The cellular basis for viral-induced immunodeficiency: analysis by monoclonal antibodies.

TLDR

Viral infections are often linked to immunodeficiency, yet the precise role of T lymphocytes in this suppression remains unclear. The study characterized T lymphocytes from six infectious mononucleosis patients during acute and convalescent phases using monoclonal antibodies against T4, T5, T3, and Ia antigens. Acute infectious mononucleosis is marked by activation and expansion of suppressor T cells (T5+, Ia+), which inhibit autologous T cell proliferation and B cell antibody production, while convalescence restores normal T cell subsets and immune function, demonstrating that viral infection can selectively activate a T cell subset and suppress overall immunity.

Abstract

Abstract Viral infections are often associated with immunodeficiency states. Although T lymphocytes have been thought to suppress the host's response, the precise etiology remains unclear. Therefore, we characterized T lymphocytes from six patients during both acute and convalescent phases of infectious mononucleosis (IM) with monoclonal antibodies (titer, 10(-5) to 10(-7) to antigens restricted to the TH2- helper (T4) and TH2 suppressor (T5) T cell subsets as well as to a common T cell antigen (T3) and HLA-D related Ia antigens. It was found that during acute infectious mononucleosis, there is both activation and increase of suppressor T cells (T5+, Ia+ phenotype). Fuctionally, the acute IM lymphocytes suppress autologous T cell proliferation to antigens as well as pokeweed mitogen driven B cell immunoglobulin production. In contrast, convalescence is associated with a return to normal of T cell subsets and immune function. These results demonstrate that viral infections can preferentially activate a specific T cell subset and suppress the overall human immune response.