Abstract

Summary After recovery of mice from encephalomyocarditis virus (EMC) infection of the nervous system, little or no antibody could be detected in brain extracts. Intracerebral injection of antibody, in excess of the amount produced after recovery, failed to protect mice if the infection was already established in the nervous system. In contrast a passively induced elevated temperature protected mice even at a time when virus had reached greatest titer in the brain. This finding that elevated temperature is protective later in the course of EMC infection of mouse brain than is antibody is interpreted to favor the concept that nonimmune antiviral factors are more likely to account for recovery from established viral infection than is antibody.

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