IgG subclass distribution of primary and secondary immune responses concomitant with viral infection

Abstract

Infection with mouse hepatitis virus was found to selectively increase the proportion of IgG2a in antibodies elicited by a concomitant administration of unrelated T cell-dependent protein Ag. In contrast, T cell-independent responses were only marginally affected. This isotypic bias, which occurred when the virus was inoculated shortly before or after a primary immunization, persisted in subsequent secondary responses. However, infection concomitant to secondary antibody responses did not affect their isotypic distribution. These observations suggest that the virus can durably modify unrelated T cell responses that are initiated at the time of infection, which could have implications in the pathogenesis of autoimmune reactions.