ArticleJournal of virology2011
Virological and immunological factors associated with HIV-1 differential disease progression in HLA-B 58:01-positive individuals.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Characterisation of HIV-1 Gag Cytotoxic T-Lymphocyte Epitopes in the Southern African Region-A Systematic Review.Immunology · 2026Pooled it
- Role of transmitted Gag CTL polymorphisms in defining replicative capacity and early HIV-1 pathogenesis.PLoS pathogens · 2012Trial
- No Difference in the Prevalence of HIV-1Vaccines · 2023Article
- Exome Sequencing Reveals a Putative Role for HLA-C*03:02 in Control of HIV-1 in African Pediatric Populations.Frontiers in genetics · 2021Article
- A de novo approach to inferring within-host fitness effects during untreated HIV-1 infection.PLoS pathogens · 2020Article
- Modelling andVirus evolution · 2019Article
- Early evolution of human leucocyte antigen-associated escape mutations in variable Gag proteins predicts CD4+ decline in HIV-1 subtype C-infected women.AIDS (London, England) · 2017Article
- HIV-1 Tat and Viral Latency: What We Can Learn from Naturally Occurring Sequence Variations.Frontiers in microbiology · 2017Review
- Genetic determinants of Nef-mediated CD4 and HLA class I down-regulation differences between HIV-1 subtypes B and C.Virology journal · 2015Article
- Structured observations reveal slow HIV-1 CTL escape.PLoS genetics · 2015Article
- Preexisting compensatory amino acids compromise fitness costs of a HIV-1 T cell escape mutation.Retrovirology · 2014Article
- tat Exon 1 exhibits functional diversity during HIV-1 subtype C primary infection.Journal of virology · 2013Article
- Rapid, complex adaptation of transmitted HIV-1 full-length genomes in subtype C-infected individuals with differing disease progression.AIDS (London, England) · 2013Article
- HIV-1 Env C2-V4 diversification in a slow-progressor infant reveals a flat but rugged fitness landscape.PloS one · 2013Article
- Intersubtype differences in the effect of a rare p24 gag mutation on HIV-1 replicative fitness.Journal of virology · 2012Article
- Temporal association of HLA-B*81:01- and HLA-B*39:10-mediated HIV-1 p24 sequence evolution with disease progression.Journal of virology · 2012Article
- Functional avidity: a measure to predict the efficacy of effector T cells?Clinical & developmental immunology · 2012Review
- Immune-mediated attenuation of HIV-1.Future virology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Molecular epidemiology studies have identified HLA-B 58:01 as a protective HIV allele. However, not all B 58:01-expressing persons exhibit slow HIV disease progression. We followed six HLA-B 58:01-positive, HIV subtype C-infected individuals for up to 31 months from the onset of infection and observed substantial variability in their clinical progression despite comparable total breadths of T cell responses. We therefore investigated additional immunological and virological factors that could explain their different disease trajectories. Cytotoxic T-lymphocyte (CTL) responses during acute infection predominantly targeted the TW10 and KF9 epitopes in p24(Gag) and Nef, respectively. Failure to target the TW10 epitope in one B 58:01-positive individual was associated with low CD4(+) counts and rapid disease progression. Among those targeting TW10, escape mutations arose within 2 to 15 weeks of infection. Rapid escape was associated with preexisting compensatory mutations in the transmitted viruses, which were present at a high frequency (69%) in the study population. At 1 year postinfection, B 58:01-positive individuals who targeted and developed escape mutations in the TW10 epitope (n = 5) retained significantly higher CD4(+) counts (P = 0.04), but not lower viral loads, than non-B 58:01-positive individuals (n = 17). The high population-level frequency of these compensatory mutations may be limiting the protective effect of the B 58:01 allele.
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Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.