Abstract
Measles virus, upon infection, caused cytopathic effects in BHK-21 cells while it readily established persistent infection in a mutant strain of BHK-21 cells which possessed a temperature sensitive defect in DNA synthesis (BN2). This finding demonstrated that host function can be involved in allowing the establishment of persistent infection. When BN2 and infected BN2 cells were incubated at the non-permissive temperature (39.5° C), DNA synthesis was inhibited in a similar manner in both cells types, suggesting that viral functions do not interfere with the expression of the host mutation. Thets mutation which blocked the DNA synthesis also caused inhibition of viral yield, viral antigen expression and viral RNA synthesis at 39.5° C. The results suggest that continued DNA synthesis is necessary for the expression of measles functions.