ArticlePloS one2010
Unexpected diversity of cellular immune responses against Nef and Vif in HIV-1-infected patients who spontaneously control viral replication.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- The role of MHC class I gene products in SIV infection of macaques.Immunogenetics · 2017Review
- Uniquely altered transcripts are associated with immune preservation in HIV infection.PloS one · 2017Article
- Cellular immune correlates analysis of an HIV-1 preexposure prophylaxis trial.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Improvement in efficacy of DNA vaccine encoding HIV-1 Vif by LIGHT gene adjuvant.Viral immunology · 2013Article
- Frequency of subtype B and F1 dual infection in HIV-1 positive, Brazilian men who have sex with men.Virology journal · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundHIV-1-infected individuals who spontaneously control viral replication represent an example of successful containment of the AIDS virus. Understanding the anti-viral immune responses in these individuals may help in vaccine design. However, immune responses against HIV-1 are normally analyzed using HIV-1 consensus B 15-mers that overlap by 11 amino acids. Unfortunately, this method may underestimate the real breadth of the cellular immune responses against the autologous sequence of the infecting virus. METHODOLOGY AND PRINCIPAL
findingsHere we compared cellular immune responses against nef and vif-encoded consensus B 15-mer peptides to responses against HLA class I-predicted minimal optimal epitopes from consensus B and autologous sequences in six patients who have controlled HIV-1 replication. Interestingly, our analysis revealed that three of our patients had broader cellular immune responses against HLA class I-predicted minimal optimal epitopes from either autologous viruses or from the HIV-1 consensus B sequence, when compared to responses against the 15-mer HIV-1 type B consensus peptides. CONCLUSION AND SIGNIFICANCE: This suggests that the cellular immune responses against HIV-1 in controller patients may be broader than we had previously anticipated.
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Registered trials
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