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HIV dynamics linked to memory CD4+ T cell homeostasis.

John M Murray1, John Zaunders2, Sean Emery3

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HIV dynamics and viral load are influenced by memory CD4+ T cell homeostasis. Mathematical modeling explains HIV DNA and plasma viral level changes during antiretroviral therapy (ART).

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Area of Science:

  • Immunology
  • Virology
  • Mathematical Biology

Background:

  • Latent HIV infection involves resting and activated memory CD4+ T cells.
  • Antiretroviral therapy (ART) impacts HIV dynamics but residual viremia persists.
  • HIV's effect on CD4+ T cell homeostasis is a key factor in viral persistence.

Purpose of the Study:

  • To investigate if HIV's impact on memory CD4+ T cell homeostasis explains plasma viral level (pVL) and HIV DNA dynamics.
  • To model the multiphasic dynamics of pVL and HIV DNA during long-term ART.

Main Methods:

  • Mathematical modeling of HIV DNA and pVL dynamics.
  • Analysis of HIV DNA (total, 2-LTR, integrated) and pVL in primary (PHI) and chronic (CHI) HIV-infected individuals on ART.
  • Simulation of ART intensification.

Main Results:

  • Mathematical model accurately reproduced multiphasic dynamics of pVL and HIV DNA over 3 years of ART.
  • Residual viremia originated from reactivated latently infected cells, primarily from clonal expansion in resting cells.
  • HIV DNA decay rates correlated with memory CD4+ T cell turnover rates (activated vs. resting).

Conclusions:

  • HIV's impact on memory CD4+ T cell homeostasis largely explains observed viral dynamics under ART.
  • Clonal expansion of latently infected cells contributes to persistent viremia, unaffected by ART.
  • Modeling suggests ongoing low-level infection may contribute to early HIV DNA dynamics.