The role of antibodies in natural and acquired resistance of mice to vesicular stomatitis virus.

Abstract

Mice infected with live vesicular stomatitis virus (VSV) produced primary antibody responses more efficiently (with doses greater than 10(2) pfu) than those injected with UV-inactivated VSV (greater than 10(6) pfu) or purified VSV glycoprotein G (equivalent to 10(7) pfu) by producing neutralizing antibodies. Very low doses of live VSV (less than 10(2) pfu) failed to prime mice. Normal mouse serum had the capacity to inactivate VSV by heat-labile and immunoglobulin-mediated mechanisms in vitro independently of specifically induced antibodies. Studies using B cell-depleted agammaglobulinaemic mice showed that their serum lacked VSV-neutralizing capacity in vitro and that naturally resistant mice became susceptible to VSV-induced paralytic disease which could be prevented by adoptive transfer of immune but also of normal serum.