Low CD4 counts rather than superantigenic-like effects account for differences in expressed T-cell receptor (TCR) repertoires between HIV-1 seropositive long-term non-progressors and individuals with progressive disease

Br J Haematol. 1998 Sep;102(5):1187-96. doi: 10.1046/j.1365-2141.1998.00912.x.

Abstract

Analysis of HIV-infected individuals who have stable CD4 counts many years after seroconversion may provide an insight as to how the host's immune system can successfully control HIV infection. In this study we analysed the T-cell receptor (TCR) Vbeta repertoire in 13 HIV+ individuals, seven of whom were classed as long-term non-progressors (LTNP), using a technique which couples anchor PCR (AnPCR) amplification of beta-chain cDNA to differential probe hybridization with non-radioactively labelled Vbeta family specific oligonucleotide probes. There were no significant differences in the expressed TCR repertoires between the LTNP group and the other HIV-infected individuals. However, there was a statistically significant inverse correlation between CD4 count and the number of Vbeta family-specific perturbations in the recent seroconverters (SC) and those with progressive infection (PI), consistent with other shared features of clinical disease progression (Th1/Th2 switch and high frequency of viral isolation). We conclude that long-term clinical non-progression in HIV-1 infection is not associated with the loss or expansion of a particular Vbeta family; instead, low CD4 count in the PI and SC individuals was correlated with increased number of Vbeta family-specific perturbations relative to the LTNP group and that it is hence unlikely that HIV encodes a superantigen.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • CD4 Lymphocyte Count
  • Cytokines / biosynthesis
  • Disease Progression
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • HIV Infections / immunology*
  • Humans
  • Male
  • Polymerase Chain Reaction / methods
  • Pregnancy
  • Receptors, Antigen, T-Cell / immunology*
  • Superantigens / immunology*

Substances

  • Cytokines
  • Receptors, Antigen, T-Cell
  • Superantigens