ArticlePloS one2007
Adaptation of HIV-1 depends on the host-cell environment.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Concomitant Enhancement of HIV-1 Replication Potential and Neutralization-Resistance in Concert With Three Adaptive Mutations in Env V1/C2/C4 Domains.Frontiers in microbiology · 2019Article
- Genetically integrated traits and rugged adaptive landscapes in digital organisms.BMC evolutionary biology · 2015Article
- Role of pleiotropy during adaptation of TEM-1 β-lactamase to two novel antibiotics.Evolutionary applications · 2015Article
- Intercompartmental recombination of HIV-1 contributes to env intrahost diversity and modulates viral tropism and sensitivity to entry inhibitors.Journal of virology · 2011Article
- Fitness ranking of individual mutants drives patterns of epistatic interactions in HIV-1.PloS one · 2011Article
- Article
- Multiple T-cell epitopes overlap positively-selected residues in the p1 spacer protein of HIV-1 gag.AIDS (London, England) · 2009Article
- The evolution of viruses in multi-host fitness landscapes.The open virology journal · 2009Article
- Clinical severe acute respiratory syndrome coronavirus 2 isolation and antiviral testing.Antiviral chemistry & chemotherapyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many viruses have the ability to rapidly develop resistance against antiviral drugs and escape from the host immune system. To which extent the host environment affects this adaptive potential of viruses is largely unknown. Here we show that for HIV-1, the host-cell environment is key to the adaptive potential of the virus. We performed a large-scale selection experiment with two HIV-1 strains in two different T-cell lines (MT4 and C8166). Over 110 days of culture, both virus strains adapted rapidly to the MT4 T-cell line. In contrast, when cultured on the C8166 T-cell line, the same strains did not show any increase in fitness. By sequence analyses and infections with viruses expressing either yellow or cyan fluorescent protein, we were able to show that the absence of adaptation was linked to a lower recombination rate in the C8166 T-cell line. Our findings suggest that if we can manipulate the host-cellular factors that mediate viral evolution, we may be able to significantly retard viral adaptability.
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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.