ABSTRACT
A sine qua non of persistent virus infection is survival of both host and virus, i.e., normally "susceptible" host cells in the presence of "lethal" virus. Defective interfering (DI) virus particles have been postulated to play a key role in persistent infection of cells by vesicular stomatitis virus and rabies virus — model systems for studying this phenomenon. There are numerous observations which show that persistent infection of cells by normally cytopathic virus is accompanied by a shift from a "wild-type" to a "temperature-sensitive" phenotype. Host-range mutants of vesicular stomatitis virus (VSV) have been described but, as yet, not implicated in persistent infections. No integrated genetically stable relationship between virus and cell has been reported for persistent infections with rhabdoviruses. In addition to sparing cells from the lethal action of the carrier virus, interferon action on rhabdoviruses may also serve to maintain levels of infectious and DI particles compatible with continued survival of both cell and virus.
