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You searched for +publisher:"University of KwaZulu-Natal" +contributor:("Carr, William Henry"). Showing records 1 – 2 of 2 total matches.

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University of KwaZulu-Natal

1. Ndlovu, Bongiwe Goodness. Innate immune mechanisms in limiting HIV-1 pathogenesis among South African adults and mother-infant pairs.

Degree: M.Med.Sc., Paediatrics and child health, 2013, University of KwaZulu-Natal

This study was conducted to investigate the role of natural killer cell surface receptors, KIRs and their cognate HLA ligands in preventing HIV-1 acquisition and disease progression in HIV-1 exposed infants. Using DBS stored for 8 years from 21 pregnant South African women we evaluated 3 methods of gDNA extraction with and without whole genome amplification (WGA) to characterize immune-related genes: IL-10, KIR and HLA class I. However, IL-10 SNP typing was only for testing the quality of gDNA. QIAamp DNA mini kit yielded the highest gDNA quality (p<0.05; Wilcoxon Signed Rank Test) with sufficient yield for subsequent analyses. In contrast, WGA was not reliable for SSP-PCR analysis of KIR2DL1, KIR2DS1, KIR2DL5, and KIR2DL3 or high resolution HLA genotyping using a sequence-based approach. A cohort of 370 infants; 124 HIV-1 perinatally infected, 120 exposed uninfected and 126 unexposed healthy infants was used for KIR and HLA genotyping. After adjustment for viral load and multiple comparisons, the frequency of HLA-Cw*04:01 allele was likely to be associated with susceptibility to mother-to-child acquisition of HIV-1 in exposed infected (EI) infants (p=0.05; Logistic Regression analysis). HLA-A*23:01 was likely to be associated with decreased CD4 T lymphocyte count in HIV-1 infected infants (p=0.01; ANOVA), whereas HLA-B*81 tended to be associated with higher CD4 T lymphocyte count (p=0.04, ANOVA). We speculate that HLA-Cw*04:01 interacts with KIR2DL1 and inhibit NK cell responses which predispose the infants to HIV-1 infection. KIR2DS1 and KIR2DL5 were both associated with faster HIV-1 disease progression. Identified protective HLA-class I alleles could be used to present viral epitopes to either NK cells via KIRs or CTLs and enhance immune activation which may promote resistance to HIV-1 infection. Advisors/Committee Members: Carr, William Henry (advisor).

Subjects/Keywords: Immunology.

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

APA (6th Edition):

Ndlovu, B. G. (2013). Innate immune mechanisms in limiting HIV-1 pathogenesis among South African adults and mother-infant pairs. (Masters Thesis). University of KwaZulu-Natal. Retrieved from http://hdl.handle.net/10413/9971

Chicago Manual of Style (16th Edition):

Ndlovu, Bongiwe Goodness. “Innate immune mechanisms in limiting HIV-1 pathogenesis among South African adults and mother-infant pairs.” 2013. Masters Thesis, University of KwaZulu-Natal. Accessed July 19, 2019. http://hdl.handle.net/10413/9971.

MLA Handbook (7th Edition):

Ndlovu, Bongiwe Goodness. “Innate immune mechanisms in limiting HIV-1 pathogenesis among South African adults and mother-infant pairs.” 2013. Web. 19 Jul 2019.

Vancouver:

Ndlovu BG. Innate immune mechanisms in limiting HIV-1 pathogenesis among South African adults and mother-infant pairs. [Internet] [Masters thesis]. University of KwaZulu-Natal; 2013. [cited 2019 Jul 19]. Available from: http://hdl.handle.net/10413/9971.

Council of Science Editors:

Ndlovu BG. Innate immune mechanisms in limiting HIV-1 pathogenesis among South African adults and mother-infant pairs. [Masters Thesis]. University of KwaZulu-Natal; 2013. Available from: http://hdl.handle.net/10413/9971


University of KwaZulu-Natal

2. Naranbhai, Vivek. The role of natural killer cells in preventing HIV-1 acquisition and controlling disease progression.

Degree: PhD, Virology, 2013, University of KwaZulu-Natal

In sub-Saharan Africa, women carry a disproportionate burden of the Human Immunodeficiency Virus Type 1 (HIV-1) pandemic. The high risk of HIV acquisition in these women and the variability in their disease progression is not fully understood. Natural Killer (NK) cells, which are innate immune antiviral lymphocytes, present systemically and at mucosal surfaces, may play a role in preventing HIV acquisition and/or altering disease progression, as they are key early mediators of the response to viral infections and are equipped to kill infected cells. The purpose of this study was to evaluate the role of NK cells in HIV-1 acquisition and following acquisition, in disease progression. The study participants were selected women who were participating in a randomized controlled trial assessing the effectiveness of 1% Tenofovir gel in preventing HIV-1 (CAPRISA 004 trial). The study design was a case-control study nested within the cohorts followed up in the CAPRISA 004 trial. In this trial, 889 sexually-active women aged 18-40 years were randomized to receive Tenofovir or placebo gel and prospectively followed. Assessment of HIV infection was performed monthly by rapid HIV-1 antibody tests, supplemented by HIV-1 RNA polymerase chain reaction (PCR), p24 Western blotting and/or ELISA. Samples obtained prior to the first positive rapid antibody test were retrospectively tested by HIV specific PCR to identify window period infections. The date of infection in this study was estimated as the midpoint between the last negative and first positive antibody test, or 14 days prior to the first HIV-1 RNA-PCR positive result. Multi-parametric flow cytometry techniques developed and validated in healthy blood donors were used to asses the bidirectional relationship between NK cells and HIV-1. To simulate in vivo interaction between NK cells and autologous HIV infected cells, an in vitro infection and coculture assay was used in addition to conventional assays of NK cell recognition of HLA-deficient cell lines. These were supplemented with measurement of plasma cytokines by Luminex and microbial products by ELISA. In this study, 44 cases who acquired HIV-1 were sampled prior to infection and 39 controls who remained HIV-1 negative despite high behavioural exposure at the timepoint when their preceding sexual activity was highest. To understand how HIV infection affected NK cells during early HIV-1 infection, the first sample obtained after acquisition was studied and compared to preinfection samples from the same participant. The case and control groups were broadly similar in the proportions using tenofovir gel, proportions infected with HSV-2 and number of sexual partners but tended to be marginally older than cases (27.6 vs 23.3 years). By design control women had higher sexual activity than cases (mean 11 vs. 5.7 sex acts per month). The frequency of IFN-γ secreting NK cells from women who acquired HIV infection were significantly lower than from women who remained uninfected in response to 721 cells-an EBV transformed B cell line… Advisors/Committee Members: Abdool Karim, Salim Safurdeen (advisor), Carr, William Henry (advisor).

Subjects/Keywords: Virology.

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

APA (6th Edition):

Naranbhai, V. (2013). The role of natural killer cells in preventing HIV-1 acquisition and controlling disease progression. (Doctoral Dissertation). University of KwaZulu-Natal. Retrieved from http://hdl.handle.net/10413/10857

Chicago Manual of Style (16th Edition):

Naranbhai, Vivek. “The role of natural killer cells in preventing HIV-1 acquisition and controlling disease progression.” 2013. Doctoral Dissertation, University of KwaZulu-Natal. Accessed July 19, 2019. http://hdl.handle.net/10413/10857.

MLA Handbook (7th Edition):

Naranbhai, Vivek. “The role of natural killer cells in preventing HIV-1 acquisition and controlling disease progression.” 2013. Web. 19 Jul 2019.

Vancouver:

Naranbhai V. The role of natural killer cells in preventing HIV-1 acquisition and controlling disease progression. [Internet] [Doctoral dissertation]. University of KwaZulu-Natal; 2013. [cited 2019 Jul 19]. Available from: http://hdl.handle.net/10413/10857.

Council of Science Editors:

Naranbhai V. The role of natural killer cells in preventing HIV-1 acquisition and controlling disease progression. [Doctoral Dissertation]. University of KwaZulu-Natal; 2013. Available from: http://hdl.handle.net/10413/10857

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