Mice infected with live vesicular stomatitis virus (VSV) produced primary antibody responses more efficiently (with doses > 102 pfu) than those injected with UV-inactivated VSV ( > 106 pfu) or purified VSV glycoprotein G (equivalent to 107 pfu) by producing neutralizing antibodies. Very low doses of live VSV ( < 102 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 agammaglobulineamic 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.

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