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A transient heritable memory regulates HIV reactivation from latency.

Yiyang Lu1, Harpal Singh1, Abhyudai Singh2

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Reactivation of human immunodeficiency virus 1 (HIV-1) from latent T cells is a cure barrier. A transient heritable memory regulates HIV-1 reactivation, impacting future therapies.

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Reactivation of latent human immunodeficiency virus 1 (HIV-1) from infected T cells is a major obstacle to achieving a cure.
  • The precise mechanism governing individual latent cell reactivation—stochastic or deterministic—remains unclear.

Purpose of the Study:

  • To investigate the nature of single-cell responses to latency reversal agents (LRAs).
  • To characterize the dynamics of HIV-1 reactivation at the single-cell level.

Main Methods:

  • Utilized the Luria-Delbrück fluctuation test by isolating single T cells and exposing them to LRAs after colony expansion.
  • Applied mathematical modeling to analyze fluctuations in reactivation rates over time.

Main Results:

  • Observed significant colony-to-colony variations in the fraction of reactivating cells, with a skewed distribution.
  • Identified a transient, heritable memory state that influences HIV-1 reactivation, lasting several weeks.

Conclusions:

  • HIV-1 reactivation is regulated by a dynamic, transient cellular memory, not solely stochastic events.
  • Fluctuation-based assays can reveal hidden cellular states, aiding the design of novel HIV-1 eradication therapies.