ArticleProceedings of the National Academy of Sciences of the United States of America2008
HIV rebounds from latently infected cells, rather than from continuing low-level replication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers.
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Who cites it
214 citing papers in PubMed.
- HIV-1 variants are archived throughout infection and persist in the reservoir.PLoS pathogens · 2020Trial
- Plasmacytoid dendritic cells sense HIV replication before detectable viremia following treatment interruption.The Journal of clinical investigation · 2020Trial
- Dynamics of HIV DNA reservoir seeding in a cohort of superinfected Kenyan women.PLoS pathogens · 2020Trial
- HIV-1 in lymph nodes is maintained by cellular proliferation during antiretroviral therapy.The Journal of clinical investigation · 2019Trial
- Characterization of the HIV-1 transcription profile after romidepsin administration in ART-suppressed individuals.AIDS (London, England) · 2019Trial
- Size, Composition, and Evolution of HIV DNA Populations during Early Antiretroviral Therapy and Intensification with Maraviroc.Journal of virology · 2018Trial
- No evidence of HIV replication in children on antiretroviral therapy.The Journal of clinical investigation · 2017Trial
- Broad activation of latent HIV-1 in vivo.Nature communications · 2016Trial
- The Effect of Therapeutic HIV Vaccination With ALVAC-HIV With or Without Remune on the Size of the Viral Reservoir (A CTN 173 Substudy).Journal of acquired immune deficiency syndromes (1999) · 2015Trial
- Restriction of V3 region sequence divergence in the HIV-1 envelope gene during antiretroviral treatment in a cohort of recent seroconverters.Retrovirology · 2013Trial
- Residual plasma viraemia and infectious HIV-1 recovery from resting memory CD4 cells in patients on antiretroviral therapy: results from ACTG A5173.Antiviral therapy · 2013Trial
- Phosphorylation of CDK9 at Ser175 enhances HIV transcription and is a marker of activated P-TEFb in CD4(+) T lymphocytes.PLoS pathogens · 2013Trial
- HIV-1 Tat B-cell epitope vaccination was ineffectual in preventing viral rebound after ART cessation: HIV rebound with current ART appears to be due to infection with new endogenous founder virus and not to resurgence of pre-existing Tat-dependent viremia.Human vaccines & immunotherapeutics · 2012Trial
- Evaluation of HIV-1 ambiguous nucleotide frequency during antiretroviral treatment interruption.Journal of acquired immune deficiency syndromes (1999) · 2012Trial
- Trial
- Reappearance of minority K103N HIV-1 variants after interruption of ART initiated during primary HIV-1 infection.PloS one · 2011Trial
- Trial
- Dynamics of natural and pharmacologic control of an SIV variant with an envelope trafficking defect.The Journal of experimental medicine · 2026Article
- Phylogenetics and molecular evolution to understand and curb the HIV pandemic.Nature reviews. Microbiology · 2026Review
- Mild HIV-specific selective forces overlaying natural CD4+ T cell dynamics explain the clonality and decay dynamics of HIV reservoir cells.Cell systems · 2025Article
154 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Rapid rebound of plasma viremia in patients after interruption of long-term combination antiretroviral therapy (cART) suggests persistence of low-level replicating cells or rapid reactivation of latently infected cells. To further characterize rebounding virus, we performed extensive longitudinal clonal evolutionary studies of HIV env C2-V3-C3 regions and exploited the temporal relationships of rebounding plasma viruses with regard to pretreatment sequences in 20 chronically HIV-1-infected patients having undergone multiple 2-week structured treatment interruptions (STI). Rebounding virus during the short STI was homogeneous, suggesting mono- or oligoclonal origin during reactivation. No evidence for a temporal structure of rebounding virus in regard to pretreatment sequences was found. Furthermore, expansion of distinct lineages at different STI cycles emerged. Together, these findings imply stochastic reactivation of different clones from long-lived latently infected cells rather than expansion of viral populations replicating at low levels. After treatment was stopped, diversity increased steadily, but pretreatment diversity was, on average, achieved only >2.5 years after the start of STI when marked divergence from preexisting quasispecies also emerged. In summary, our results argue against persistence of ongoing low-level replication in patients on suppressive cART. Furthermore, a prolonged delay in restoration of pretreatment viral diversity after treatment interruption demonstrates a surprisingly sustained evolutionary bottleneck induced by punctuated antiretroviral therapy.
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