ArticleJournal of virology2010
Mathematical modeling of ultradeep sequencing data reveals that acute CD8+ T-lymphocyte responses exert strong selective pressure in simian immunodeficiency virus-infected macaques but still fail to clear founder epitope sequences.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Restriction of V3 region sequence divergence in the HIV-1 envelope gene during antiretroviral treatment in a cohort of recent seroconverters.Retrovirology · 2013Trial
- Modelling HIV-1 control and remission.NPJ systems biology and applications · 2024Review
- Kinetics of HIV-Specific CTL Responses Plays a Minimal Role in Determining HIV Escape Dynamics.Frontiers in immunology · 2018Article
- The HIV-1 transmission bottleneck.Retrovirology · 2017Article
- Broad CTL Response in Early HIV Infection Drives Multiple Concurrent CTL Escapes.PLoS computational biology · 2015Article
- Deep sequencing analysis of viral infection and evolution allows rapid and detailed characterization of viral mutant spectrum.Bioinformatics (Oxford, England) · 2015Article
- Comparison of Major and Minor Viral SNPs Identified through Single Template Sequencing and Pyrosequencing in Acute HIV-1 Infection.PloS one · 2015Article
- Indel and Carryforward Correction (ICC): a new analysis approach for processing 454 pyrosequencing data.Bioinformatics (Oxford, England) · 2013Article
- Article
- Previously transmitted HIV-1 strains are preferentially selected during subsequent sexual transmissions.The Journal of infectious diseases · 2012Article
- Next generation deep sequencing and vaccine design: today and tomorrow.Trends in biotechnology · 2012Review
- A quantitative quasispecies theory-based model of virus escape mutation under immune selection.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Whole genome deep sequencing of HIV-1 reveals the impact of early minor variants upon immune recognition during acute infection.PLoS pathogens · 2012Article
- The efficiency of the human CD8+ T cell response: how should we quantify it, what determines it, and does it matter?PLoS computational biology · 2012Article
- Systems biology approaches to new vaccine development.Current opinion in immunology · 2011Review
- CD8(+)T-cell-mediated control of HIV-1 and SIV infection.Immunologic research · 2011Review
- Epitope-specific CD8+ T lymphocytes cross-recognize mutant simian immunodeficiency virus (SIV) sequences but fail to contain very early evolution and eventual fixation of epitope escape mutations during SIV infection.Journal of virology · 2011Article
- Transmission of single HIV-1 genomes and dynamics of early immune escape revealed by ultra-deep sequencing.PloS one · 2010Article
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Authors and funding
5 authors.
Funding
Abstract
The prominent role of antiviral cytotoxic CD8(+) T-lymphocytes (CD8-TL) in containing the acute viremia of human and simian immunodeficiency viruses (HIV-1 and SIV) has rationalized the development of T-cell-based vaccines. However, the presence of escape mutations in the acute stage of infection has raised a concern that accelerated escape from vaccine-induced CD8-TL responses might undermine vaccine efficacy. We reanalyzed previously published data of 101,822 viral genomes of three CD8-TL epitopes, Nef(103-111)RM9 (RM9), Tat(28-35)SL8 (SL8), and Gag(181-189)CM9 (CM9), sampled by ultradeep pyrosequencing from eight macaques. Multiple epitope variants appeared during the resolution of acute viremia, followed by the predominance of a single mutant epitope. By fitting a mathematical model, we estimated the first acute escape rate as 0.36 day(-1) within escape-prone epitopes, RM9 and SL8, and the chronic escape rate as 0.014 day(-1) within the CM9 epitope. Our estimate of SIV acute escape rates was found to be comparable to very early HIV-1 escape rates. The timing of the first escape was more highly correlated with the timing of the peak CD8-TL response than with the magnitude of the CD8-TL response. The transmitted epitope decayed more than 400 times faster during the acute viral decline stage than predicted by a neutral evolution model. However, the founder epitope persisted as a minor population even at the viral set point; in contrast, the majority of acute escape epitopes were completely cleared. Our results suggest that a reservoir of SIV infection is preferentially formed by virus with the transmitted epitope.
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