Cellular response to rabies virus infection.
The effects of rabies virus on host cells were studied and compared to those obtained with another rhabdovirus, vesicular stomatitis virus [J. Virol. 34, 777-781 (1980)]. We show here: (1) that rabies infection has no effect on cell morphology, while infection with vesicular stomatitis virus caused cell retraction. Thus, only vesicular stomatitis virus induced a depolymerization of the microfilaments; and (2) that microtubules and microfilaments do not play a major role in rabies virus production, as it is suggested by results obtained with several effectors (colcemid, colchicine and cytochalasin-B) which directly or indirectly affect cytoskeleton organization. The same properties were observed with directly or indirectly affect cytoskeleton organization. The same properties were observed with vesicular stomatitis virus. Furthermore, the use of cytochalasin-B shows that an inhibition of glycosylation of the virion spike protein occurs only in rabies infected cells. As vesicular stomatitis viral glycosylation is normal in cytochalasin-B treated cells, results obtained indicate that two types of interactions can occur between a virion and the host-cell depending on the rhabdovirus type.
D000818:Animals; D002460:Cell Line; D002472:Cell Transformation, Viral / Q000187:drug effects; D002642:Chick Embryo; D003078:Colchicine / Q000494:pharmacology; D006224:Cricetinae; D003571:Cytochalasin B / Q000494:pharmacology; D015638:Cytochalasin D; D003572:Cytochalasins / Q000494:pharmacology; D003703:Demecolcine / Q000494:pharmacology; D007668:Kidney; D007700:Kinetics; D011820:Rabies virus / Q000235:genetics*; D014721:Vesicular stomatitis Indiana virus / Q000235:genetics*; D014764:Viral Proteins / Q000235:genetics*; D014771:Virion / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects
D003572:Cytochalasins; D014764:Viral Proteins; D015638:Cytochalasin D; D003571:Cytochalasin B; D003078:Colchicine; D003703:Demecolcine