CD8+ T cells specific for EBV, cytomegalovirus, and influenza virus are activated during primary HIV infection

J Immunol. 2004 Aug 15;173(4):2410-8. doi: 10.4049/jimmunol.173.4.2410.

Abstract

Primary viral infections, including primary HIV infection, trigger intense activation of the immune system, with marked expansion of CD38(+)CD8(+) T cells. Whether this expansion involves only viral-specific cells or includes a degree of bystander activation remains a matter of debate. We therefore examined the activation status of EBV-, CMV-, and influenza virus (FLU)-specific CD8(+) T cells during primary HIV infection, in comparison to HIV-specific CD8(+) T cells. The activation markers CD38 and HLA-DR were strongly expressed on HIV-specific CD8(+) T cells. Surprisingly, CD38 expression was also up-regulated on CD8(+) T cells specific for other viruses, albeit to a lesser extent. Activation marker expression returned to normal or near-normal values after 1 year of highly active antiretroviral therapy. HIV viral load correlated with CD38 expression on HIV-specific CD8(+) T cells but also on EBV-, CMV-, and FLU-specific CD8(+) T cells. In primary HIV infection, EBV-specific CD8(+) T cells also showed increased Ki67 expression and decreased Bcl-2 expression, compared with values observed in HIV-seronegative control subjects. These results show that bystander activation occurs during primary HIV infection, even though HIV-specific CD8(+) T cells express the highest level of activation. The role of this bystander activation in lymphocyte homeostasis and HIV pathogenesis remains to be determined.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADP-ribosyl Cyclase / biosynthesis
  • ADP-ribosyl Cyclase / immunology
  • ADP-ribosyl Cyclase 1
  • Adult
  • Animals
  • Antigens, CD / biosynthesis
  • Antigens, CD / immunology
  • Antigens, Differentiation / biosynthesis
  • Antigens, Differentiation / immunology
  • Antiretroviral Therapy, Highly Active
  • CD8-Positive T-Lymphocytes / immunology*
  • Cytomegalovirus / immunology*
  • Female
  • HIV / immunology
  • HIV Infections / drug therapy
  • HIV Infections / immunology*
  • HLA-DR Antigens / biosynthesis
  • HLA-DR Antigens / immunology
  • Herpesvirus 4, Human / immunology*
  • Humans
  • Ki-67 Antigen / biosynthesis
  • Ki-67 Antigen / immunology
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology
  • Male
  • Membrane Glycoproteins
  • Orthomyxoviridae / immunology*
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / immunology
  • Viral Load

Substances

  • Antigens, CD
  • Antigens, Differentiation
  • HLA-DR Antigens
  • Ki-67 Antigen
  • Membrane Glycoproteins
  • Proto-Oncogene Proteins c-bcl-2
  • ADP-ribosyl Cyclase
  • CD38 protein, human
  • ADP-ribosyl Cyclase 1