Predominance of MHC class II-restricted CD4+ cytotoxic T cells against mouse hepatitis virus A59.

Coronavirus-induced acute hepatitis is a complex event and the role of different components of the immune system with regard to defined viral proteins and the course of the infection is not yet clear. We have analysed the cytotoxic T-lymphocyte (CTL) response in mouse hepatitis virus (MHV-A59) infection. Surprisingly, we detected only a very clear virus-specific major histocompatibility complex (MHC) class II-restricted cytotoxicity in mice infected with MHV-A59.

Activation of virus-specific major histocompatibility complex class II-restricted CD8+ cytotoxic T cells in CD4-deficient mice.

Acute enteritic or respiratory disease is a consequence of coronavirus infection in man and rodents. Mouse hepatitis virus, stain A59 (MHV-A59) causes acute hepatitis in mice and rats and induces a response of major histocompatibility complex (MHC) class II-restricted CD4+ cytotoxic T cells, protecting mice against acute infection. In the present study we show that MHV-A59 infection of mice that lack a functional CD4 gene activates effector cells of the CD8+ phenotype.

Treatment with monoclonal anti-CD3 antibody protects against lethal Sendai virus infection by induction of natural killer cells.

C57BL/6 mice are protected from a lethal pneumonia caused by Sendai virus when treated with low doses of mAb directed to the CD3 Ag. The protective mechanism is not due to an accelerated Sendai virus-specific Th cell, CTL, or antibody response but to a strong NK cell response via the in vivo induction of lymphokines. Antibodies directed against the NK1.