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Biphasic rate of CD4+ cell count decline during progression to AIDS correlates with HIV-1 phenotype

P T Schellekens1, M Tersmette, M T Roos

  • 1Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam.

Insights

In HIV-1-infected men, CD4+ lymphocyte decline accelerates significantly about 18 months before AIDS diagnosis. This rapid decline correlates with a more virulent, fast-replicating HIV-1 phenotype.

Area of Science:

  • Immunology
  • Virology
  • Epidemiology

Background:

  • Human Immunodeficiency Virus type 1 (HIV-1) infection leads to a progressive decline in CD4+ lymphocytes, a hallmark of disease progression.
  • Understanding the kinetics of CD4+ cell loss is crucial for predicting disease progression and therapeutic timing.

Purpose of the Study:

  • To investigate the rate of CD4+ lymphocyte decline in asymptomatic HIV-1-infected homosexual men.
  • To correlate the kinetics of CD4+ cell decline with HIV-1 biological phenotype and progression to Acquired Immunodeficiency Syndrome (AIDS).

Main Methods:

  • A cohort of 187 initially asymptomatic homosexual men infected with HIV-1 were monitored every 3 months for 5 years.
  • CD4+ lymphocyte counts were enumerated, and progression to AIDS (excluding Kaposi's sarcoma) was recorded.
  • The rate of CD4+ cell decline was analyzed in relation to HIV-1 biological phenotype in 43 participants.

Main Results:

  • CD4+ lymphocyte counts showed a slow, continuous decline in asymptomatic HIV-1-infected individuals.
  • A biphasic decline was observed in men who progressed to AIDS, with a significant threefold to fivefold acceleration starting approximately 18 months before diagnosis.
  • Rapid CD4+ cell decline was associated with syncytium-inducing, fast-replicating HIV-1 isolates, while non-syncytium-inducing isolates predominated during slower decline phases.

Conclusions:

  • A significant increase in the rate of CD4+ lymphocyte loss occurs around 18 months prior to AIDS diagnosis.
  • This accelerated decline may be linked to the emergence of a more virulent HIV-1 phenotype, characterized by fast replication and syncytium induction.
Abstract

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