Residual low-level viral replication could explain discrepancies between viral load and CD4+ cell response in human immunodeficiency virus-infected patients receiving antiretroviral therapy

Clin Infect Dis. 2000 Feb;30(2):392-4. doi: 10.1086/313660.

Abstract

We report the evolution of chronic infection with human immunodeficiency virus type 1 (HIV-1) in a patient treated with stavudine plus didanosine, whose CD4+ lymphocyte count progressively decreased, despite a sustained plasma viral load <20 copies/mL. After 12 months of therapy, treatment was switched to zidovudine plus lamivudine plus nelfinavir. CD4+ T cell count decreased from 559 x 10(6)/L at month 0 to 259 x 10(6)/L at month 12. Plasma viral load decreased from 21,665 HIV-1 RNA copies/mL at baseline (month 0) to <20 copies/mL after 1 month of therapy with stavudine plus didanosine, and remained below 20 copies/mL until month 12, but always >5 copies/mL. Viral load in tonsilar tissue at month 12 was 125,000 copies/mg of tissue. After the change to triple-drug therapy, the plasma viral load decreased to 5 copies/mL, the CD4+ T cell count increased to 705 x 10(6)/L, and the viral load in tonsilar tissue decreased to <40 copies/mg of tissue at month 24. A low level of HIV-1 replication could explain the lack of immunologic response in patients with apparent virological response.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoids / pathology
  • Adenoids / virology*
  • Anti-HIV Agents / administration & dosage*
  • Biopsy, Needle
  • CD4 Lymphocyte Count / drug effects
  • CD4-CD8 Ratio / drug effects
  • CD4-Positive T-Lymphocytes / drug effects*
  • Drug Therapy, Combination
  • Flow Cytometry
  • Follow-Up Studies
  • HIV Infections / diagnosis
  • HIV Infections / drug therapy*
  • HIV Infections / immunology
  • HIV Infections / virology*
  • HIV-1 / drug effects*
  • HIV-1 / pathogenicity
  • Humans
  • Monitoring, Physiologic
  • T-Lymphocyte Subsets / drug effects*
  • Treatment Outcome
  • Viral Load*

Substances

  • Anti-HIV Agents