1. A CRISPR View of Cleavage.

    Cell 161(5):964 (2015) PMID 26000476

    Seminal studies showed that CRISPR-Cas systems provide adaptive immunity in prokaryotes and promising gene-editing tools from bacteria to humans. Yet, reports diverged on whether some CRISPR systems naturally target DNA or RNA. Here, Samai and colleagues unify the studies, showing that a single ...
  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) 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...
  4. 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...
  5. 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...
  6. 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...
  7. The case for transmissible antivirals to control population-wide infectious disease.

    Trends in Biotechnology 32(8):400 (2014) PMID 25017994

    Infectious disease control faces significant challenges including: how to therapeutically target the highest-risk populations, circumvent behavioral barriers, and overcome pathogen persistence and resistance mechanisms. We review a recently proposed solution to overcome these challenges: antivir...
  8. Stochastic fate selection in HIV-infected patients.

    Cell 155(3):497 (2013) PMID 24243007

    Classic studies proposed that stochastic variability ("noise") can drive biological fate switching, enhancing evolutionary success. Now, Ho et al. report that HIV's reactivation from dormant (latently infected) patient cells-the major barrier to an HIV cure-is inherently stochastic. Eradicating ...
  9. Stochastic Fate Selection in HIV-Infected Patients

    Cell 155(3):497 (2013)

    Classic studies proposed that stochastic variability (“noise”) can drive biological fate switching, enhancing evolutionary success. Now, Ho et al. report that HIV’s reactivation from dormant (latently infected) patient cells—the major barrier to an HIV cure—is inherently stochastic. Er...
  10. CRISPR-Cas: To Take Up DNA or Not—That Is the Question

    Cell Host & Microbe 12(2):125 (2012)

    Landmark experiments in the 1920s showed that capsule switching is critical for Streptococcus pneumonia survival. Further studies demonstrated that capsule “transformation” occurs via DNA uptake. In this issue of Cell Host and Microbe, Bikard et al. (2012) show that CRISPR-Cas systems ...
  11. CRISPR-Cas: to take up DNA or not-that is the question.

    Cell Host & Microbe 12(2):125 (2012) PMID 22901532 PMCID PMC3427645

    Landmark experiments in the 1920s showed that capsule switching is critical for Streptococcus pneumonia survival. Further studies demonstrated that capsule "transformation" occurs via DNA uptake. In this issue of Cell Host and Microbe, Bikard et al. (2012) show that CRISPR-Cas systems inhibit DN...
  12. Persisting viral sequences shape microbial CRISPR-based immunity.

    PLoS computational biology 8(4):e1002475 (2012) PMID 22532794 PMCID PMC3330103

    Well-studied innate immune systems exist throughout bacteria and archaea, but a more recently discovered genomic locus may offer prokaryotes surprising immunological adaptability. Mediated by a cassette-like genomic locus termed Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR),...
  13. Persisting viral sequences shape microbial CRISPR-based immunity.

    PLoS computational biology 8(4):e1002475 (2012) PMID 22532794 PMCID PMC3330103

    Well-studied innate immune systems exist throughout bacteria and archaea, but a more recently discovered genomic locus may offer prokaryotes surprising immunological adaptability. Mediated by a cassette-like genomic locus termed Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR),...
  14. An Evolutionary Role for HIV Latency in Enhancing Viral Transmission

    Cell (2012)

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

    Cell (2012)

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

    Cell (2012)

    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...
  17. Viral diversity threshold for adaptive immunity in prokaryotes.

    mBio 3(6):e00456 (2012) PMID 23221803 PMCID PMC3517865

    Bacteria and archaea face continual onslaughts of rapidly diversifying viruses and plasmids. Many prokaryotes maintain adaptive immune systems known as clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated genes (Cas). CRISPR-Cas systems are genomic sensors tha...
  18. Persistence and emergence of X4 virus in HIV infection.

    Mathematical Biosciences and Engineering 8(2):605 (2011) PMID 21631149 PMCID PMC3118547

    Approximately 50% of late-stage HIV patients develop CXCR4-tropic (X4) virus in addition to CCR5-tropic (R5) virus. X4 emergence occurs with a sharp decline in CD4+ T cell counts and accelerated time to AIDS. Why this phenotypic switch to X4 occurs is not well understood. Previously, we used num...
  19. Persistence and emergence of X4 virus in HIV infection.

    Mathematical Biosciences and Engineering 8(2):605 (2011) PMID 21631149 PMCID PMC3118547

    Approximately 50% of late-stage HIV patients develop CXCR4-tropic (X4) virus in addition to CCR5-tropic (R5) virus. X4 emergence occurs with a sharp decline in CD4+ T cell counts and accelerated time to AIDS. Why this phenotypic switch to X4 occurs is not well understood. Previously, we used num...
  20. Accelerated immunodeficiency by anti-CCR5 treatment in HIV infection.

    PLoS computational biology 5(8):e1000467 (2009) PMID 19680436 PMCID PMC2715863

    In 50% of progressing HIV-1 patients, CXCR4-tropic (X4) virus emerges late in infection, often overtaking CCR5-tropic (R5) virus as the dominant viral strain. This "phenotypic switch" is strongly associated with rapidly declining CD4(+) T cell counts and AIDS onset, yet its causes remain unknown...