctoral thesis we try to record epidemiology of Hepatitis C virus (HCV) in Greece, since there are no sufficient relative scientific studies concerning our country.The collection of samples was performed in individuals who visited the Department of Sexually Transmitted Diseases and AIDS in “ANDREAS SYNGROS” Hospital during the period from 2004 till the end of 2012. 1.543 individuals were identified as positive to Hepatitis C (HCV) and these data consist the database of the present study.We applied Pearson statistical tool on this database and we attempted to statistically correlate with selective agents-variables, such as other STDs (Sexually Transmitted Diseases), age, sex, educational attainment, origin, sexual orientation, number of partners, usage of condom, usage of toxic substances, as well as with the parameter ‘economical refugee’.The laboratory methods used for the detection of HCV were the routine methods used in the Sexually Transmitted Diseases and AIDS Laboratory of ‘Andreas Syngros’ Hospital, which are immuno-serological and molecular methods. In the first case ELISA and immunoblotting methods were used, while the samples that gave uncertain result with the above mentioned methods were further proceeded with molecular detection.Studying the findings we noted that the most frequently observed groups by category are the following: in terms of toxic substances usage are the users of i.v. drugs, in terms of educational attainment are the elementary school graduates and higher education graduates, in terms of origin Greek people are far more prevalent, in terms of age the most popular group belongs to age category from 31 to 40 years old, in terms of gender men prevail, in terms of sexual orientation are the heterosexuals, in terms of number of partners are the ones with less than 5 partners during the last six months, in terms of coinfections presence the most common case is this of HIV, in terms of condom usage the highest percentage declares rare usage of condom and finally, in terms of the parameter ‘economical refugee’, only a small percentage belongs in this category.With respect to the joined variables HCV+STD, assessing a demographic characterization, our main conclusion was that only the parameter of age is representing a risk factor, while assessing an epidemiological characterization, our main conclusion was that the usage of toxic substances, the number of partners during the last six months and sexual orientation definitely are risk factors.The result of the present study is the accomplishment of an epidemiological study which can be used as a tool for clinicians, enabling them to categorize the potential carriers of the disease and contribute to early prognosis and timely treatment.

Στην παρούσα διδακτορική διατριβή γίνεται προσπάθεια καταγραφής της επιδημιολογίας του ιού της ηπατίτιδας C (HCV) στην Ελλάδα, καθώς δεν υπάρχουν αντίστοιχες επαρκείς επιστημονικές μελέτες στη χώρα μας.Η συλλογή των δειγμάτων αφορά σε άτομα που προσήλθαν στo Τμήμα Σεξουαλικώς Μεταδιδομένων…

Subjects/Keywords: Ηπατίτιδα C; Επιδημιολογία HCV; HCV-συλλοιμώξεις; ΣΜΝ; Hepatitis C; Eoidemiology HCV; HCV-HIV; HCV-coinfections; STDS

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

APA (6^th Edition):

Vounatsou, M. (2014). Επιδημιολογία της λοίμωξης από τον ιό της ηπατίτιδας C σε ασθενείς κλινικής σεξουαλικών μεταδιδόμενων νοσημάτων και AIDS. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/41110

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):

Vounatsou, Myrsini. “Επιδημιολογία της λοίμωξης από τον ιό της ηπατίτιδας C σε ασθενείς κλινικής σεξουαλικών μεταδιδόμενων νοσημάτων και AIDS.” 2014. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed February 16, 2020. http://hdl.handle.net/10442/hedi/41110.

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

MLA Handbook (7^th Edition):

Vounatsou, Myrsini. “Επιδημιολογία της λοίμωξης από τον ιό της ηπατίτιδας C σε ασθενείς κλινικής σεξουαλικών μεταδιδόμενων νοσημάτων και AIDS.” 2014. Web. 16 Feb 2020.

Vancouver:

Vounatsou M. Επιδημιολογία της λοίμωξης από τον ιό της ηπατίτιδας C σε ασθενείς κλινικής σεξουαλικών μεταδιδόμενων νοσημάτων και AIDS. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/10442/hedi/41110.

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

Council of Science Editors:

Vounatsou M. Επιδημιολογία της λοίμωξης από τον ιό της ηπατίτιδας C σε ασθενείς κλινικής σεξουαλικών μεταδιδόμενων νοσημάτων και AIDS. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. Available from: http://hdl.handle.net/10442/hedi/41110

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

Indian Institute of Science

11. Bhat, Prasanna. Characterization of Host Protein Interactions with HCV RNA : Implications in Viral Translation, Replication and Design of Antivirals.

Degree: 2014, Indian Institute of Science

URL: http://etd.iisc.ernet.in/2005/3496 ; http://etd.iisc.ernet.in/abstracts/4363/G26604-Abs.pdf

► HCV genome is a positive sense single-stranded RNA containing a single open reading frame (ORF) flanked by untranslated regions (UTRs), 5’UTR and 3’UTR.Initiation of HCV… (more)

▼ HCV genome is a positive sense single-stranded RNA containing a single open reading frame (ORF) flanked by untranslated regions (UTRs), 5’UTR and 3’UTR.Initiation of HCV RNA translation is mediated by internal ribosome entry site (IRES) present in 5’ UTR and this process is independent of cap-structure and requires only a small subset of canonical initiation factors. Hence, HCV IRES-mediated translation initiation mechanism is quite different from canonical cellular mRNA translation initiation. The IRES is organized into highly structured domains, namely domain II, III and IV. High affinity interactions between structured RNA elements present in the IRES and 40S ribosomal proteins mediate 40S recruitment to HCV IRES. However, details of the RNA elements and region of ribosomal proteins involved in these interactions are poorly understood. In recent days, RNA-based molecules like siRNAs, antisense RNAs and RNA decoys have become promising candidates for antiviral molecules. So designing short RNA molecules that target unique HCV translation initiation mechanism might help in developing novel anti-HCV molecules. HCV 3’UTR and antisense-5’ UTRs serve as sites for replication initiation to synthesize negative and positive strand and this process is catalyzed by NS5B protein (RNA-dependent RNA polymerase). Hence, host proteins binding to both 3’UTR and antisense-5’UTR might play important role in HCV replication. This puts the study of HCV RNA–host protein interactions and its role in viral translation and replication in perspective. Studying the HCV IRES-ribosomal protein S5 interactions and its role in HCV IRES function Previous studies from our laboratory have demonstrated that binding of La protein to GCAC close to initiator AUG enhances ribosomal protein S5 (RPS5) binding with HCV IRES and stimulates HCV translation. However in-detail study on HCV IRES–RPS5 interactions and its implication on HCV translation initiation were lacking. In present study computational modelling suggested that domain II and IV interact majorly with the beta hairpin structure and C-terminal helix of RPS5. Filter-binding and UV cross-linking studies with peptides derived from predicated RNA-binding region of RPS5 and mutational studies with RPS5 demonstrated that beta hairpin structure present in RPS5 is critical for IRES–RPS5 interaction. In parallel, we have studied RNA elements involved in the IRES–RPS5 interactions using deletions and substitution mutations, which we had generated on the basis of the computational model. Direct and competition UV cross-linking experiments performed with these IRES mutants and 40S subunits as a source of RPS5 suggested that structure and sequence of both domain II and IV play crucial role in IRES–RPS5 interactions. We further investigated the effect of these mutations on IRES activity by in vitro translation assay and found that all the mutants that were compromised in binding to RPS5 showed reduced IRES activity. Moreover, ribosome assembly experiments on HCV IRES demonstrated that mutations affecting… Advisors/Committee Members: Das, Saumitra.

Subjects/Keywords: Hepatitis C Virus (HCV) RNA; HCV RNA Host Protein Interactions; HVC Infection; HCV RNA Translation; HCV Genomes; HCV Replication; HCV IRES RNA; HCV IRES; HCV Replication; HCV-IRES; HCV-IRES; HCV RNA; Virus-Host Protein Interactions; Viral RNA Replication; Microbiology and Cell Biology

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

APA (6^th Edition):

Bhat, P. (2014). Characterization of Host Protein Interactions with HCV RNA : Implications in Viral Translation, Replication and Design of Antivirals. (Thesis). Indian Institute of Science. Retrieved from http://etd.iisc.ernet.in/2005/3496 ; http://etd.iisc.ernet.in/abstracts/4363/G26604-Abs.pdf

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):

Bhat, Prasanna. “Characterization of Host Protein Interactions with HCV RNA : Implications in Viral Translation, Replication and Design of Antivirals.” 2014. Thesis, Indian Institute of Science. Accessed February 16, 2020. http://etd.iisc.ernet.in/2005/3496 ; http://etd.iisc.ernet.in/abstracts/4363/G26604-Abs.pdf.

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

MLA Handbook (7^th Edition):

Bhat, Prasanna. “Characterization of Host Protein Interactions with HCV RNA : Implications in Viral Translation, Replication and Design of Antivirals.” 2014. Web. 16 Feb 2020.

Vancouver:

Bhat P. Characterization of Host Protein Interactions with HCV RNA : Implications in Viral Translation, Replication and Design of Antivirals. [Internet] [Thesis]. Indian Institute of Science; 2014. [cited 2020 Feb 16]. Available from: http://etd.iisc.ernet.in/2005/3496 ; http://etd.iisc.ernet.in/abstracts/4363/G26604-Abs.pdf.

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

Council of Science Editors:

Bhat P. Characterization of Host Protein Interactions with HCV RNA : Implications in Viral Translation, Replication and Design of Antivirals. [Thesis]. Indian Institute of Science; 2014. Available from: http://etd.iisc.ernet.in/2005/3496 ; http://etd.iisc.ernet.in/abstracts/4363/G26604-Abs.pdf

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

12. Da Costa, Daniel. Study of cell host factors involved in Hepatitis C virus tropism : Etude des facteurs cellulaires de l'hôte impliqués dans le tropisme du virus de l'hépatite C.

Degree: Docteur es, Virologie : aspects moléculaires et médicaux, 2012, Université de Strasbourg

URL: http://www.theses.fr/2012STRAJ071

►

Le virus de l’hépatite C (HCV) est un problème majeur de santé publique. Le développement de nouveaux traitements pour lutter contre le HCV a été… (more)

▼

Le virus de l’hépatite C (HCV) est un problème majeur de santé publique. Le développement de nouveaux traitements pour lutter contre le HCV a été ralenti par l’absence de modèles d’études in vitro et in vivo convenables. Le but de mon travail de thèse a été, dans un premier temps, de caractériser les facteurs déterminant le tropisme hépatique du HCV. En exprimant des facteurs clés dans une lignée cellulaire humaine non-hépatocytaire, nous avons reconstitué in fine l’ensemble du cycle viral dans ces cellules. L’entrée du virus dans la cellule hôte fait intervenir différents récepteurs d’entrée dont CD81, occludin (OCLN), claudin-1 (CLDN1) et scavenger receptor class B type I (SR-BI). L’expression de ces quatre récepteurs sur cette lignée la rend hautement permissive à l’entrée du virus, mais ne permet pas de rétablir la réplication du virus. L’expression du micro-ARN 122, un micro-RNA important pour l’infection du HCV, dans les cellules exprimant les quatre récepteurs, restaure une forte réplication de l’ARN viral mais ne permet pas de détecter une production de particules infectieuses. L’expression de l’apolipoprotein E (apoE), jouant un rôle primordial dans l’assemblage et la sécrétion, rétablis cette dernière étape du cycle viral du HCV dans la lignée cellulaire humaine non-hépatocytaire. Dans un second temps, j’ai utilisé la stratégie, précédemment établie, pour étudier la spécificité d’espèce de l’infection du HCV dans plusieurs lignées hépatocytaires murines. Nous avons pu rendre ces cellules permissives à l’entrée du HCV et pu détecter une très faible réplication. L’ensemble de mes travaux apportent de nouvelles informations sur la compréhension des facteurs clés nécessaire au cycle viral du HCV dans des cellules murines et humaines.

Hepatitis C virus (HCV) is a global health burden. The development of new therapeutics to treat HCV infection has been hampered by the lack of convenient in vitro and in vivo model systems. The goal of my PhD work was, in a first time, to characterize the factors determining the hepatotropism of HCV. By expressing key factors within a non-hepatic cell line, we reconstituted in fine the full HCV life cycle in those cells. Virus entry into the host cell requires different entry factors which are CD81, occludin (OCLN), claudin-1 (CLDN1) and the scavenger receptor class B type I (SR-BI). The expression of these four factors in this cell line renders it highly permissive to viral entry, but does not allow restoring replication of the virus. The expression of miR-122, a micro-RNA important for HCV infection, into the cell lines expressing the four HCV entry factors restore a strong replication of the HCV RNA but does not allow detecting infectious viral particle production. Further expression of the apolipoprotein E (apoE), which plays a critical role in the assembly and release process, restore the last step of the HCV life cycle in a non-hepatic cell line. In a second part of my PhD, I have used the previously developed strategy to study the species specificity of HCV infection…

Advisors/Committee Members: Baumert, Thomas (thesis director).

Subjects/Keywords: Intéraction virus-hôte; Tropisme du HCV; Spécificité d’espèce du HCV; Entrée du HCV; Replication du HCV; Assemblage du HCV et modèle murin du HCV; Hepatitis C virus infection; Virus-host interaction; HCV tropism; HCV species specificity; HCV entry; HCV replication; HCV assembly and HCV mouse model; 579.2; 616.91; 572.8

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

APA (6^th Edition):

Da Costa, D. (2012). Study of cell host factors involved in Hepatitis C virus tropism : Etude des facteurs cellulaires de l'hôte impliqués dans le tropisme du virus de l'hépatite C. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2012STRAJ071

Chicago Manual of Style (16^th Edition):

Da Costa, Daniel. “Study of cell host factors involved in Hepatitis C virus tropism : Etude des facteurs cellulaires de l'hôte impliqués dans le tropisme du virus de l'hépatite C.” 2012. Doctoral Dissertation, Université de Strasbourg. Accessed February 16, 2020. http://www.theses.fr/2012STRAJ071.

MLA Handbook (7^th Edition):

Da Costa, Daniel. “Study of cell host factors involved in Hepatitis C virus tropism : Etude des facteurs cellulaires de l'hôte impliqués dans le tropisme du virus de l'hépatite C.” 2012. Web. 16 Feb 2020.

Vancouver:

Da Costa D. Study of cell host factors involved in Hepatitis C virus tropism : Etude des facteurs cellulaires de l'hôte impliqués dans le tropisme du virus de l'hépatite C. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2012. [cited 2020 Feb 16]. Available from: http://www.theses.fr/2012STRAJ071.

Council of Science Editors:

Da Costa D. Study of cell host factors involved in Hepatitis C virus tropism : Etude des facteurs cellulaires de l'hôte impliqués dans le tropisme du virus de l'hépatite C. [Doctoral Dissertation]. Université de Strasbourg; 2012. Available from: http://www.theses.fr/2012STRAJ071

University of Alberta

13. Samrat, Subodh Kr. MODULATION OF IMMUNE RESPONSE BY HCV-DERIVED F, CORE AND NS3 PROTEINS.

Degree: PhD, Department of Surgery, 2013, University of Alberta

URL: https://era.library.ualberta.ca/files/vm40xt06s

► The hepatitis C virus leads to chronic infection in the majority of infected individuals; however, in a minority of patients, acute infection is followed by… (more)

▼ The hepatitis C virus leads to chronic infection in the majority of infected individuals; however, in a minority of patients, acute infection is followed by viral clearance. The immune correlates of viral clearance are not yet clear, but have been extensively investigated, suggesting the role of multispecific and multifunctional cellular immunity. In the current studies, we demonstrated that endogenous expression of the F protein in human DCs leads to contrasting effects on activation and apoptosis of DCs, allowing the activated DCs to efficiently internalize apoptotic DCs. These in turn result in the efficient ability of DCs to process and present antigen, and prime and stimulate antigen-specific T cells from HCV-naive individuals. Our in vivo studies show that mice immunized with F- or core-containing adenovector induce dysfunctional T cells with reduced granzyme B (GrB) expression which are unable to kill peptide-loaded target cells. Exogenous addition of IL-2 in in vitro cultures, as well as immunization with the toll-like receptor (TLR) agonist poly I:C restores the GrB expression in T cells. Thus, we have discovered a new mechanism of T cell modulation by HCV-derived antigens and we have also delineated strategies to overcome this dysfunction. Further, we have analyzed the early immune events in the mice immunized with recombinant adenovector containing core and NS3 in a time-course manner. Our results demonstrate that despite efficient expression of both antigens at the site of immunization, T cell proliferation and IL-2, IL-6 and IL-12 production were significantly higher in NS3-immunized mice at 12-48 hours after immunization compared to the core-immunized mice. These studies have implied that early events in antigen encounters imprint the subsequent immunity and the final outcome; two distinct patterns of early events in immunity can be demonstrated for the antigens core and NS3. Over all, my studies have discovered a new mechanism of immune modulation by HCV-derived antigens that could help in designing both prophylactic and therapeutic vaccine candidates against the HCV.

Subjects/Keywords: HCV; Immunology; DCs modulation

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

APA (6^th Edition):

Samrat, S. K. (2013). MODULATION OF IMMUNE RESPONSE BY HCV-DERIVED F, CORE AND NS3 PROTEINS. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/vm40xt06s

Chicago Manual of Style (16^th Edition):

Samrat, Subodh Kr. “MODULATION OF IMMUNE RESPONSE BY HCV-DERIVED F, CORE AND NS3 PROTEINS.” 2013. Doctoral Dissertation, University of Alberta. Accessed February 16, 2020. https://era.library.ualberta.ca/files/vm40xt06s.

MLA Handbook (7^th Edition):

Samrat, Subodh Kr. “MODULATION OF IMMUNE RESPONSE BY HCV-DERIVED F, CORE AND NS3 PROTEINS.” 2013. Web. 16 Feb 2020.

Vancouver:

Samrat SK. MODULATION OF IMMUNE RESPONSE BY HCV-DERIVED F, CORE AND NS3 PROTEINS. [Internet] [Doctoral dissertation]. University of Alberta; 2013. [cited 2020 Feb 16]. Available from: https://era.library.ualberta.ca/files/vm40xt06s.

Council of Science Editors:

Samrat SK. MODULATION OF IMMUNE RESPONSE BY HCV-DERIVED F, CORE AND NS3 PROTEINS. [Doctoral Dissertation]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/vm40xt06s

Texas A&M University

14. Reddy Chinnaswamy, Sreedhar. De Novo Initiated RNA Synthesis by the Hepatitis C Virus RNA-dependent RNA Polymerase.

Degree: 2011, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7816

► Hepatitis C Virus (HCV) is a positive-strand RNA virus that has infected more than 3% of the world population. Chronic infections by the virus lead… (more)

▼ Hepatitis C Virus (HCV) is a positive-strand RNA virus that has infected more than 3% of the world population. Chronic infections by the virus lead to cirrhosis and hepatocellular carcinoma. HCV is currently the leading cause for liver transplantation in the US. The nonstructural protein NS5B of HCV is the RNA-dependent RNA polymerase (RdRp) that replicates the viral RNA on host derived membranous structures. Structurally NS5B has the characteristic fingers, thumb and palm domains seen in all polymerase proteins. However, extensive interactions between the fingers and thumb domains completely encircle the active site of NS5B as seen in solved X-ray diffraction crystal structures. These interactions are primarily mediated by a short (35 residues) flexible loop called the Delta 1 loop. NS5B produced from heterologous systems can initiate RNA synthesis by a de novo initiation mechanism from 3?ends of RNA templates or can also extend from 3'ends of primers that are annealed stably to a template RNA in biochemical assays. The closed conformation of NS5B as per X-ray crystal structures can only accommodate a ssRNA but not a dsRNA, hence necessitating a conformational change between de novo initiation and elongation. The details of these conformational changes are not known and will prove to be important to design potent polymerase inhibitors. The study performed for this dissertation focused on the conformational requirements of NS5B during de novo initiation and primer extension (or elongation). Biochemical assays utilizing template RNAs that can lead to both de novo initiation and primer extension products were utilized, and a systematic mutational analysis of the template channel of the RdRp was performed. Mutants W397A and H428A were identified that showed only primer extension but no de novo initiation. Structural analysis of NS5B suggested that these residues were important contact points in the Delta 1 loop and thumb domain interactions. A deletion mutant, m26-30 with a five amino acid deletion at the apex of the Delta 1 loop also failed in de novo initiation but not primer extension reactions. Biophysical and gel shift assays showed that m26-30 was in a more open conformation than the WT enzyme. Furthermore, oligomerization of NS5B was demonstrated and its role in RNA synthesis was examined. It was found that the de novo initiation competent conformation of NS5B is maintained by oligomeric contacts between individual subunits, likely by stabilizing the Delta 1 loop and thumb domain interactions. Mutations disrupting the Delta 1 loop and thumb domain interactions as well as those in the allosteric GTP binding site induced conformational changes in the protein partially explaining the defect in de novo initiation activity in enzymes carrying those mutations. These results not only contribute to the overall mechanism of RNA synthesis in viral RdRps but also open new avenues for developing HCV polymerase inhibitors. Advisors/Committee Members: Kao, Cheng C. (advisor), Young, Ryland F. (advisor), Leibowitz, Julian L. (committee member), Scholtz, Martin J. (committee member).

Subjects/Keywords: HCV; RdRp; Polymerase; Conformation; Oligomerization

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

APA (6^th Edition):

Reddy Chinnaswamy, S. (2011). De Novo Initiated RNA Synthesis by the Hepatitis C Virus RNA-dependent RNA Polymerase. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7816

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):

Reddy Chinnaswamy, Sreedhar. “De Novo Initiated RNA Synthesis by the Hepatitis C Virus RNA-dependent RNA Polymerase.” 2011. Thesis, Texas A&M University. Accessed February 16, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7816.

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

MLA Handbook (7^th Edition):

Reddy Chinnaswamy, Sreedhar. “De Novo Initiated RNA Synthesis by the Hepatitis C Virus RNA-dependent RNA Polymerase.” 2011. Web. 16 Feb 2020.

Vancouver:

Reddy Chinnaswamy S. De Novo Initiated RNA Synthesis by the Hepatitis C Virus RNA-dependent RNA Polymerase. [Internet] [Thesis]. Texas A&M University; 2011. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7816.

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

Council of Science Editors:

Reddy Chinnaswamy S. De Novo Initiated RNA Synthesis by the Hepatitis C Virus RNA-dependent RNA Polymerase. [Thesis]. Texas A&M University; 2011. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7816

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

Texas A&M University

15. Simeon, Rudo Lyndon. Selecting a path against Hepatitis C Virus.

Degree: 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151941

► Hepatitis C virus (HCV) currently affects ~5% of the world?s population and has relatively limited treatment options for infected patients. Genetic suppressor elements (GSE) derived… (more)

▼ Hepatitis C virus (HCV) currently affects ~5% of the world?s population and has relatively limited treatment options for infected patients. Genetic suppressor elements (GSE) derived from a gene or genome of interest can act as transdominant inhibitors of a particular biology function presumably by binding to and blocking an essential interaction surface for protein activity. Taking advantage of hepatoma cell line n4mBid, that supports all stages of the HCV life cycle and strongly report HCV infection by a cell-death phenotype, we developed an iterative selection/enrichment strategy for the identification of GSE against HCV. Using this strategy, a library expressing random fragments of the HCV genome was screened for sequences able to suppress HCV infection. A 244 amino acid gene fragment, B1, was strongly enriched after 5 rounds of selection. B1 has a very high net positive charge of 43 at neutral pH and a high charge-to-mass (kDa) ratio of 1.5. We show that B1 expression specifically inhibits HCV replication, apparently due to its high positive charge. We also show that recombinant positively charged proteins can inhibit HCV infection, when supplied in vitro.In addition, eGFP-fused B1 potently penetrates both adherent and suspension cells with >80% of cells taking up the protein. Importantly, we show that B1 not only facilitates cellular uptake, but allows protein cargo to reach sites of biological relevance. B1 also delivers non-covalently conjugated RNA and DNA across the cell membrane to cytosolic and nuclear sites, with efficiency comparable to commercially available cationic lipid reagents. Our data suggest that B1 utilizes cell-surface glycans and multiple competing endocytic pathways to enter and traffic through cells.During a separate screening carried out in our lab, we identified a TACR3 inhibitor SB 222200 that had significant HCV activity. We go on to show that both TACR1 and TACR3 receptors are expressed in the HCV-permissive Huh 7.5 cell line. We also show that both TACR1 and TACR3 inhibitors significantly inhibit HCV infection. These results point to the potential for TACR1 antagonists in treating patients infected with both HCV and HIV. Advisors/Committee Members: Chen, Zhilei (advisor), Jayaraman, Arul (committee member), Karim, Nazmul (committee member), Leibowitz, Julian (committee member).

Subjects/Keywords: HCV; biomolecules; biotherapeutics; transfection; transduction

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

APA (6^th Edition):

Simeon, R. L. (2013). Selecting a path against Hepatitis C Virus. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151941

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):

Simeon, Rudo Lyndon. “Selecting a path against Hepatitis C Virus.” 2013. Thesis, Texas A&M University. Accessed February 16, 2020. http://hdl.handle.net/1969.1/151941.

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

MLA Handbook (7^th Edition):

Simeon, Rudo Lyndon. “Selecting a path against Hepatitis C Virus.” 2013. Web. 16 Feb 2020.

Vancouver:

Simeon RL. Selecting a path against Hepatitis C Virus. [Internet] [Thesis]. Texas A&M University; 2013. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/1969.1/151941.

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

Council of Science Editors:

Simeon RL. Selecting a path against Hepatitis C Virus. [Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151941

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

Texas A&M University

16. Chamoun Emanuelli, Ana M. Characterization of Viral Entry Inhibitors.

Degree: 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/153447

► Hepatitis C virus (HCV), Human Immunodeficiency virus (HIV) and Herpes Simplex virus (HSV) are pathogenic viruses known to cause liver disorder, acquired immunodeficiency and skin… (more)

Subjects/Keywords: HCV; HSV; HIV; entry inhibitors

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APA (6^th Edition):

Chamoun Emanuelli, A. M. (2014). Characterization of Viral Entry Inhibitors. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153447

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):

Chamoun Emanuelli, Ana M. “Characterization of Viral Entry Inhibitors.” 2014. Thesis, Texas A&M University. Accessed February 16, 2020. http://hdl.handle.net/1969.1/153447.

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

MLA Handbook (7^th Edition):

Chamoun Emanuelli, Ana M. “Characterization of Viral Entry Inhibitors.” 2014. Web. 16 Feb 2020.

Vancouver:

Chamoun Emanuelli AM. Characterization of Viral Entry Inhibitors. [Internet] [Thesis]. Texas A&M University; 2014. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/1969.1/153447.

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

Council of Science Editors:

Chamoun Emanuelli AM. Characterization of Viral Entry Inhibitors. [Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153447

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

Duquesne University

17. Schrott, Valerie. Characterization of the Hepatitis C Virus Genome Interactions with the microRNA miR-122: Potential New Therapeutic Targets for Peptide Nucleic Acid Based Strategies.

Degree: MS, Chemistry and Biochemistry, 2012, Duquesne University

URL: https://dsc.duq.edu/etd/1157

► Hepatitis C virus (HCV), a positive-sense RNA virus that chronically infects between 2.7 and 3.9 million Americans, is highly mutational, making the HCV infection difficult… (more)

Subjects/Keywords: HCV; miR-122; PNA

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

APA (6^th Edition):

Schrott, V. (2012). Characterization of the Hepatitis C Virus Genome Interactions with the microRNA miR-122: Potential New Therapeutic Targets for Peptide Nucleic Acid Based Strategies. (Masters Thesis). Duquesne University. Retrieved from https://dsc.duq.edu/etd/1157

Chicago Manual of Style (16^th Edition):

Schrott, Valerie. “Characterization of the Hepatitis C Virus Genome Interactions with the microRNA miR-122: Potential New Therapeutic Targets for Peptide Nucleic Acid Based Strategies.” 2012. Masters Thesis, Duquesne University. Accessed February 16, 2020. https://dsc.duq.edu/etd/1157.

MLA Handbook (7^th Edition):

Schrott, Valerie. “Characterization of the Hepatitis C Virus Genome Interactions with the microRNA miR-122: Potential New Therapeutic Targets for Peptide Nucleic Acid Based Strategies.” 2012. Web. 16 Feb 2020.

Vancouver:

Schrott V. Characterization of the Hepatitis C Virus Genome Interactions with the microRNA miR-122: Potential New Therapeutic Targets for Peptide Nucleic Acid Based Strategies. [Internet] [Masters thesis]. Duquesne University; 2012. [cited 2020 Feb 16]. Available from: https://dsc.duq.edu/etd/1157.

Council of Science Editors:

Schrott V. Characterization of the Hepatitis C Virus Genome Interactions with the microRNA miR-122: Potential New Therapeutic Targets for Peptide Nucleic Acid Based Strategies. [Masters Thesis]. Duquesne University; 2012. Available from: https://dsc.duq.edu/etd/1157

18. Papachristou, Eleni. Μελέτη της πολυμορφίας του HCV στην Ελλάδα: αναζήτηση σπανίων στελεχών και μέθοδοι προσδιορισμού τους.

Degree: 2017, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/41393

►

The discovery of the HCV virus as the etiologic factor for the non A, non B hepatitis cases, led to the development of many methods… (more)

▼

The discovery of the HCV virus as the etiologic factor for the non A, non B hepatitis cases, led to the development of many methods and technologies for its detection and identification. HCV is a flavivirus and its genome is a single stranded RNA molecule which encodes for a polyprotein which provides the structural and non structural proteins of the virus. The target cells for HCV are the hepatocytes as well as B and T lymphocytes, dendritic and mononuclear cells which the virus enters throygh endocytosis. Although the immune system manages to clear the virus a large number (80-85%) of patients become chronic carriers from which about 5-25% will develop chirrossis, end stage liver disease and hepatocellular carcinoma.HCV has a great genetic diversity, is spread worldwide having infected more than 150 million of people and is classified in seven major genotypes and many subtypes. The detection and quantification of thw HCV RNA are valuable tools for monitoring the chronic infection and the outcome of the therapy. Furthermore, knowing the genotype with which a patient is infected is crucial for the choice of the therary regimen. The aim of this study was to develop two in house methods a) for the detection and quantification of the HCV RNA and b) for the determination of the genotype in order to study the diversity of HCV in Greece.For the quantification method we targeted at the 3’UTR end of the genome in contrast to all the commercially available methods which target the 5’end. After experimenting with different types of reagents and enzymes and on different platforms we finally chose the technology of one step real time RT PCR on the Light Cycler platform (Roche). The method was validated with international standards and was evaluated with two commercially available methods from Abbott and Roche with excellent results. The method is quick, reliable and low cost and can be further developed.For the HCV genotyping we developed a method based on the sequencing of the NS5B region of the genome. We designed primers and tried many PCR protocols. The obtained sequences were analysed with phylogenetic analysis methods. The method was validated with international standards and was certified by ΕΣΥΔ. With this method we genotyped most of the undetermined samples (by other methods) in our lab and mainly we studied the HCV dispersal pattern among IDUs (intravenous drug users) in Athens as part of the “Aristotle” programme.

Η ανακάλυψη και ταυτοποίηση του ιού HCV ως τον αιτιολογικό παράγοντα των περιστατικών μη-Α, μη-Β ηπατίτιδας ήταν η αρχή για την ανάπτυξη διαφόρων μεθόδων και τεχνολογιών για την ανίχνευση και τυποποίησή του. Ο ιός HCV ανήκει στην οικογένεια Flaviviridae, γένος hepacivirus και το γονιδίωμά του είναι μονόκλωνο RNA θετικής πολικότητας που κωδικοποιεί μια πολυπρωτεϊνη από την οποία προκύπτουν οι δομικές και οι μη δομικές πρωτεϊνες του. Κύτταρα-στόχοι του ιού – στα οποία εισέρχεται με ενδοκύτωση μετά από πρόσδεση σε ειδικούς υποδοχείς- είναι τα ηπατοκύτταρα αλλά αναφέρονται και τα λεμφοκύτταρα (Β και Τ) καθώς…

Subjects/Keywords: Ηπατίτιδα C; HCV-RNA; Γονότυπος HCV; ΧΕΝ; Δίκτυα μετάδοσης; Hepatitis C; HCV-RNA; HCV genotype; IDU; Transmission networks

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

APA (6^th Edition):

Papachristou, E. (2017). Μελέτη της πολυμορφίας του HCV στην Ελλάδα: αναζήτηση σπανίων στελεχών και μέθοδοι προσδιορισμού τους. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/41393

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):

Papachristou, Eleni. “Μελέτη της πολυμορφίας του HCV στην Ελλάδα: αναζήτηση σπανίων στελεχών και μέθοδοι προσδιορισμού τους.” 2017. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed February 16, 2020. http://hdl.handle.net/10442/hedi/41393.

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

MLA Handbook (7^th Edition):

Papachristou, Eleni. “Μελέτη της πολυμορφίας του HCV στην Ελλάδα: αναζήτηση σπανίων στελεχών και μέθοδοι προσδιορισμού τους.” 2017. Web. 16 Feb 2020.

Vancouver:

Papachristou E. Μελέτη της πολυμορφίας του HCV στην Ελλάδα: αναζήτηση σπανίων στελεχών και μέθοδοι προσδιορισμού τους. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2017. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/10442/hedi/41393.

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

Council of Science Editors:

Papachristou E. Μελέτη της πολυμορφίας του HCV στην Ελλάδα: αναζήτηση σπανίων στελεχών και μέθοδοι προσδιορισμού τους. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2017. Available from: http://hdl.handle.net/10442/hedi/41393

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

19. 西村, 知裕; ニシムラ, トモヒロ. Clarification of the mechanism of p53 inactivation by the novel HCV infection-related protein 3β-hydroxysterol Δ24-reductase : シンキ HCV カンレンインシ 3β hydroxysterol Δ24 reductase ニヨル p53 キノウヨクセイキコウノカイメイ; 新規HCV関連因子 3β-hydroxysterol Δ24-reductase によるp53 機能抑制機構の解明.

Degree: Kumamoto University / 熊本大学

URL: http://hdl.handle.net/2298/21804

► The hepatitis C virus (HCV) is one of the most important causes of chronic liver disease. This chronic infection induces chronic hepatitis, hepatic cirrhosis and… (more)

Subjects/Keywords: HCV; DHCR24

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APA (6^th Edition):

西村, 知裕; ニシムラ, �. (n.d.). Clarification of the mechanism of p53 inactivation by the novel HCV infection-related protein 3β-hydroxysterol Δ24-reductase : シンキ HCV カンレンインシ 3β hydroxysterol Δ24 reductase ニヨル p53 キノウヨクセイキコウノカイメイ; 新規HCV関連因子 3β-hydroxysterol Δ24-reductase によるp53 機能抑制機構の解明. (Thesis). Kumamoto University / 熊本大学. Retrieved from http://hdl.handle.net/2298/21804

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

西村, 知裕; ニシムラ, トモヒロ. “Clarification of the mechanism of p53 inactivation by the novel HCV infection-related protein 3β-hydroxysterol Δ24-reductase : シンキ HCV カンレンインシ 3β hydroxysterol Δ24 reductase ニヨル p53 キノウヨクセイキコウノカイメイ; 新規HCV関連因子 3β-hydroxysterol Δ24-reductase によるp53 機能抑制機構の解明.” Thesis, Kumamoto University / 熊本大学. Accessed February 16, 2020. http://hdl.handle.net/2298/21804.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

西村, 知裕; ニシムラ, トモヒロ. “Clarification of the mechanism of p53 inactivation by the novel HCV infection-related protein 3β-hydroxysterol Δ24-reductase : シンキ HCV カンレンインシ 3β hydroxysterol Δ24 reductase ニヨル p53 キノウヨクセイキコウノカイメイ; 新規HCV関連因子 3β-hydroxysterol Δ24-reductase によるp53 機能抑制機構の解明.” Web. 16 Feb 2020.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

西村, 知裕; ニシムラ �. Clarification of the mechanism of p53 inactivation by the novel HCV infection-related protein 3β-hydroxysterol Δ24-reductase : シンキ HCV カンレンインシ 3β hydroxysterol Δ24 reductase ニヨル p53 キノウヨクセイキコウノカイメイ; 新規HCV関連因子 3β-hydroxysterol Δ24-reductase によるp53 機能抑制機構の解明. [Internet] [Thesis]. Kumamoto University / 熊本大学; [cited 2020 Feb 16]. Available from: http://hdl.handle.net/2298/21804.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

西村, 知裕; ニシムラ �. Clarification of the mechanism of p53 inactivation by the novel HCV infection-related protein 3β-hydroxysterol Δ24-reductase : シンキ HCV カンレンインシ 3β hydroxysterol Δ24 reductase ニヨル p53 キノウヨクセイキコウノカイメイ; 新規HCV関連因子 3β-hydroxysterol Δ24-reductase によるp53 機能抑制機構の解明. [Thesis]. Kumamoto University / 熊本大学; Available from: http://hdl.handle.net/2298/21804

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

20. ALBUQUERQUE, Diego Araújo Pessoa de. Perfil Proteômico e Imunômico da Lectina Ligadora de Manose (Mbl) em Indivíduos Portadores do Vírus da Hepatite .

Degree: 2010, Universidade Federal de Pernambuco

URL: http://repositorio.ufpe.br/handle/123456789/1811

► A lectina ligadora de manose (mannan binding lectin - MBL) é membro das glicoproteínas plasmáticas, um grupo de proteínas que se caracteriza pela interação com… (more)

▼ A lectina ligadora de manose (mannan binding lectin - MBL) é membro das glicoproteínas plasmáticas, um grupo de proteínas que se caracteriza pela interação com um ou mais resíduos de açúcares específicos expressos em vários sistemas biológicos. Concentrações reduzidas de MBL tem sido relacionadas com a diminuição na resposta a varias doenças infecciosas. Inúmeras formas oligoméricas da MBL, com diferentes capacidades funcionais, são encontradas no sangue humano. Estudos controversos lidam com a possível associação entre mutações no gene da MBL e a infecção com o vírus da hepatite C (hepatitis C vírus - HCV). Não existem associações significativas entre pacientes com baixos níveis séricos de MBL e as características de desenvolvimento da doença, incluindo a resposta a terapia antiviral. O presente estudo teve como objetivo propor um ensaio prático para purificação de formas moleculares de MBL em amostras de soro de pacientes infectados com HCV visando investigar a estrutura e o genótipo desta lectina. Os resultados do ensaio de dot-N-man demonstraram uma boa eficiência na separação da MBL utilizando membrana de nitrocelulose revestida de manana. A identificação de MBL foi confirmada em todos os genótipos por método convencional de dot-ELISA. Bandas protéicas em gel de eletroforese revelaram diferentes padrões de migração entre os genótipos AA, A0 e 00, entre 50-90 KDa, e 270 KDa, relacionadas com a variação de baixa e alta massa molecular da subunidade estrutural de MBL, respectivamente. Nas amostras de SDS-PAGE não redutora observou-se uma maior variedade de massas moleculares, como dímeros, trímeros, e as unidades estruturais de MBL, principalmente em indivíduos AA. A analise de western blotting confirmou a presença de alta (128 KDa) e baixa (32KDa) massas moleculares da MBL. Foi também observada a presença de MBL com massa molecular de 128 KDa, a qual não é muito comum. Os resultados mostraram que ambas, baixa e alta formas moleculares, foram identificadas e também houve variação com a genotipagem dos pacientes. Os resultados descrevendo o proteoma das formas moleculares de MBL em pacientes com HCV contribuíram para melhor compreensão da estrutura/genótipo da MBL nesta patologia que pode estar associada à resposta ao tratamento Advisors/Committee Members: CARVALHO JUNIOR, Luiz Bezerra de (advisor).

Subjects/Keywords: dot-N-man; HCV; MBL

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

APA (6^th Edition):

ALBUQUERQUE, D. A. P. d. (2010). Perfil Proteômico e Imunômico da Lectina Ligadora de Manose (Mbl) em Indivíduos Portadores do Vírus da Hepatite . (Thesis). Universidade Federal de Pernambuco. Retrieved from http://repositorio.ufpe.br/handle/123456789/1811

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):

ALBUQUERQUE, Diego Araújo Pessoa de. “Perfil Proteômico e Imunômico da Lectina Ligadora de Manose (Mbl) em Indivíduos Portadores do Vírus da Hepatite .” 2010. Thesis, Universidade Federal de Pernambuco. Accessed February 16, 2020. http://repositorio.ufpe.br/handle/123456789/1811.

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

MLA Handbook (7^th Edition):

ALBUQUERQUE, Diego Araújo Pessoa de. “Perfil Proteômico e Imunômico da Lectina Ligadora de Manose (Mbl) em Indivíduos Portadores do Vírus da Hepatite .” 2010. Web. 16 Feb 2020.

Vancouver:

ALBUQUERQUE DAPd. Perfil Proteômico e Imunômico da Lectina Ligadora de Manose (Mbl) em Indivíduos Portadores do Vírus da Hepatite . [Internet] [Thesis]. Universidade Federal de Pernambuco; 2010. [cited 2020 Feb 16]. Available from: http://repositorio.ufpe.br/handle/123456789/1811.

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

Council of Science Editors:

ALBUQUERQUE DAPd. Perfil Proteômico e Imunômico da Lectina Ligadora de Manose (Mbl) em Indivíduos Portadores do Vírus da Hepatite . [Thesis]. Universidade Federal de Pernambuco; 2010. Available from: http://repositorio.ufpe.br/handle/123456789/1811

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

Penn State University

21. Aligo, Jason Alan. Defining the Role of the Nonstructural Protein 4B C-Terminal Domain in Hepatitis C Virus Replication.

Degree: PhD, Genetics, 2009, Penn State University

URL: https://etda.libraries.psu.edu/catalog/9944

► Like most positive-strand RNA viruses, the Hepatitis C Virus (HCV) replication complex is associated with rearranged cytoplasmic membranes. For HCV, a novel membrane structure, termed… (more)

▼ Like most positive-strand RNA viruses, the Hepatitis C Virus (HCV) replication complex is associated with rearranged cytoplasmic membranes. For HCV, a novel membrane structure, termed the membranous web, has been observed in HCV-infected cells or in cells expressing the mature NS4B. However, we still do not understand the role of NS4B protein in HCV genome replication. NS4B could contribute by forming the web structure, providing the scaffold for other replicase proteins, or in binding HCV RNA. To better understand the role of NS4B in HCV genome replication, we introduced mutations in the poorly characterized C-terminal domain (CTD) in the context of the HCV subgenomic replicon. Interestingly, these mutants all resulted in a significant decrease in HCV replication as determined by colony formation assay. Transient expression of mutant replicons, followed by immunofluorescence indicated that certain NS4B CTD point mutantss resulted in reticular staining rather than punctate foci shown in cells expressing the WT replicon. These same mutants caused redistribution of NS5A to these reticular structures, indicating that the CTD may play a role in membranous web formation or in recruitment of other replicase proteins (or both). To test the hypothesis that the NS4B CTD might play a role in membranous web formation, we deleted the entire CTD in the context of NS4B protein alone. Deletion or removal of parts of this domain resulted in loss of webs as visualized via electron microscopy. However, expression of the CTD alone did not result in web formation, arguing that the NS4B CTD was required but not sufficient to form the web structure. Further, our data indicate that deletion of the NS4B CTD prevents NS4B from co-localizing with Rab5, an early endosomal GTPase that our laboratory has previously found to be required for HCV replication. Finally, studies with an NS4B protein from an HCV-related pestivirus (Bovine Viral Diarrhea Virus - BVDV) indicated that a chimeric protein consisting of the HCV N-terminus of NS4B and the C-terminus from BVDV NS4B induces the formation of foci. However, these foci were of a different morphology compared to those formed after expression of HCV NS4B. The chimeric NS4B protein also failed to co-localize with Rab5. These results suggest that although the NS4B CTD from related flaviviruses play a role in the formation of NS4B-asociated foci, that these structures may have alternate functions or utilize different host factors. These factors may also be unique to the host cell utilized by these viruses. The significance of these findings and the ramifications for the flavivirus family is discussed.

Subjects/Keywords: HCV; NS4B; Virus; Replication; CTD

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

APA (6^th Edition):

Aligo, J. A. (2009). Defining the Role of the Nonstructural Protein 4B C-Terminal Domain in Hepatitis C Virus Replication. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/9944

Chicago Manual of Style (16^th Edition):

Aligo, Jason Alan. “Defining the Role of the Nonstructural Protein 4B C-Terminal Domain in Hepatitis C Virus Replication.” 2009. Doctoral Dissertation, Penn State University. Accessed February 16, 2020. https://etda.libraries.psu.edu/catalog/9944.

MLA Handbook (7^th Edition):

Aligo, Jason Alan. “Defining the Role of the Nonstructural Protein 4B C-Terminal Domain in Hepatitis C Virus Replication.” 2009. Web. 16 Feb 2020.

Vancouver:

Aligo JA. Defining the Role of the Nonstructural Protein 4B C-Terminal Domain in Hepatitis C Virus Replication. [Internet] [Doctoral dissertation]. Penn State University; 2009. [cited 2020 Feb 16]. Available from: https://etda.libraries.psu.edu/catalog/9944.

Council of Science Editors:

Aligo JA. Defining the Role of the Nonstructural Protein 4B C-Terminal Domain in Hepatitis C Virus Replication. [Doctoral Dissertation]. Penn State University; 2009. Available from: https://etda.libraries.psu.edu/catalog/9944

22. GOMES, Daniel Christiano de Albuquerque. Disfunção cognitiva em pacientes com infecção crônica pelo vírus da hepatite C: estudo transversal na cidade do Recife e revisão de literatura .

Degree: 2011, Universidade Federal de Pernambuco

URL: https://repositorio.ufpe.br/handle/123456789/29281

► A hepatite C crônica constitui atualmente importante problema de saúde pública, visto que acomete cerca de 2% da população mundial. Representa uma das principais causas… (more)

▼ A hepatite C crônica constitui atualmente importante problema de saúde pública, visto que acomete cerca de 2% da população mundial. Representa uma das principais causas de cirrose hepática, hepatocarcinoma e transplante hepático. Embora suas principais conseqüências se devam ao comprometimento hepático, manifestações extra-hepáticas da doença têm sido bem documentadas. Ao longo dos últimos anos, pesquisas com a utilização de diferentes ferramentas diagnósticas têm apontado a ocorrência de disfunção cognitiva nesta população. O presente trabalho é composto por dois artigos. O primeiro deles é um artigo de revisão, o qual visa a abordar as evidências mais atuais dos efeitos neurocognitivos da infecção crônica pelo HCV. São revisados os tipos e a prevalência de alterações cerebrais identificadas nos variados métodos diagnósticos empregados, assim como os mecanismos patogênicos propostos para a disfunção cognitiva. Embora sejam notadas controvérsias na literatura revisada, identifica-se que prejuízos em atenção, velocidade de processamento mental e memória de trabalho têm sido os mais comumente descritos na hepatite C crônica, configurando um padrão compatível com disfunção frontal-subcortical. Além disso, na parte final do artigo, são comentados os principais impactos da co-infecção HCV/HIV e da terapia antiviral à cognição.Já o segundo é um artigo original, que descreve um estudo transversal realizado em Recife, no Nordeste do Brasil. A pesquisa objetivou avaliar, através da aplicação de testes neuropsicológicos, a ocorrência de déficits cognitivos numa amostra constituída por pacientes não cirróticos com hepatite C crônica, inclusos no grupo de casos, e indivíduos curados da infecção pelo HCV, estes pertencentes ao grupo controle. Foram excluídos do estudo indivíduos com condições clínicas que sabidamente acarretam declínio cognitivo. Identificou-se elevada ocorrência de desempenho deficitário em ambos os grupos em vários dos testes aplicados, sobretudo em medidas de atenção, velocidade de processamento mental, flexibilidade mental e memória de trabalho. Diferentemente do que tem sido descrito na literatura, o presente estudo evidenciou ainda ocorrência significativa de déficits em habilidades aritméticas e construcionais visuoespaciais. Entre os grupos, houve diferenças significativas apenas em dois subtestes de linguagem, com pior desempenho do grupo de casos. Este trabalho, portanto, corroborou alguns dos achados previamente referidos na literatura, bem como evidenciou peculiaridades até então pouco descritas. Advisors/Committee Members: LOPES NETO, Edmundo Pessoa de Almeida (advisor), http://lattes.cnpq.br/1738354802121443 (advisor).

Subjects/Keywords: Hepatite C; HCV; Disfunção cognitiva

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APA (6^th Edition):

GOMES, D. C. d. A. (2011). Disfunção cognitiva em pacientes com infecção crônica pelo vírus da hepatite C: estudo transversal na cidade do Recife e revisão de literatura . (Masters Thesis). Universidade Federal de Pernambuco. Retrieved from https://repositorio.ufpe.br/handle/123456789/29281

Chicago Manual of Style (16^th Edition):

GOMES, Daniel Christiano de Albuquerque. “Disfunção cognitiva em pacientes com infecção crônica pelo vírus da hepatite C: estudo transversal na cidade do Recife e revisão de literatura .” 2011. Masters Thesis, Universidade Federal de Pernambuco. Accessed February 16, 2020. https://repositorio.ufpe.br/handle/123456789/29281.

MLA Handbook (7^th Edition):

GOMES, Daniel Christiano de Albuquerque. “Disfunção cognitiva em pacientes com infecção crônica pelo vírus da hepatite C: estudo transversal na cidade do Recife e revisão de literatura .” 2011. Web. 16 Feb 2020.

Vancouver:

GOMES DCdA. Disfunção cognitiva em pacientes com infecção crônica pelo vírus da hepatite C: estudo transversal na cidade do Recife e revisão de literatura . [Internet] [Masters thesis]. Universidade Federal de Pernambuco; 2011. [cited 2020 Feb 16]. Available from: https://repositorio.ufpe.br/handle/123456789/29281.

Council of Science Editors:

GOMES DCdA. Disfunção cognitiva em pacientes com infecção crônica pelo vírus da hepatite C: estudo transversal na cidade do Recife e revisão de literatura . [Masters Thesis]. Universidade Federal de Pernambuco; 2011. Available from: https://repositorio.ufpe.br/handle/123456789/29281

University of Toronto

23. Khattar, Ramzi. Targeted Deletion of Fibrinogen-like Protein 2 (FGL2) ENHANCES Immunity in a Murine Model of Acute Viral Hepatitis Caused by Lymphocytic Choriomeningitis Virus (LCMV).

Degree: 2011, University of Toronto

URL: http://hdl.handle.net/1807/31278

►

Viral hepatitis infection represents a significant epidemiological and economic burden on society. Following infection, some patients mount a blunted immune response to the virus, which… (more)

Subjects/Keywords: LCMV; HCV pathogenesis; 0982

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APA (6^th Edition):

Khattar, R. (2011). Targeted Deletion of Fibrinogen-like Protein 2 (FGL2) ENHANCES Immunity in a Murine Model of Acute Viral Hepatitis Caused by Lymphocytic Choriomeningitis Virus (LCMV). (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/31278

Chicago Manual of Style (16^th Edition):

Khattar, Ramzi. “Targeted Deletion of Fibrinogen-like Protein 2 (FGL2) ENHANCES Immunity in a Murine Model of Acute Viral Hepatitis Caused by Lymphocytic Choriomeningitis Virus (LCMV).” 2011. Masters Thesis, University of Toronto. Accessed February 16, 2020. http://hdl.handle.net/1807/31278.

MLA Handbook (7^th Edition):

Khattar, Ramzi. “Targeted Deletion of Fibrinogen-like Protein 2 (FGL2) ENHANCES Immunity in a Murine Model of Acute Viral Hepatitis Caused by Lymphocytic Choriomeningitis Virus (LCMV).” 2011. Web. 16 Feb 2020.

Vancouver:

Khattar R. Targeted Deletion of Fibrinogen-like Protein 2 (FGL2) ENHANCES Immunity in a Murine Model of Acute Viral Hepatitis Caused by Lymphocytic Choriomeningitis Virus (LCMV). [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/1807/31278.

Council of Science Editors:

Khattar R. Targeted Deletion of Fibrinogen-like Protein 2 (FGL2) ENHANCES Immunity in a Murine Model of Acute Viral Hepatitis Caused by Lymphocytic Choriomeningitis Virus (LCMV). [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/31278

Kwame Nkrumah University of Science and Technology

24. Layden, Jennifer E.; Phillips, Richard O.; Owusu-Ofori, Shirley; Sarfo, Fred Stephen; Kliethermes, Stephanie. High Frequency of Active HCV Infection Among Seropositive Cases in West Africa and Evidence for Multiple Transmission Pathways.

Degree: 2014, Kwame Nkrumah University of Science and Technology

URL: http://dspace.knust.edu.gh:8080/jspui/handle/123456789/11855

►

Sub-Saharan Africa (SSA) has one of the highest global hepatitis C virus (HCV) prevalence estimates. However, reports that suggest high rates of serologic false positives… (more)

Subjects/Keywords: HCV; Africa; prevalence; transmission.

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APA (6^th Edition):

Layden, Jennifer E.; Phillips, Richard O.; Owusu-Ofori, Shirley; Sarfo, Fred Stephen; Kliethermes, S. (2014). High Frequency of Active HCV Infection Among Seropositive Cases in West Africa and Evidence for Multiple Transmission Pathways. (Thesis). Kwame Nkrumah University of Science and Technology. Retrieved from http://dspace.knust.edu.gh:8080/jspui/handle/123456789/11855

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):

Layden, Jennifer E.; Phillips, Richard O.; Owusu-Ofori, Shirley; Sarfo, Fred Stephen; Kliethermes, Stephanie. “High Frequency of Active HCV Infection Among Seropositive Cases in West Africa and Evidence for Multiple Transmission Pathways.” 2014. Thesis, Kwame Nkrumah University of Science and Technology. Accessed February 16, 2020. http://dspace.knust.edu.gh:8080/jspui/handle/123456789/11855.

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

MLA Handbook (7^th Edition):

Layden, Jennifer E.; Phillips, Richard O.; Owusu-Ofori, Shirley; Sarfo, Fred Stephen; Kliethermes, Stephanie. “High Frequency of Active HCV Infection Among Seropositive Cases in West Africa and Evidence for Multiple Transmission Pathways.” 2014. Web. 16 Feb 2020.

Vancouver:

Layden, Jennifer E.; Phillips, Richard O.; Owusu-Ofori, Shirley; Sarfo, Fred Stephen; Kliethermes S. High Frequency of Active HCV Infection Among Seropositive Cases in West Africa and Evidence for Multiple Transmission Pathways. [Internet] [Thesis]. Kwame Nkrumah University of Science and Technology; 2014. [cited 2020 Feb 16]. Available from: http://dspace.knust.edu.gh:8080/jspui/handle/123456789/11855.

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

Council of Science Editors:

Layden, Jennifer E.; Phillips, Richard O.; Owusu-Ofori, Shirley; Sarfo, Fred Stephen; Kliethermes S. High Frequency of Active HCV Infection Among Seropositive Cases in West Africa and Evidence for Multiple Transmission Pathways. [Thesis]. Kwame Nkrumah University of Science and Technology; 2014. Available from: http://dspace.knust.edu.gh:8080/jspui/handle/123456789/11855

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

University of New South Wales

25. Cunningham, Evan. Transmission and treatment of hepatitis C virus infection in people who inject drugs.

Degree: Kirby Institute, 2017, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/58947 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:48008/SOURCE02?view=true

► Background: The advent of novel, highly efficacious, and well tolerated hepatitis C virus (HCV) therapies could potentially lead to the elimination of HCV in many… (more)

▼ Background: The advent of novel, highly efficacious, and well tolerated hepatitis C virus (HCV) therapies could potentially lead to the elimination of HCV in many settings globally. A better understanding of HCV transmission and treatment among people who inject drugs (PWID) is needed for this potential to be realised. Aims: The broad aim of this research was to inform prevention and treatment of HCV infection in PWID. Specific aims included the evaluation of injecting risk behaviours and incidence of HCV infection among PWID in an Australian prison setting; to investigate HCV transmission via phylogenetic analyses in a population of street-involved youth in Vancouver, Canada; and to evaluate adherence to pegylated interferon/ribavirin therapy and sofosbuvir/velpatasvir therapy among PWID.Methods: In Chapter 2 and Chapter 3, data from the HITS-p study were analysed using Cox proportional hazard, logistic regression, and generalized estimating equation (GEE) methodologies. In Chapter 4, data from the At-Risk Youth Study (ARYS) were analysed using maximum likelihood phylogenetic and logistic regression methods. In Chapter 5 and 6, adherence and behavioural data from the ACTIVATE and SIMPLIFY studies were analysed using GEE and logistic regression methodologies. Key findings: In the HITS-p study, primary HCV infection was associated with needle/syringe sharing irrespective of injecting frequency or drug type. The incidence was high and remained stable between 2005 and 2014. Needle/syringe sharing increased following entry into prison while any injecting drug use decreased. Younger age was associated with continuing and reinitiating injecting following prison entry as well as ongoing injecting risk behaviours while in prison. Methamphetamine injecting was associated with phylogenetic clustering in street-involved youth. PWID demonstrated high adherence to both PEG-IFN/RBV and sofosbuvir/velpatasvir. Injecting cocaine or amphetamines was associated with reduced adherence to sofosbuvir/velpatasvir however any injecting at baseline was not associated with overall adherence to therapy.Conclusion: A multifaceted approach is needed to effectively reduce the prevalence and incidence of HCV infection among PWID. Scale up of HCV prevention strategies including needle and syringe programs and opioid substitution therapy are needed to supplement the scale up of DAA therapy to provide the greatest prevention benefit to meet global HCV elimination targets. Advisors/Committee Members: Grebely, Jason, Kirby Institute, Faculty of Medicine, UNSW, Applegate, Tanya, Kirby Institute, Faculty of Medicine, UNSW, Hajarizadeh, Behzad, Kirby Institute, Faculty of Medicine, UNSW, Dore, Gregory, Kirby Institute, Faculty of Medicine, UNSW, Lloyd, Andrew, Kirby Institute, Faculty of Medicine, UNSW.

Subjects/Keywords: Epidemiology; HCV; PWID; DAA

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APA (6^th Edition):

Cunningham, E. (2017). Transmission and treatment of hepatitis C virus infection in people who inject drugs. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/58947 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:48008/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Cunningham, Evan. “Transmission and treatment of hepatitis C virus infection in people who inject drugs.” 2017. Doctoral Dissertation, University of New South Wales. Accessed February 16, 2020. http://handle.unsw.edu.au/1959.4/58947 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:48008/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Cunningham, Evan. “Transmission and treatment of hepatitis C virus infection in people who inject drugs.” 2017. Web. 16 Feb 2020.

Vancouver:

Cunningham E. Transmission and treatment of hepatitis C virus infection in people who inject drugs. [Internet] [Doctoral dissertation]. University of New South Wales; 2017. [cited 2020 Feb 16]. Available from: http://handle.unsw.edu.au/1959.4/58947 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:48008/SOURCE02?view=true.

Council of Science Editors:

Cunningham E. Transmission and treatment of hepatitis C virus infection in people who inject drugs. [Doctoral Dissertation]. University of New South Wales; 2017. Available from: http://handle.unsw.edu.au/1959.4/58947 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:48008/SOURCE02?view=true

University of New South Wales

26. Baharuddin, Benny. Metabolic dysfunction in T cells during hepatitis C virus infection.

Degree: Medical Sciences, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55779 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:39271/SOURCE02?view=true

► T cell glucose metabolism is essential for the provision of energy to sustain and maintain T cell function, the so called, fuel for energy. In… (more)

▼ T cell glucose metabolism is essential for the provision of energy to sustain and maintain T cell function, the so called, fuel for energy. In hepatitis C virus (HCV) infection, the immune response is a key determinant to outcome after primary infection, and with antiviral therapy for chronic HCV infection. The overall aim of this thesis was to examine T cell glucose metabolism in HCV infection and its association with T cell responses in chronic and primary HCV infection. To achieve this, key markers of glucose metabolism and T cell activation were studied in individuals with chronic HCV infection prior to receiving antiviral therapy and prior to primary infection.This is the first study to report that patients with chronic HCV infection demonstrate impaired glucose metabolism in both CD8 and CD4 T cells. Further, patients with chronic HCV infection who achieved viral clearance with PegIFN therapy, glucose metabolism as assessed by pAkt and glucose uptake, recovered to levels of healthy subjects. This data indicates dysfunctional T cell glucose metabolism may be a viral driven effect that may impact T cell function and viral clearance.Interestingly, low pAkt level was associated with reduced T cell activation markers (measured by CD25 and PD1) in both CD8 and CD4 T cells and their antigen-experienced subpopulations. Further, reduced pAkt level and T cell activation was associated with impaired production of effector antiviral cytokines in treatment non-responders. Lastly, non-responders had reduced frequency of terminally differentiated, effector and central memory T cells. The results from this study suggest that impaired T cell glucose metabolism, may affect T cell activation, function, effector phenotype differentiation and treatment outcome.Finally, the role of host related factors in potentially influencing the observed dysfunction in T cell glucose metabolism was further studied in individuals prior to primary HCV infection, and with known outcome from infection (spontaneous clearing versus chronic infection). The studies did not show any differences between the two groups before infection in terms of pAkt or glucose metabolism. Further, known SNPs within the Akt gene was not predictive of outcome of primary HCV infection. Thus, thexxresults suggest that pre-existent host factors related to Akt does not predict acute HCV infection outcome.The data from this thesis indicate that HCV infection is associated with dysfunctional T cell glucose metabolism which may impact T cell activation, differentiation and the response to antiviral therapy. These studies are the first to report impaired T cell glucose metabolism during chronic HCV infection and improved our understanding of the relationship of HCV and T cell function. Advisors/Committee Members: Zekry, Amany, Clinical School - St George Hospital, Faculty of Medicine, UNSW, Simar, David, Medical Sciences, Faculty of Medicine, UNSW.

Subjects/Keywords: metabolism; HCV; T cell

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APA (6^th Edition):

Baharuddin, B. (2015). Metabolic dysfunction in T cells during hepatitis C virus infection. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55779 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:39271/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Baharuddin, Benny. “Metabolic dysfunction in T cells during hepatitis C virus infection.” 2015. Doctoral Dissertation, University of New South Wales. Accessed February 16, 2020. http://handle.unsw.edu.au/1959.4/55779 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:39271/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Baharuddin, Benny. “Metabolic dysfunction in T cells during hepatitis C virus infection.” 2015. Web. 16 Feb 2020.

Vancouver:

Baharuddin B. Metabolic dysfunction in T cells during hepatitis C virus infection. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2020 Feb 16]. Available from: http://handle.unsw.edu.au/1959.4/55779 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:39271/SOURCE02?view=true.

Council of Science Editors:

Baharuddin B. Metabolic dysfunction in T cells during hepatitis C virus infection. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55779 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:39271/SOURCE02?view=true

University of New South Wales

27. Bretana, Neil. Understanding the dynamics of hepatitis C virus transmission in a high-risk environment.

Degree: Medical Sciences, 2017, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/57161 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42740/SOURCE02?view=true

► HCV is mainly transmitted between people who inject drugs in developed countries. In this population, HCV prevalence is high and incarceration is recognised to be… (more)

▼ HCV is mainly transmitted between people who inject drugs in developed countries. In this population, HCV prevalence is high and incarceration is recognised to be an independent risk factor for infection. This thesis integrates epidemiology, molecular epidemiology, and computational modelling to investigate HCV transmission among inmates in NSW prisons.In the first study, HCV incidence and associated risk behaviours were calculated in a prospective cohort of inmates in NSW prisons. Thirty-eight HCV incident cases were identified in 269.94 person-years of follow-up yielding an estimated HCV incidence of 14.08 (95% CI: 9.96-19.32) per 100 person-years. Indigenous identity, injecting daily or more often, and injecting heroin were found to be associated with an increased risk of HCV infection.The second study integrated virus sequences with risk behaviour and spatio-temporal data in order to reveal transmission clusters among inmates in NSW. Three clusters of recent HCV transmission were detected consisting of four in-custody transmission events involving drug injecting and sharing between source/recipient pairs located in the same prison at the same time. Despite a large background population of prisoners with chronic HCV, transmission events from recently infected individuals were identified in the prison setting. In the third study, a computational model was developed to simulate the ongoing HCV epidemics in the NSW prisons. The model was used to predict future epidemiological trends and investigate scenarios of altered risk affecting the epidemic. The projected incidence of HCV was stable at 9.72 (95% CI: 9.36-10.08) per 100 person-years until 2020. The potential impact of changes in incarceration rates, and HCV prevention strategies to reduce HCV transmission in NSW prisons were explored. This approach of integrated epidemiological, molecular epidemiological and modeling methods to study HCV transmissions has clear capacity to inform policy and public health practice in the prison setting. Future work includes consideration of social network information, assessment of new antiviral treatment strategies in NSW prisons, and enhancing linkage with community-based research. Advisors/Committee Members: Luciani, Fabio, Medical Sciences, Faculty of Medicine, UNSW, Lloyd, Andrew, Medical Sciences, Faculty of Medicine, UNSW, Bull, Rowena, Medical Sciences, Faculty of Medicine, UNSW, Betz-Stablein, Brigid, Medical Sciences, Faculty of Medicine, UNSW.

Subjects/Keywords: Prison; HCV; Transmission; Model; Phylogenetics

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APA (6^th Edition):

Bretana, N. (2017). Understanding the dynamics of hepatitis C virus transmission in a high-risk environment. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/57161 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42740/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Bretana, Neil. “Understanding the dynamics of hepatitis C virus transmission in a high-risk environment.” 2017. Doctoral Dissertation, University of New South Wales. Accessed February 16, 2020. http://handle.unsw.edu.au/1959.4/57161 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42740/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Bretana, Neil. “Understanding the dynamics of hepatitis C virus transmission in a high-risk environment.” 2017. Web. 16 Feb 2020.

Vancouver:

Bretana N. Understanding the dynamics of hepatitis C virus transmission in a high-risk environment. [Internet] [Doctoral dissertation]. University of New South Wales; 2017. [cited 2020 Feb 16]. Available from: http://handle.unsw.edu.au/1959.4/57161 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42740/SOURCE02?view=true.

Council of Science Editors:

Bretana N. Understanding the dynamics of hepatitis C virus transmission in a high-risk environment. [Doctoral Dissertation]. University of New South Wales; 2017. Available from: http://handle.unsw.edu.au/1959.4/57161 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42740/SOURCE02?view=true

Harvard University

28. Stoeckle, Catherine Carlisle. An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies.

Degree: Doctor of Medicine, 2018, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41973520

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TITLE: An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies Purpose: To determine whether the recent development of direct acting… (more)

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TITLE: An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies Purpose: To determine whether the recent development of direct acting antiviral drugs (DAAs) has spurred an increase in the transplantation of livers from donors with hepatitis c virus (HCV) and to establish what percent of these livers come from donors with current versus cleared infection using NAT status. Methods: We retrospectively reviewed data from the United Network for Organ Sharing (UNOS) on all donors, wait-listed candidates and transplant recipients of livers, kidneys, hearts, lungs, intestines and pancreases in the United States from January 2009-March 2016. Data was analyzed using VirtualBox and SAS Studio. Results: Between 2009 and 2015, less than 5% of all liver transplants came from HCV-positive donors. However the number of HCV-positive livers used for transplant increased, particularly in 2013, when interferon-free DAAs were introduced. Most of these HCV-positive livers were transplanted into HCV-positive recipients (in 2015, 381 went to positive recipients compared to 12 to HCV-negative recipients) and the number of these D-positive/R-positive transplants increased since 2013. In terms of HCV-negative liver donors, more than half were transplanted into HCV-negative recipients, and the number transplanted into HCV-positive recipients decreased from 2014-15. This suggests an increasing propensity to give HCV-positive recipients an HCV-positive liver when previously more of those donations were discarded. Wait-list data showed that while HCV-positive recipients experience longer wait times for liver transplants compared to HCV-negative recipients, the disparity in wait times has decreased by more than 50% from 2000 to 2015. In terms of NAT status, of all organ donors (including heart, lung, liver, kidney, intestine, pancreas) evaluated for transplant between January 2015 and March 2016 that were HCV-antibody positive, two-thirds were also NAT-positive and one third were NAT-negative, reflecting current and cleared infection states, respectively. Conclusions: Our data indicate that the development of IFN-free DAAs has prompted increased usage of HCV-positive livers for transplantation, resulting in shorter wait times for all recipients. Thus enhanced use of HCV-positive donor organs offers hope for optimal organ utilization of a previously high-risk donor pool.

Scholarly Project

Subjects/Keywords: HCV; transplantation; UNOS; liver

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APA (6^th Edition):

Stoeckle, C. C. (2018). An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:41973520

Chicago Manual of Style (16^th Edition):

Stoeckle, Catherine Carlisle. “An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies.” 2018. Doctoral Dissertation, Harvard University. Accessed February 16, 2020. http://nrs.harvard.edu/urn-3:HUL.InstRepos:41973520.

MLA Handbook (7^th Edition):

Stoeckle, Catherine Carlisle. “An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies.” 2018. Web. 16 Feb 2020.

Vancouver:

Stoeckle CC. An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies. [Internet] [Doctoral dissertation]. Harvard University; 2018. [cited 2020 Feb 16]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41973520.

Council of Science Editors:

Stoeckle CC. An Analysis of Hepatitis-C-Positive Liver Donors in the Era of Direct Acting Antiviral Therapies. [Doctoral Dissertation]. Harvard University; 2018. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:41973520

University of Sydney

29. Najim, Mustafa. Hepatitis C virus induced changes in cellular trafficking and lipid metabolism - identifying novel host factors required for HCV replication .

Degree: 2018, University of Sydney

URL: http://hdl.handle.net/2123/20895

► Hepatitis C virus (HCV) infection is endemic in numerous countries and is a global health issue, placing a huge burden on health care systems and… (more)

Subjects/Keywords: HCV; TM6SF2; hnRNPC1/C2; COPI

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

APA (6^th Edition):

Najim, M. (2018). Hepatitis C virus induced changes in cellular trafficking and lipid metabolism - identifying novel host factors required for HCV replication . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20895

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):

Najim, Mustafa. “Hepatitis C virus induced changes in cellular trafficking and lipid metabolism - identifying novel host factors required for HCV replication .” 2018. Thesis, University of Sydney. Accessed February 16, 2020. http://hdl.handle.net/2123/20895.

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

MLA Handbook (7^th Edition):

Najim, Mustafa. “Hepatitis C virus induced changes in cellular trafficking and lipid metabolism - identifying novel host factors required for HCV replication .” 2018. Web. 16 Feb 2020.

Vancouver:

Najim M. Hepatitis C virus induced changes in cellular trafficking and lipid metabolism - identifying novel host factors required for HCV replication . [Internet] [Thesis]. University of Sydney; 2018. [cited 2020 Feb 16]. Available from: http://hdl.handle.net/2123/20895.

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

Council of Science Editors:

Najim M. Hepatitis C virus induced changes in cellular trafficking and lipid metabolism - identifying novel host factors required for HCV replication . [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/20895

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

30. Morel, Anthony. Etapes précoces de l'infection du virus de l'hépatite C : endocytose et rôle potentiel du FcRn dans la modulation de sa neutralisation : Early steps of hepatitis C virus infection : endocytosis and putative role of the FcRn in the modulation of its neutralization.

Degree: Docteur es, Sciences de la Vie et de la Santé, 2016, Université François-Rabelais de Tours

URL: http://www.theses.fr/2016TOUR3311

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Les étapes précoces de l’infection virale sont des évènements critiques dans le déroulement du cycle viral. Notamment, l’entrée virale est la première étape d’interaction entre… (more)

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Les étapes précoces de l’infection virale sont des évènements critiques dans le déroulement du cycle viral. Notamment, l’entrée virale est la première étape d’interaction entre un virus et une cellule permettant d’initier, de maintenir et de propager l’infection. De ce fait, cette étape constitue une cible majeure de la réponse immunitaire adaptative de l’hôte. C’est ainsi que cette étude bipartite s’est intéressée aux étapes précoces de l’infection du virus de l’hépatite C (HCV). Dans un premier temps, l’obtention de clones de cellules Huh-7.5 n’exprimant plus le récepteur néonatal des immunoglobulines, le FcRn, a permis d’analyser l’implication de ce récepteur dans la neutralisation du HCV par des anticorps neutralisants. Les résultats obtenus nous informent que le récepteur FcRn n’intervient vraisemblablement pas dans la modulation de la neutralisation du HCV. Dans un second temps, nous avons réalisé une étude préliminaire afin d’approfondir les mécanismes régissant l’endocytose du HCV : à savoir, quelles sont les protéines adaptatrices responsables du déclenchement de l’endocytose dépendante de la clathrine et s’il existe une potentielle voie d’entrée alternative pour ce virus. A ces fins, nous avons opté pour une stratégie basée sur la transfection de siRNA, couplée à l’utilisation des pseudoparticules HCVpp qui constituent une approche encore pertinente appliquée à l’étude de l’entrée du HCV.

The early steps during a viral infection are critical events in the course of the viral cycle. Particularly, the viral entry is the first step allowing the interaction between a virus and a cell to initiate, maintain and propagate an infection. Therefore, this very step is a major target for the host adaptive immunity. This bipartite study is focused on the early steps of the infection by the hepatitis C virus (HCV). First of all, generation of Huh-7.5 clones whose expression of the neonatal Fc receptor, FcRn, has been deleted gave us the opportunity to analyze the involvement of this receptor during the neutralization of HCV by neutralizing antibodies. Regarding the results, it appears unlikely that the FcRn modulates the neutralization of HCV. Then we conducted a preliminary study to further explore the mechanisms underlying the endocytosis of HCV: that is, which are the adaptor proteins that trigger the clathrine-mediated endocytosis and if there is another putative entry pathway for the virus. To these ends we opted for a RNAi based strategy coupled to the use of HCV-derived pseudo-particles (HCVpp) that are still useful and relevant tools dedicated to HCV-entry studies.

Advisors/Committee Members: Blanchard, Emmanuelle (thesis director).

Subjects/Keywords: HCV; FcRn; Neutralisation; Endocytose; Clathrine; HCV; FcRn; Neutralization; Endocytosis; Clathrin; 610

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

APA (6^th Edition):

Morel, A. (2016). Etapes précoces de l'infection du virus de l'hépatite C : endocytose et rôle potentiel du FcRn dans la modulation de sa neutralisation : Early steps of hepatitis C virus infection : endocytosis and putative role of the FcRn in the modulation of its neutralization. (Doctoral Dissertation). Université François-Rabelais de Tours. Retrieved from http://www.theses.fr/2016TOUR3311

Chicago Manual of Style (16^th Edition):

Morel, Anthony. “Etapes précoces de l'infection du virus de l'hépatite C : endocytose et rôle potentiel du FcRn dans la modulation de sa neutralisation : Early steps of hepatitis C virus infection : endocytosis and putative role of the FcRn in the modulation of its neutralization.” 2016. Doctoral Dissertation, Université François-Rabelais de Tours. Accessed February 16, 2020. http://www.theses.fr/2016TOUR3311.

MLA Handbook (7^th Edition):

Morel, Anthony. “Etapes précoces de l'infection du virus de l'hépatite C : endocytose et rôle potentiel du FcRn dans la modulation de sa neutralisation : Early steps of hepatitis C virus infection : endocytosis and putative role of the FcRn in the modulation of its neutralization.” 2016. Web. 16 Feb 2020.

Vancouver:

Morel A. Etapes précoces de l'infection du virus de l'hépatite C : endocytose et rôle potentiel du FcRn dans la modulation de sa neutralisation : Early steps of hepatitis C virus infection : endocytosis and putative role of the FcRn in the modulation of its neutralization. [Internet] [Doctoral dissertation]. Université François-Rabelais de Tours; 2016. [cited 2020 Feb 16]. Available from: http://www.theses.fr/2016TOUR3311.

Council of Science Editors:

Morel A. Etapes précoces de l'infection du virus de l'hépatite C : endocytose et rôle potentiel du FcRn dans la modulation de sa neutralisation : Early steps of hepatitis C virus infection : endocytosis and putative role of the FcRn in the modulation of its neutralization. [Doctoral Dissertation]. Université François-Rabelais de Tours; 2016. Available from: http://www.theses.fr/2016TOUR3311

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Open Access Theses and Dissertations