Abstract
The encephalitogenic potential of nine temperature-sensitive mutants of measles virus was determined in newborn golden Syrian hamsters. The parental virus produced acute encephalitis without any prior adaptation. Six of the mutants were attenuated, two were virulent, and one was associated with hydrocephalus with acute onset. The attenuated mutants, blocked before measles virus antigen and ribonucleic acid synthesis at 39 C, were all members of one complementation group. The virulent temperature-sensitive mutants, defective in hemolysin antigen synthesis at 39 C, were members of a second complementation group. The hydrocephalus-inducing mutant was genetically distinct from the other mutants. The mechanism of attenuation most probably does not involve a temperature-induced inhibition of virus replication, but rather appears to be related to the partial defectiveness of the mutants under permissive conditions.
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