Limitation of VSV infection by the host's response to VSV-associated cellular antigens.
It has been reported that during the maturation of enveloped viruses, host proteins such as H-2 antigens of the mouse associate with the budding viruses. This finding led us to investigate the possible biologic significance of this association. In our studies, we examined, with purified vesicular stomatitis virus (VSV) from various sources, the in vivo infection of mice immunized with allogeneic tumors. Immunization of H-2k mice with an H-2d tumor caused the limitation of replication, within the spleen, of VSV derived from an H-2d cell line compared with the replication of VSV derived from an H-2k line. Conversely, immunization of H-2d mice with an H-2k tumor caused the limitation of replication of VSV derived from an H-2k cell line. Viral mixture experiments ruled out indirect inactivation or inhibition of virus replication by nonspecific factors, such as immune interferon, as having a major role in the observed limitation of VSV replication. We conclude that virus infections can be limited by an immune response directed against the specific host surface antigen that the virus carries in its envelope.
D000818:Animals; D000954:Antigens, Surface / Q000276:immunology*; D002478:Cells, Cultured; D000939:Epitopes; D006183:H-2 Antigens / Q000276:immunology; D007114:Immunization; D051379:Mice; D009374:Neoplasms, Experimental / Q000276:immunology; D013154:Spleen / Q000382:microbiology; D014721:Vesicular stomatitis Indiana virus / Q000276:immunology*; D014777:Virus Diseases / Q000276:immunology*; D014779:Virus Replication
D000954:Antigens, Surface; D000939:Epitopes; D006183:H-2 Antigens