Analysis of CD8+ T lymphocyte-mediated nonlytic suppression of autologous and heterologous primary human immunodeficiency virus type 1 isolates

AIDS Res Hum Retroviruses. 1997 May 20;13(8):685-93. doi: 10.1089/aid.1997.13.685.

Abstract

Nonlytic CD8+ T lymphocyte antiviral factor (CAF) activity has been described as having an important role in the clinical course of human immunodeficiency virus type 1 (HIV-1) infection. Testing of CAF activity against autologous viruses isolated at approximately the same time points showed that CD8+ T lymphocytes from long-term survivors indeed possessed high CAF activity. However, in four of six progressors to AIDS, we observed the same amount of CAF activity in the face of increasing cellular HIV-1 load. In the other two progressors, CAF activity seemed preserved over time whereas the susceptibility of the virus isolate obtained late in infection seemed to be diminished. In a heterologous system, CAF activity of CD8+ T lymphocytes from 13 HIV-1-positive individuals did not correlate with CD4+ T lymphocyte counts. In two of three patients, syncytium-inducing (SI) HIV-1 variants, which are associated with a progressive clinical course, appeared to have a somewhat reduced susceptibility to CAF activity as compared to their coexisting non-SI HIV-1 variants. In a large donor group, suppression of SI isolates (as compared to non-SI isolates) mediated by heterologous CD8+ T lymphocytes was reduced. CD8+ T lymphocytes from five of six HIV-1-positive individuals suppressed HIV-1 replication in macrophages. CD8+ T lymphocytes from noninfected donors, even from cord blood, already had high CAF activity, suggesting that induction of this activity is neither virus nor HIV-1 specific.

MeSH terms

  • Anti-HIV Agents / metabolism
  • CD8-Positive T-Lymphocytes / metabolism
  • CD8-Positive T-Lymphocytes / virology*
  • Disease Progression
  • HIV Infections / blood
  • HIV-1 / growth & development
  • HIV-1 / metabolism*
  • Humans
  • Leukocytes, Mononuclear / virology
  • Macrophages / metabolism
  • Macrophages / virology
  • Male
  • Virus Replication / physiology*

Substances

  • Anti-HIV Agents