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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...

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Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
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Rapid CD4+ cell decrease after transient cART initiated during primary HIV infection (ANRS PRIMO and SEROCO cohorts).

Remonie Seng1, Cécile Goujard, Loïc Desquilbet

  • 1INSERM U822, Le Kremlin-Bicêtre, France.

Journal of Acquired Immune Deficiency Syndromes (1999)
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A limited course of combination antiretroviral therapy (cART) initiated during primary HIV infection (PHI) may not benefit patients long-term, as CD4 cell counts declined similarly to untreated individuals after treatment cessation.

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Area of Science:

  • Immunology
  • Virology
  • Clinical Medicine

Background:

  • Primary HIV infection (PHI) is a critical window for intervention.
  • Combination antiretroviral therapy (cART) aims to control HIV replication and preserve immune function.
  • Understanding the long-term impact of cART initiated during PHI is crucial for treatment guidelines.

Purpose of the Study:

  • To model CD4 cell count decline after stopping cART in patients who started treatment during PHI.
  • To identify factors influencing CD4 cell count kinetics post-cART cessation.
  • To compare CD4 cell count trajectories between treated and never-treated HIV cohorts.

Main Methods:

  • Mixed-effects modeling was used to analyze CD4 count kinetics on the square root scale.
  • Data from 170 patients in the PRIMO cohort (cART during PHI) and 123 in the SEROCO cohort (never-treated) were analyzed.
  • CD4 cell counts were tracked over time after cART interruption or infection diagnosis.

Main Results:

  • After cART interruption in the PHI cohort, CD4 counts rapidly declined initially, then slowed.
  • Higher CD4 count increases during cART predicted steeper declines post-cessation.
  • Three years after cART interruption, mean CD4 loss was 383 cells/microL, compared to 239 cells/microL in never-treated individuals.

Conclusions:

  • Limited courses of cART initiated within 3 months of PHI diagnosis may offer no significant long-term advantage in CD4 cell count preservation.
  • These findings challenge the established benefit of early, short-term cART initiation in PHI.
  • Further research is needed to optimize HIV treatment strategies during primary infection.