1. An Evolutionary Role for HIV Latency in Enhancing Viral Transmission.

    Cell 160(5):1002 (2015) PMID 25723173

    HIV latency is the chief obstacle to eradicating HIV but is widely believed to be an evolutionary accident providing no lentiviral fitness advantage. However, findings of latency being "hardwired" into HIV's gene-regulatory circuitry appear inconsistent with latency being an evolutionary acciden...
  2. An Evolutionary Role for HIV Latency in Enhancing Viral Transmission.

    Cell 160(5):1002 (2015) PMID 25723173

    HIV latency is the chief obstacle to eradicating HIV but is widely believed to be an evolutionary accident providing no lentiviral fitness advantage. However, findings of latency being "hardwired" into HIV's gene-regulatory circuitry appear inconsistent with latency being an evolutionary acciden...
  3. An Evolutionary Role for HIV Latency in Enhancing Viral Transmission

    Cell 160(5):1002 (2015)

    HIV latency is the chief obstacle to eradicating HIV but is widely believed to be an evolutionary accident providing no lentiviral fitness advantage. However, findings of latency being “hardwired” into HIV’s gene-regulatory circuitry appear inconsistent with latency being an evolutiona...
  4. An evolutionary role for HIV latency in enhancing viral transmission.

    Cell 160(5):1002 (2015) PMID 25723173 PMCID PMC4488136

    HIV latency is the chief obstacle to eradicating HIV but is widely believed to be an evolutionary accident providing no lentiviral fitness advantage. However, findings of latency being "hardwired" into HIV's gene-regulatory circuitry appear inconsistent with latency being an evolutionary acciden...
  5. A Hardwired HIV Latency Program.

    Cell 160(5):990 (2015) PMID 25723172

    Biological circuits can be controlled by two general schemes: environmental sensing or autonomous programs. For viruses such as HIV, the prevailing hypothesis is that latent infection is controlled by cellular state (i.e., environment), with latency simply an epiphenomenon of infected cells tran...
  6. A Hardwired HIV Latency Program.

    Cell 160(5):990 (2015) PMID 25723172

    Biological circuits can be controlled by two general schemes: environmental sensing or autonomous programs. For viruses such as HIV, the prevailing hypothesis is that latent infection is controlled by cellular state (i.e., environment), with latency simply an epiphenomenon of infected cells tran...
  7. The route of HIV escape from immune response targeting multiple sites is determined by the cost-benefit tradeoff of escape mutations.

    PLoS computational biology 10(10):e1003878 (2014) PMID 25356981 PMCID PMC4214571

    Cytotoxic T lymphocytes (CTL) are a major factor in the control of HIV replication. CTL arise in acute infection, causing escape mutations to spread rapidly through the population of infected cells. As a result, the virus develops partial resistance to the immune response. The factors controllin...
  8. The route of HIV escape from immune response targeting multiple sites is determined by the cost-benefit tradeoff of escape mutations.

    PLoS computational biology 10(10):e1003878 (2014) PMID 25356981 PMCID PMC4214571

    Cytotoxic T lymphocytes (CTL) are a major factor in the control of HIV replication. CTL arise in acute infection, causing escape mutations to spread rapidly through the population of infected cells. As a result, the virus develops partial resistance to the immune response. The factors controllin...
  9. Stochastic variability in HIV affects viral eradication.

    PNAS 111(37):13251 (2014) PMID 25201951 PMCID PMC4169906

  10. Stochastic variability in HIV affects viral eradication.

    PNAS 111(37):13251 (2014) PMID 25201951 PMCID PMC4169906

  11. An Evolutionary Role for HIV Latency in Enhancing Viral Transmission

    Cell (2014)

    HIV latency is the chief obstacle to eradicating HIV, but is widely believed to be an evolutionary accident providing no lentiviral fitness advantage. However, findings of latency being ‘hardwired’ into HIV’s gene-regulatory circuitry appear inconsistent with latency being an evolution...
  12. Fifteen years later: hard and soft selection sweeps confirm a large population number for HIV in vivo.

    PLoS Genetics 10(2):e1004179 (2014) PMID 24586204 PMCID PMC3930503

  13. Fifteen years later: hard and soft selection sweeps confirm a large population number for HIV in vivo.

    PLoS Genetics 10(2):e1004179 (2014) PMID 24586204 PMCID PMC3930503

  14. Fifteen years later: hard and soft selection sweeps confirm a large population number for HIV in vivo.

    PLoS Genetics 10(2):e1004179 (2014) PMID 24586204 PMCID PMC3930503

  15. Reply to "Coadaptive stability of interfering particles with HIV-1 when there is an evolutionary conflict".

    Journal of Virology 87(17):9960 (2013) PMID 23943740 PMCID PMC3754088

  16. Reply to "Coadaptive stability of interfering particles with HIV-1 when there is an evolutionary conflict".

    Journal of Virology 87(17):9960 (2013) PMID 23943740 PMCID PMC3754088

  17. Design requirements for interfering particles to maintain coadaptive stability with HIV-1.

    Journal of Virology 87(4):2081 (2013) PMID 23221552 PMCID PMC3571494

    Defective interfering particles (DIPs) are viral deletion mutants lacking essential transacting or packaging elements and must be complemented by wild-type virus to propagate. DIPs transmit through human populations, replicating at the expense of the wild-type virus and acting as molecular paras...
  18. Design requirements for interfering particles to maintain coadaptive stability with HIV-1.

    Journal of Virology 87(4):2081 (2013) PMID 23221552 PMCID PMC3571494

    Defective interfering particles (DIPs) are viral deletion mutants lacking essential transacting or packaging elements and must be complemented by wild-type virus to propagate. DIPs transmit through human populations, replicating at the expense of the wild-type virus and acting as molecular paras...
  19. Distribution of fixed beneficial mutations and the rate of adaptation in asexual populations.

    PNAS 109(13):4950 (2012) PMID 22371564 PMCID PMC3323973

    When large asexual populations adapt, competition between simultaneously segregating mutations slows the rate of adaptation and restricts the set of mutations that eventually fix. This phenomenon of interference arises from competition between mutations of different strengths as well as competit...
  20. Distribution of fixed beneficial mutations and the rate of adaptation in asexual populations.

    PNAS 109(13):4950 (2012) PMID 22371564 PMCID PMC3323973

    When large asexual populations adapt, competition between simultaneously segregating mutations slows the rate of adaptation and restricts the set of mutations that eventually fix. This phenomenon of interference arises from competition between mutations of different strengths as well as competit...