Differential growth of MHV(PRI) and MHV(C3H) in genetically resistant C3H mice rendered susceptible by eperythrozoon infection

Summary Mice of the C₃H strain, which are genetically resistant to mouse hepatitis virus, MHV(PRI), became highly susceptible to that virus when preinfected with the murine blood parasite,Eperythrozoon coccoides (E. coccoides). Peak virus titers and deaths occurred 2 or more days later inE. coccoides-infected C₃H mice than those events in genetically susceptible Princeton (PRI) mice. Growth curves and infectivity analyses of progeny virus in cultures of susceptible PRI and resistant C₃H cells demonstrated that MHV(PRI) itself multiplied to high titer inE. coccoides- infected C₃H mice. Variant virus, MHV(C₃H), was also produced, but appeared later in the infection and comprised only a small fraction of the progeny virus. On subsequent passage of progeny virus inE. coccoides-infected C₃H mice, MHV(PRI) continued to be produced far in excess of MHV(C₃H). In normal (E. coccoides-free) C₃H mice, progeny virus caused deaths or lesions indicative of the presence of variant virus, and the latter was recovered at a high titer. The action ofE. coccoides, whereby MHV(PRI) multiplication is initiated in genetically resistant (nonpermissive) C₃H cells, could not be reproducedin vitro.