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A hardwired HIV latency program.

Brandon S Razooky1, Anand Pai2, Katherine Aull3

  • 1The Gladstone Institutes (Virology and Immunology), San Francisco, California Institute of Quantitative Biosciences, University of California, San Francisco, 94158; Biophysics Graduate Group, California Institute of Quantitative Biosciences, University of California, San Francisco, 94158.

Cell
|February 28, 2015
PubMed
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This summary is machine-generated.

Human immunodeficiency virus (HIV) latency is controlled by an autonomous viral program, not just cellular state. HIV

Area of Science:

  • Virology and Molecular Biology
  • Systems Biology
  • Synthetic Biology

Background:

  • Biological circuits are typically controlled by environmental sensing or autonomous programs.
  • The prevailing hypothesis for human immunodeficiency virus (HIV) latency is control by cellular state, with latency as an epiphenomenon of cell activation state.
  • HIV expression has been observed to persist despite transitions between activated and resting cellular states.

Purpose of the Study:

  • To investigate the control mechanisms underlying HIV latency.
  • To test the hypothesis that HIV latency is regulated by an autonomous viral program.
  • To decouple viral transcription from cellular activation state using synthetic biology.

Main Methods:

  • Mathematical modeling of HIV circuitry.

Related Experiment Videos

  • Synthetic biology to create circuits that decouple viral dependence on cellular environment from viral transcription.
  • Experimental validation of synthetic circuits to control viral transcription independently of cellular activation.

    • Main Results:

    • HIV expression persists through cellular state transitions, contradicting the cellular control hypothesis.
    • Mathematical modeling indicated that HIV's Tat positive-feedback circuitry is crucial for persistence and latency control.
    • Synthetic circuits demonstrated that Tat feedback is sufficient to regulate HIV latency independently of cellular activation.

    Conclusions:

    • HIV latency is primarily governed by a largely autonomous, viral-encoded program, specifically the Tat positive-feedback loop.
    • This viral autonomous program explains the persistence of HIV expression irrespective of the host cell's activation state.
    • The findings suggest a potential reason for the incomplete penetrance of cell-targeted latency-reversing agents in HIV treatment.