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Journal articles on the topic 'HIV-1, HLA-C'

Author: Grafiati
Published: 11 March 2023
Last updated: 31 July 2025

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1

Muccini, Camilla, Monica Guffanti, Vincenzo Spagnuolo, et al. "Association between low levels of HIV-1 DNA and HLA class I molecules in chronic HIV-1 infection." PLOS ONE 17, no. 3 (2022): e0265348. http://dx.doi.org/10.1371/journal.pone.0265348.

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Background HLA-B27 and -B57 were found in people with low levels of HIV-1 DNA, suggesting that HLA class I molecules may influence the size of HIV-1 reservoir. Aim of the study was to explore the association between HLA class I molecules and HIV-1 DNA in people with chronic HIV-1 infection. Methods Post-hoc analysis of the APACHE trial, on adults with chronic HIV-1 infection, prolonged suppressive antiretroviral therapy and good immunological profile. HIV-1 DNA was quantified in peripheral blood mononuclear cells (PBMCs); HLA-A, -B and -C were tested on genomic DNA. Crude odds ratios (OR) with
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2

Zipeto, Donato, and Alberto Beretta. "C3 HIV-1 Env and HLA-C." JAIDS Journal of Acquired Immune Deficiency Syndromes 59 (April 2012): 77. http://dx.doi.org/10.1097/01.qai.0000413798.79651.e7.

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3

Apps, Richard, Gregory Q. Del Prete, Pramita Chatterjee, et al. "HIV-1 Vpu Mediates HLA-C Downregulation." Cell Host & Microbe 19, no. 5 (2016): 686–95. http://dx.doi.org/10.1016/j.chom.2016.04.005.

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4

Barker, Edward, and David T. Evans. "HLA-C Downmodulation by HIV-1 Vpu." Cell Host & Microbe 19, no. 5 (2016): 570–71. http://dx.doi.org/10.1016/j.chom.2016.04.023.

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5

Nii-Trebi, Nicholas I., Saori Matsuoka, Ai Kawana-Tachikawa, et al. "Super high-resolution single-molecule sequence-based typing of HLA class I alleles in HIV-1 infected individuals in Ghana." PLOS ONE 17, no. 6 (2022): e0269390. http://dx.doi.org/10.1371/journal.pone.0269390.

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Polymorphisms in human leukocyte antigen (HLA) class I loci are known to have a great impact on disease progression in HIV-1 infection. Prevailing HIV-1 subtypes and HLA genotype distribution are different all over the world, and the HIV-1 and host HLA interaction could be specific to individual areas. Data on the HIV-1 and HLA interaction have been accumulated in HIV-1 subtype B- and C-predominant populations but not fully obtained in West Africa where HIV-1 subtype CRF02_AG is predominant. In the present study, to obtain accurate HLA typing data for analysis of HLA association with disease p
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6

Kyobe, Samuel, Savannah Mwesigwa, Gyaviira Nkurunungi, et al. "Identification of a Clade-Specific HLA-C*03:02 CTL Epitope GY9 Derived from the HIV-1 p17 Matrix Protein." International Journal of Molecular Sciences 25, no. 17 (2024): 9683. http://dx.doi.org/10.3390/ijms25179683.

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Efforts towards an effective HIV-1 vaccine have remained mainly unsuccessful. There is increasing evidence for a potential role of HLA-C-restricted CD8+ T cell responses in HIV-1 control, including our recent report of HLA-C*03:02 among African children. However, there are no documented optimal HIV-1 CD8+ T cell epitopes restricted by HLA-C*03:02; additionally, the structural influence of HLA-C*03:02 on epitope binding is undetermined. Immunoinformatics approaches provide a fast and inexpensive method to discover HLA-restricted epitopes. Here, we employed immunopeptidomics to identify HLA-C*03
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7

Bachtel, Nathaniel D., Gisele Umviligihozo, Suzanne Pickering, et al. "HLA-C downregulation by HIV-1 adapts to host HLA genotype." PLOS Pathogens 14, no. 9 (2018): e1007257. http://dx.doi.org/10.1371/journal.ppat.1007257.

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8

Specht, Anke, Amalio Telenti, Raquel Martinez, et al. "Counteraction of HLA-C-Mediated Immune Control of HIV-1 by Nef." Journal of Virology 84, no. 14 (2010): 7300–7311. http://dx.doi.org/10.1128/jvi.00619-10.

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ABSTRACT A host genetic variant (−35C/T) correlates with increased human leukocyte antigen C (HLA-C) expression and improved control of HIV-1. HLA-C-mediated immunity may be particularly protective because HIV-1 is unable to remove HLA-C from the cell surface, whereas it can avoid HLA-A- and HLA-B-mediated immunity by Nef-mediated down-modulation. However, some individuals with the protective −35CC genotype exhibit high viral loads. Here, we investigated whether the ability of HIV-1 to replicate efficiently in the “protective” high-HLA-C-expression host environment correlates with specific fun
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9

Adnan, Sama, Arumugam Balamurugan, Alicja Trocha, et al. "Nef interference with HIV-1–specific CTL antiviral activity is epitope specific." Blood 108, no. 10 (2006): 3414–19. http://dx.doi.org/10.1182/blood-2006-06-030668.

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AbstractHIV-1 Nef and HIV-1–specific cytotoxic T lymphocytes (CTLs) have important and opposing roles in the immunopathogenesis of HIV-1 infection. Nef-mediated down-modulation of HLA class I on infected cells can confer resistance to CTL clearance, but the factors determining the efficiency of this process are unknown. This study examines the impact of Nef on the antiviral activity of several CTL clones recognizing epitopes from early and late HIV-1 proteins, restricted by HLA-A, -B, and -C molecules. CTL-targeting epitopes in early proteins remained susceptible to the effects of Nef, althoug
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10

Ende, Zachary, Martin J. Deymier, Daniel T. Claiborne, et al. "HLA Class I Downregulation by HIV-1 Variants from Subtype C Transmission Pairs." Journal of Virology 92, no. 7 (2018): e01633-17. http://dx.doi.org/10.1128/jvi.01633-17.

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ABSTRACTHIV-1 downregulates human leukocyte antigen A (HLA-A) and HLA-B from the surface of infected cells primarily to evade CD8 T cell recognition. HLA-C was thought to remain on the cell surface and bind inhibitory killer immunoglobulin-like receptors, preventing natural killer (NK) cell-mediated suppression. However, a recent study found HIV-1 primary viruses have the capacity to downregulate HLA-C. The goal of this study was to assess the heterogeneity of HLA-A, HLA-B, and HLA-C downregulation among full-length primary viruses from six chronically infected and six newly infected individua
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11

Stefani, Chiara, Antonella Sangalli, Elena Locatelli, et al. "Increased Prevalence of Unstable HLA-C Variants in HIV-1 Rapid-Progressor Patients." International Journal of Molecular Sciences 23, no. 23 (2022): 14852. http://dx.doi.org/10.3390/ijms232314852.

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HIV-1 infection in the absence of treatment results in progression toward AIDS. Host genetic factors play a role in HIV-1 pathogenesis, but complete knowledge is not yet available. Since less-expressed HLA-C variants are associated with poor HIV-1 control and unstable HLA-C variants are associated with higher HIV-1 infectivity, we investigated whether there was a correlation between the different stages of HIV-1 progression and the presence of specific HLA-C allotypes. HLA-C genotyping was performed using allele-specific PCR by analyzing a treatment-naïve cohort of 96 HIV-1-infected patients f
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12

Derrien, Muriel, Nathalie Pizzato, Guillermina Dolcini, et al. "Human immunodeficiency virus 1 downregulates cell surface expression of the non-classical major histocompatibility class I molecule HLA-G1." Journal of General Virology 85, no. 7 (2004): 1945–54. http://dx.doi.org/10.1099/vir.0.79867-0.

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Human immunodeficiency virus 1 (HIV-1) downregulates cell surface expression of HLA-A and HLA-B but not HLA-C or HLA-E to ultimately escape immune defences. Here, it is shown that cell surface expression of the non-classical HLA-G1 is also downregulated by HIV-1, by using co-transfection experiments and infection with cell-free HIV-1 of HLA-G1-expressing U87 glioma cells or macrophages in primary culture. Moreover, co-transfection experiments using proviruses deleted in either nef or vpu or plasmids encoding HIV-1 Nef and Vpu mixed together with a HLA-G1-expressing construct demonstrated that
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13

Akahoshi, Tomohiro, Hiroyuki Gatanaga, Nozomi Kuse, et al. "T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics." PLOS Pathogens 16, no. 12 (2020): e1009177. http://dx.doi.org/10.1371/journal.ppat.1009177.

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HIV-1 strains harboring immune escape mutations can persist in circulation, but the impact of selection by multiple HLA alleles on population HIV-1 dynamics remains unclear. In Japan, HIV-1 Reverse Transcriptase codon 135 (RT135) is under strong immune pressure by HLA-B*51:01-restricted and HLA-B*52:01-restricted T cells that target a key epitope in this region (TI8; spanning RT codons 128–135). Major population-level shifts have occurred at HIV-1 RT135 during the Japanese epidemic, which first affected hemophiliacs (via imported contaminated blood products) and subsequently non-hemophiliacs (
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14

Tam, Tran Thi Minh, Nguyen Thuy Linh, Phan Ha My, and Nguyen Thi Lan Anh. "Characteristics allelic of Human Leukocyte Antigen class I genotype and association with viral load and CD4 cell count in HIV-1 infected patients, Hanoi 2014 – 2016." Tạp chí Y học Dự phòng 31, no. 4 (2021): 43–50. http://dx.doi.org/10.51403/0868-2836/2021/335.

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Human Leukocyte Antigen (HLA) class I plays a regulatory role in cellular immune response to HIV-1 infection. The role of HLA alleles in HIV progression via viral load and CD4 cell count is well known. HLA class I is polymorphic and distributed differently by nation. This descriptive cross-sectional study was performed on 303 HIV-1 infected patients in 2014 - 2016, with aims to (i) characterize HLA class I genotype with 4-digit nomenclature and (ii) identify specifc alleles in correlate with CD4 cell counts and HIV viral load. 117 allele genotypes have been identifed, including 28 HLA-A allele
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15

Lazaryan, Aleksandr, Elena Lobashevsky, Joseph Mulenga, et al. "Human Leukocyte Antigen B58 Supertype and Human Immunodeficiency Virus Type 1 Infection in Native Africans." Journal of Virology 80, no. 12 (2006): 6056–60. http://dx.doi.org/10.1128/jvi.02119-05.

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ABSTRACT Human leukocyte antigen (HLA) class I alleles can be grouped into supertypes according to their shared peptide binding properties. We examined alleles of the HLA-B58 supertype (B58s) in treatment-naïve human immunodeficiency virus type 1 (HIV-1)-seropositive Africans (423 Zambians and 202 Rwandans). HLA-B and HLA-C alleles were resolved to four digits by a combination of molecular methods, and their respective associations with outcomes of HIV-1 infection were analyzed by statistical procedures appropriate for continuous or categorical data. The effects of the individual alleles on n
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16

Yindom, Louis-Marie, Aleksandra Leligdowicz, Maureen P. Martin, et al. "Influence of HLA Class I and HLA-KIR Compound Genotypes on HIV-2 Infection and Markers of Disease Progression in a Manjako Community in West Africa." Journal of Virology 84, no. 16 (2010): 8202–8. http://dx.doi.org/10.1128/jvi.00116-10.

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ABSTRACT Overall, the time to AIDS after HIV-2 infection is longer than with HIV-1, and many individuals infected with HIV-2 virus remain healthy throughout their lives. Multiple HLA and KIR gene products have been implicated in the control of HIV-1, but the effect of variation at these loci on HIV-2 disease is unknown. We show here for the first time that HLA-B*1503 is associated significantly with poor prognosis after HIV-2 infection and that HLA-B*0801 is associated with susceptibility to infection. Interestingly, previous data indicate that HLA-B*1503 is associated with low viral loads in
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17

Yang, Hongbing, Margarida Rei, Simon Brackenridge, et al. "HLA-E–restricted, Gag-specific CD8+ T cells can suppress HIV-1 infection, offering vaccine opportunities." Science Immunology 6, no. 57 (2021): eabg1703. http://dx.doi.org/10.1126/sciimmunol.abg1703.

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Human leukocyte antigen-E (HLA-E) normally presents an HLA class Ia signal peptide to the NKG2A/C-CD94 regulatory receptors on natural killer (NK) cells and T cell subsets. Rhesus macaques immunized with a cytomegalovirus-vectored simian immunodeficiency virus (SIV) vaccine generated Mamu-E (HLA-E homolog)–restricted T cell responses that mediated post-challenge SIV replication arrest in >50% of animals. However, HIV-1–specific, HLA-E–restricted T cells have not been observed in HIV-1–infected individuals. Here, HLA-E–restricted, HIV-1–specific CD8+ T cells were primed in vitro. These T cel
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18

Kulpa, Deanna A., and Kathleen L. Collins. "The emerging role of HLA-C in HIV-1 infection." Immunology 134, no. 2 (2011): 116–22. http://dx.doi.org/10.1111/j.1365-2567.2011.03474.x.

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19

Pai, Sara I., J. Jack Lee, Thomas E. Carey, et al. "Intact APM and PD-1:PD-L1 pathway upregulation in HIV-infected head and neck cancer patients." Journal of Clinical Oncology 35, no. 15_suppl (2017): 6058. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.6058.

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6058 Background: HIV-infected individuals have a higher incidence of oral infection with human papillomavirus (HPV) and possibly a higher incidence of head and neck cancer (HNC). Whether this observation reflects defects in the ability of this Òimmune-compromisedÓ patient population to mount sufficient tumor specific immune responses and/or reflects activation of immune escape mechanisms is not known. To address this question, we investigated the expression of HLA class I antigen processing machinery (APM) components and PD-1:PD-L1 pathway activation in HIV(+) HNC patients. Methods: 62 HIV(+)
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20

Mori, Masahiko, Ellen Leitman, Bruce Walker, Thumbi Ndung’u, Mary Carrington, and Philip Goulder. "Impact of HLA Allele-KIR Pairs on HIV Clinical Outcome in South Africa." Journal of Infectious Diseases 219, no. 9 (2018): 1456–63. http://dx.doi.org/10.1093/infdis/jiy692.

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Abstract Background HLA class I contributes to HIV immune control through antigen presentation to cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. In contrast to investigations of CTL, studies of NK cells in HIV control through HLA-killer immunoglobulin-like receptor (KIR) interactions remain sparse in African cohorts. Methods Treatment-naive, chronically HIV-infected adults (N = 312) were recruited from South Africa, and the effects of HLA-KIR pairs on clinical outcome were analyzed. Results There was no significant difference in viral load among all subjects with HLA alleles fro
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21

Leslie, Alasdair, Philippa C. Matthews, Jennifer Listgarten, et al. "Additive Contribution of HLA Class I Alleles in the Immune Control of HIV-1 Infection." Journal of Virology 84, no. 19 (2010): 9879–88. http://dx.doi.org/10.1128/jvi.00320-10.

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ABSTRACT Previous studies have identified a central role for HLA-B alleles in influencing control of HIV infection. An alternative possibility is that a small number of HLA-B alleles may have a very strong impact on HIV disease outcome, dominating the contribution of other HLA alleles. Here, we find that even following the exclusion of subjects expressing any of the HLA-B class I alleles (B*57, B*58, and B*18) identified to have the strongest influence on control, the dominant impact of HLA-B alleles on virus set point and absolute CD4 count variation remains significant. However, we also find
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22

Stoll, Andrej, Silke Bergmann, Christiane Mummert, et al. "Identification of HLA-C restricted, HIV-1-specific CTL epitopes by peptide induced upregulation of HLA-C expression." Journal of Immunological Methods 418 (March 2015): 9–18. http://dx.doi.org/10.1016/j.jim.2015.01.005.

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23

Dalal, Bhavik Ashok, Aruna Shankarkumar, and Amar Pazare. "MHC class I and II genes dependent hypersensitivity to nevirapine and efavirenz in Indian HIV-1 patients." Journal of Immunology 202, no. 1_Supplement (2019): 177.11. http://dx.doi.org/10.4049/jimmunol.202.supp.177.11.

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Abstract OBJECTIVE The present study demonstrates and investigates the involvement of differences in human leukocyte antigens (HLA) class I and class II genes in the risk of hypersensitive reaction to nevirapine and efavirenz among Indian HIV- 1 infected patients. METHODS Thirty-three HIV-positive patients treated with efavirenz and nevirapine were studied. The HLA class I and II molecular typing in both Non-tolerant and tolerant patients were performed using the sequence-specific primers (SSP), the Olerup HLA-A-B-C and DQ-DR SSP Combi Tray. Odds ratios (OR) with 95 % confidence intervals (CI)
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24

Matucci, Andrea, Paola Rossolillo, Miriam Baroni, Antonio G. Siccardi, Alberto Beretta, and Donato Zipeto. "HLA-C increases HIV-1 infectivity and is associated with gp120." Retrovirology 5, no. 1 (2008): 68. http://dx.doi.org/10.1186/1742-4690-5-68.

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25

Matucci, Andrea, Paola Rossolillo, Marco Turci, et al. "137 Presence and role of HLA-C in HIV-1 infection." JAIDS Journal of Acquired Immune Deficiency Syndromes 51 (June 2009): 1. http://dx.doi.org/10.1097/01.qai.0000351094.48019.b6.

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26

Turci, Marco, Pierpaolo Racchiolli, Serena Ziglio, Dalila Astone, Almudena Blanco, and Donato Zipeto. "157a HLA-C Associates with Env and Increases HIV-1 Infectivity." JAIDS Journal of Acquired Immune Deficiency Syndromes 56 (April 2011): 65. http://dx.doi.org/10.1097/01.qai.0000397343.00180.17.

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27

Wright, Jaclyn K., Zabrina L. Brumme, Jonathan M. Carlson, et al. "Gag-Protease-Mediated Replication Capacity in HIV-1 Subtype C Chronic Infection: Associations with HLA Type and Clinical Parameters." Journal of Virology 84, no. 20 (2010): 10820–31. http://dx.doi.org/10.1128/jvi.01084-10.

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ABSTRACT The mechanisms underlying HIV-1 control by protective HLA class I alleles are not fully understood and could involve selection of escape mutations in functionally important Gag epitopes resulting in fitness costs. This study was undertaken to investigate, at the population level, the impact of HLA-mediated immune pressure in Gag on viral fitness and its influence on HIV-1 pathogenesis. Replication capacities of 406 recombinant viruses encoding plasma-derived Gag-protease from patients chronically infected with HIV-1 subtype C were assayed in an HIV-1-inducible green fluorescent protei
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Porter, Kristen, Lauren Kelley, Michael Nekorchuk, et al. "CIITA enhances HIV-1 attachment to CD4+ T cells leading to enhanced infection and cell depletion (154.27)." Journal of Immunology 186, no. 1_Supplement (2011): 154.27. http://dx.doi.org/10.4049/jimmunol.186.supp.154.27.

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Abstract Activated CD4+ T cells are more susceptible to HIV infection than resting T cells; the reason for this remains unresolved. Induction of CIITA and subsequent expression of the MHC class II isotype HLA-DR are hallmarks of CD4+ T cell activation; therefore, we investigated the role of CIITA expression in T cells during HIV infection. CIITA-expressing SupT1 cells display enhanced virion attachment in a gp160/CD4-dependent manner, resulting in increased HIV infection, virus release, and T cell depletion. Although increased attachment and infection of T cells correlated with HLA-DR surface
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29

DeGottardi, M. Quinn, Anke Specht, Benjamin Metcalf, Amitinder Kaur, Frank Kirchhoff, and David T. Evans. "Selective Downregulation of Rhesus Macaque and Sooty Mangabey Major Histocompatibility Complex Class I Molecules by Nef Alleles of Simian Immunodeficiency Virus and Human Immunodeficiency Virus Type 2." Journal of Virology 82, no. 6 (2008): 3139–46. http://dx.doi.org/10.1128/jvi.02102-07.

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ABSTRACT Human immunodeficiency virus type 1 (HIV-1) Nef downregulates HLA-A and -B molecules, but not HLA-C or -E molecules, based on amino acid differences in their cytoplasmic domains to simultaneously evade cytotoxic T lymphocyte (CTL) and natural killer cell surveillance. Rhesus macaques and sooty mangabeys express orthologues of HLA-A, -B, and -E, but not HLA-C, and many of these molecules have unique amino acid differences in their cytoplasmic tails. We found that these differences also resulted in differential downregulation by primary simian immunodeficiency virus (SIV) SIVsmm/mac and
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30

Rousseau, Christine M., Marcus G. Daniels, Jonathan M. Carlson, et al. "HLA Class I-Driven Evolution of Human Immunodeficiency Virus Type 1 Subtype C Proteome: Immune Escape and Viral Load." Journal of Virology 82, no. 13 (2008): 6434–46. http://dx.doi.org/10.1128/jvi.02455-07.

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ABSTRACT Human immunodeficiency virus type 1 (HIV-1) mutations that confer escape from cytotoxic T-lymphocyte (CTL) recognition can sometimes result in lower viral fitness. These mutations can then revert upon transmission to a new host in the absence of CTL-mediated immune selection pressure restricted by the HLA alleles of the prior host. To identify these potentially critical recognition points on the virus, we assessed HLA-driven viral evolution using three phylogenetic correction methods across full HIV-1 subtype C proteomes from a cohort of 261 South Africans and identified amino acids c
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Murakoshi, Hayato, Tomohiro Akahoshi, Madoka Koyanagi, et al. "Clinical Control of HIV-1 by Cytotoxic T Cells Specific for Multiple Conserved Epitopes." Journal of Virology 89, no. 10 (2015): 5330–39. http://dx.doi.org/10.1128/jvi.00020-15.

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ABSTRACTIdentification and characterization of CD8+T cells effectively controlling HIV-1 variants are necessary for the development of AIDS vaccines and for studies of AIDS pathogenesis, although such CD8+T cells have been only partially identified. In this study, we sought to identify CD8+T cells controlling HIV-1 variants in 401 Japanese individuals chronically infected with HIV-1 subtype B, in which protective alleles HLA-B*57 and HLA-B*27 are very rare, by using comprehensive and exhaustive methods. We identified 13 epitope-specific CD8+T cells controlling HIV-1 in Japanese individuals, th
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32

Mann, Jaclyn K., Erasha Rajkoomar, Steven W. Jin, et al. "Consequences of HLA‐associated mutations in HIV‐1 subtype C Nef on HLA‐I downregulation ability." Journal of Medical Virology 92, no. 8 (2020): 1182–90. http://dx.doi.org/10.1002/jmv.25676.

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Gong, XiaoYan, WeiWei Gai, JunQiang Xu, Wei Zhou, and Po Tien. "Glycoprotein 96-Mediated Presentation of Human Immunodeficiency Virus Type 1 (HIV-1)-Specific Human Leukocyte Antigen Class I-Restricted Peptide and Humoral Immune Responses to HIV-1 p24." Clinical and Vaccine Immunology 16, no. 11 (2009): 1595–600. http://dx.doi.org/10.1128/cvi.00160-09.

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ABSTRACT Viral antigens complexed to heat shock proteins (HSPs) can enhance antiviral immunity. The present study evaluated the immunogenicity of a novel human immunodeficiency virus type 1B′ (HIV-1B′)-specific, human leukocyte antigen A2 (HLA-A2)-restricted peptide (FLQSRPEPTA, Gag448-457) and the cellular immune adjuvant effect of HSP gp96 using the HLA-A2 transgenic mouse model. It was found that gp96 could augment cytotoxic-T-lymphocyte responses specific for the 10-mer peptide of HIV-1B′. This study also evaluated the humoral immune adjuvant effect of HSP gp96 and its N-terminal fragment
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Hadida, F., G. Haas, N. Zimmermann, et al. "CTLs from lymphoid organs recognize an optimal HLA-A2-restricted and HLA-B52-restricted nonapeptide and several epitopes in the C-terminal region of HIV-1 Nef." Journal of Immunology 154, no. 8 (1995): 4174–86. http://dx.doi.org/10.4049/jimmunol.154.8.4174.

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Abstract In a previous analysis of HIV-1-specific CTLs in lymphoid organs from HIV-seropositive patients, we reported high frequencies of in vivo differentiated CTLs directed against two immunodominant regions in the central and in the C-terminal part of the HIV-1 Nef protein. The present study analyzes the epitopes recognized by CTLs in the carboxyl terminus of Nef (amino acids 182-205). In addition to several epitopes that are recognized in association with different HLA molecules (A1, A2, A25(10), B35, B52), we defined an optimal nonapeptide (190-198). This nonapeptide was recognized by CTL
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Honeyborne, Isobella, Francisco M. Codoñer, Alasdair Leslie, et al. "HLA-Cw*03-Restricted CD8+ T-Cell Responses Targeting the HIV-1 Gag Major Homology Region Drive Virus Immune Escape and Fitness Constraints Compensated for by Intracodon Variation." Journal of Virology 84, no. 21 (2010): 11279–88. http://dx.doi.org/10.1128/jvi.01144-10.

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ABSTRACT The potential importance of HLA-C-restricted CD8+ cytotoxic T lymphocytes (CTL) in HIV infection remains undetermined. We studied the dominant HLA-Cw*03-restricted CTL response to YVDRFFKTL296-304 (YL9), within the conserved major homology region (MHR) of the Gag protein, in 80 HLA-Cw*03-positive individuals with chronic HIV infection to better define the efficacy of the YL9 HLA-C-restricted response. The HLA-Cw*03 allele is strongly associated with HIV sequence changes from Thr-303 to Val, Ile, or Ala at position 8 within the YL9 epitope (P = 1.62 × 10−10). In vitro studies revealed
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Koofhethile, Catherine K., Zaza M. Ndhlovu, Christina Thobakgale-Tshabalala, et al. "CD8+T Cell Breadth andEx VivoVirus Inhibition Capacity Distinguish between Viremic Controllers with and without Protective HLA Class I Alleles." Journal of Virology 90, no. 15 (2016): 6818–31. http://dx.doi.org/10.1128/jvi.00276-16.

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ABSTRACTThe mechanisms of viral control and loss of viral control in chronically infected individuals with or without protective HLA class I alleles are not fully understood. We therefore characterized longitudinally the immunological and virological features that may explain divergence in disease outcome in 70 HIV-1 C-clade-infected antiretroviral therapy (ART)-naive South African adults, 35 of whom possessed protective HLA class I alleles. We demonstrate that, over 5 years of longitudinal study, 35% of individuals with protective HLA class I alleles lost viral control compared to none of the
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Geels, Mark J., Sheri A. Dubey, Kiersten Anderson, et al. "Broad Cross-Clade T-Cell Responses to Gag in Individuals Infected with Human Immunodeficiency Virus Type 1 Non-B Clades (A to G): Importance of HLA Anchor Residue Conservation." Journal of Virology 79, no. 17 (2005): 11247–58. http://dx.doi.org/10.1128/jvi.79.17.11247-11258.2005.

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ABSTRACT We aimed to identify cross-clade human immunodeficiency virus type 1 (HIV-1) specific T-cell responses among 10 HLA-typed individuals who were infected with non-B HIV-1 strains (A, AG, C, D, G, or F) and to correlate these responses with genetic variation in documented T-cell epitopes. T-cell reactivity was tested against peptide pools spanning clade B Gag, Pol, Nef, Rev, and Tat consensus, with Gag and Nef providing the highest responses. Nine individuals who responded to clade B Gag demonstrated cross-reactive T-cell responses against clade A and C Gag pools, while six of seven resp
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Hu, Qinxue, Ines Frank, Vennansha Williams, et al. "Blockade of Attachment and Fusion Receptors Inhibits HIV-1 Infection of Human Cervical Tissue." Journal of Experimental Medicine 199, no. 8 (2004): 1065–75. http://dx.doi.org/10.1084/jem.20022212.

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Identification of cellular factors involved in HIV-1 entry and transmission at mucosal surfaces is critical for understanding viral pathogenesis and development of effective prevention strategies. Here we describe the evaluation of HIV-1 entry inhibitors for their ability to prevent infection of, and dissemination from, human cervical tissue ex vivo. Blockade of CD4 alone or CCR5 and CXCR4 together inhibited localized mucosal infection. However, simultaneous blockade of CD4 and mannose-binding C-type lectin receptors including dendritic cell–specific intercellular adhesion molecule–grabbing in
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Crawford, Hayley, Wendy Lumm, Alasdair Leslie, et al. "Evolution of HLA-B*5703 HIV-1 escape mutations in HLA-B*5703–positive individuals and their transmission recipients." Journal of Experimental Medicine 206, no. 4 (2009): 909–21. http://dx.doi.org/10.1084/jem.20081984.

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HLA-B*57 is the class I allele most consistently associated with control of human immunodeficiency virus (HIV) replication, which may be linked to the specific HIV peptides that this allele presents to cytotoxic T lymphocytes (CTLs), and the resulting efficacy of these cellular immune responses. In two HIV C clade–infected populations in South Africa and Zambia, we sought to elucidate the role of HLA-B*5703 in HIV disease outcome. HLA-B*5703–restricted CTL responses select for escape mutations in three Gag p24 epitopes, in a predictable order. We show that the accumulation of these mutations s
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McLaren, Paul J., Cedric Coulonges, István Bartha, et al. "Polymorphisms of large effect explain the majority of the host genetic contribution to variation of HIV-1 virus load." Proceedings of the National Academy of Sciences 112, no. 47 (2015): 14658–63. http://dx.doi.org/10.1073/pnas.1514867112.

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Previous genome-wide association studies (GWAS) of HIV-1–infected populations have been underpowered to detect common variants with moderate impact on disease outcome and have not assessed the phenotypic variance explained by genome-wide additive effects. By combining the majority of available genome-wide genotyping data in HIV-infected populations, we tested for association between ∼8 million variants and viral load (HIV RNA copies per milliliter of plasma) in 6,315 individuals of European ancestry. The strongest signal of association was observed in the HLA class I region that was fully expl
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Mahmud, Rizwan, Zoë Krullaars, Jolieke van Osch, et al. "Computational and Population-Based HLA Permissiveness to HIV Drug Resistance-Associated Mutations." Pathogens 14, no. 3 (2025): 207. https://doi.org/10.3390/pathogens14030207.

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The presentation of HIV peptides by the human leukocyte antigen (HLA) complex to CD8+ cytotoxic T-cells (CTLs) is critical to limit viral pathogenesis. HIV can mutate to evade HLA-restricted CTL responses and resist antiretroviral drugs, raising questions about how it balances these evolutionary pressures. Here, we used a computational approach to assess how drug resistance-associated mutations (RAMs) affect the binding of HIV-1 subtype B or C peptides to the most prevalent HLA alleles in US, European, and South African populations. We predict RAMs that may be favored in certain populations an
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42

Novitsky, V., P. Gilbert, T. Peter, et al. "Association between Virus-Specific T-Cell Responses and Plasma Viral Load in Human Immunodeficiency Virus Type 1 Subtype C Infection." Journal of Virology 77, no. 2 (2003): 882–90. http://dx.doi.org/10.1128/jvi.77.2.882-890.2003.

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ABSTRACT Virus-specific T-cell immune responses are important in restraint of human immunodeficiency virus type 1 (HIV-1) replication and control of disease. Plasma viral load is a key determinant of disease progression and infectiousness in HIV infection. Although HIV-1 subtype C (HIV-1C) is the predominant virus in the AIDS epidemic worldwide, the relationship between HIV-1C-specific T-cell immune responses and plasma viral load has not been elucidated. In the present study we address (i) the association between the level of plasma viral load and virus-specific immune responses to different
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Yu, Xu G., Mathias Lichterfeld, Senica Chetty, et al. "Mutually Exclusive T-Cell Receptor Induction and Differential Susceptibility to Human Immunodeficiency Virus Type 1 Mutational Escape Associated with a Two-Amino-Acid Difference between HLA Class I Subtypes." Journal of Virology 81, no. 4 (2006): 1619–31. http://dx.doi.org/10.1128/jvi.01580-06.

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ABSTRACT The relative contributions of HLA alleles and T-cell receptors (TCRs) to the prevention of mutational viral escape are unclear. Here, we examined human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses restricted by two closely related HLA class I alleles, B*5701 and B*5703, that differ by two amino acids but are both associated with a dominant response to the same HIV-1 Gag epitope KF11 (KAFSPEVIPMF). When this epitope is presented by HLA-B*5701, it induces a TCR repertoire that is highly conserved among individuals, cross-recognizes viral epitope variants, and is
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Mkhwanazi, Nompumelelo, Christina F. Thobakgale, Mary van der Stok, et al. "Immunodominant HIV-1-specific HLA-B- and HLA-C-restricted CD8+ T cells do not differ in polyfunctionality." Virology 405, no. 2 (2010): 483–91. http://dx.doi.org/10.1016/j.virol.2010.06.002.

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45

Tang, Jianming, Shenghui Tang, Elena Lobashevsky, et al. "Favorable and Unfavorable HLA Class I Alleles and Haplotypes in Zambians Predominantly Infected with Clade C Human Immunodeficiency Virus Type 1." Journal of Virology 76, no. 16 (2002): 8276–84. http://dx.doi.org/10.1128/jvi.76.16.8276-8284.2002.

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ABSTRACT The setpoint of viral RNA concentration (viral load [VL]) during chronic human immunodeficiency virus type 1 (HIV-1) infection reflects a virus-host equilibration closely related to CD8+ cytotoxic T-lymphocyte (CTL) responses, which rely heavily on antigen presentation by the human major histocompatibility complex (MHC) (i.e., HLA) class I molecules. Differences in HIV-1 VL among 259 mostly clade C virus-infected individuals (137 females and 122 males) in the Zambia-UAB HIV Research Project (ZUHRP) were associated with several HLA class I alleles and haplotypes. In particular, general
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Celsi, Fulvio, Eulalia Catamo, Giulio Kleiner, Paola Maura Tricarico, Josef Vuch, and Sergio Crovella. "HLA-G/C, miRNAs, and Their Role in HIV Infection and Replication." BioMed Research International 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/693643.

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In recent years, a number of different mechanisms regulating gene expressions, either in normal or in pathological conditions, have been discovered. This review aims to highlight some of the regulatory pathways involved during the HIV-1 infection and disease progression, focusing on the novel discovered microRNAs (miRNAs) and their relation with immune system’s agents. Human leukocyte antigen (HLA) family of proteins plays a key role because it is a crucial modulator of the immune response; here we will examine recent findings, centering especially on HLA-C and -G, novel players lately discove
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Matthews, Philippa C., Andrew Prendergast, Alasdair Leslie, et al. "Central Role of Reverting Mutations in HLA Associations with Human Immunodeficiency Virus Set Point." Journal of Virology 82, no. 17 (2008): 8548–59. http://dx.doi.org/10.1128/jvi.00580-08.

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ABSTRACT Much uncertainty still exists over what T-cell responses need to be induced by an effective human immunodeficiency virus (HIV) vaccine. Previous studies have hypothesized that the effective CD8+ T-cell responses are those driving the selection of escape mutations that reduce viral fitness and therefore revert posttransmission. In this study, we adopted a novel approach to define better the role of reverting escape mutations in immune control of HIV infection. This analysis of sequences from 710 study subjects with chronic C-clade HIV type 1 infection demonstrates the importance of mut
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Santos-Pereira, Ana, Vera Triunfante, Pedro M. M. Araújo, et al. "Nationwide Study of Drug Resistance Mutations in HIV-1 Infected Individuals under Antiretroviral Therapy in Brazil." International Journal of Molecular Sciences 22, no. 10 (2021): 5304. http://dx.doi.org/10.3390/ijms22105304.

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The success of antiretroviral treatment (ART) is threatened by the emergence of drug resistance mutations (DRM). Since Brazil presents the largest number of people living with HIV (PLWH) in South America we aimed at understanding the dynamics of DRM in this country. We analyzed a total of 20,226 HIV-1 sequences collected from PLWH undergoing ART between 2008–2017. Results show a mild decline of DRM over the years but an increase of the K65R reverse transcriptase mutation from 2.23% to 12.11%. This increase gradually occurred following alterations in the ART regimens replacing zidovudine (AZT)
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Hake, Anna, Anja Germann, Corena de Beer, et al. "Insights to HIV-1 coreceptor usage by estimating HLA adaptation with Bayesian generalized linear mixed models." PLOS Computational Biology 19, no. 12 (2023): e1010355. http://dx.doi.org/10.1371/journal.pcbi.1010355.

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The mechanisms triggering the human immunodeficiency virus type I (HIV-1) to switch the coreceptor usage from CCR5 to CXCR4 during the course of infection are not entirely understood. While low CD4+ T cell counts are associated with CXCR4 usage, a predominance of CXCR4 usage with still high CD4+ T cell counts remains puzzling. Here, we explore the hypothesis that viral adaptation to the human leukocyte antigen (HLA) complex, especially to the HLA class II alleles, contributes to the coreceptor switch. To this end, we sequence the viral gag and env protein with corresponding HLA class I and II
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Currier, Jeffrey R., Mark deSouza, Penprapa Chanbancherd, Wendy Bernstein, Deborah L. Birx, and Josephine H. Cox. "Comprehensive Screening for Human Immunodeficiency Virus Type 1 Subtype-Specific CD8 Cytotoxic T Lymphocytes and Definition of Degenerate Epitopes Restricted by HLA-A0207 and -CW0304 Alleles." Journal of Virology 76, no. 10 (2002): 4971–86. http://dx.doi.org/10.1128/jvi.76.10.4971-4986.2002.

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ABSTRACT For this report, the rapid identification and characterization of human immunodeficiency virus type 1 (HIV-1)-derived broadly cross-subtype-reactive CD8 cytotoxic T lymphocyte (CTL) epitopes were performed. Using a gamma interferon (IFN-γ) Elispot assay-based approach and a panel of recombinant vaccinia viruses expressing gag, env, pol, and nef genes representing the seven most predominant subtypes and one circulating recombinant form of HIV-1, the subtype specificity and cross-subtype reactivity of a CD8 response were directly measured from circulating peripheral blood mononuclear ce
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