Polyclonality of the cytotoxic T lymphocyte response to virus infection.

Abstract

For many years, it has been known that certain viral infections induce a polyclonal B cell activation that can lead to the generation of antibody against self-antigens and nonviral foreign antigens (1–8). More recently, it has been shown that viruses can also be potent polyclonal cytotoxic T lymphocyte (CTL) inducers, spontaneously stimulating the generation of high levels of allospecific CTL (9, 10) and reactivating memory CTL specific for unrelated viruses from previous infections (11). Virus-induced stimulation of self-reactive or “autoimmune” CTL has also been reported in some systems (12–14). Stimulation of allospecific CTL has been observed in humans during episodes of acute infectious mononucleosis (Epstein-Barr virus [EBV] infection) (10, 15, 16) and in the mouse during acute infections with lymphocytic choriomeningitis virus (LCMV), vaccinia virus (VV), Pichinde virus, and murine cytomegalovirus (11). One might expect that acute viral infections would, therefore, be detrimental to allograft survi...