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G Lanman

Publications and source records attributed to G Lanman.

4 recordsLinked to original sources

Characterization of virulent isolates of vesicular stomatitis virus in relation to interference by defective particles.

To investigate the role that defective interfering (DI) particles might conceivably play in the epizootiology of vesicular stomatitis, two virulent New Jersey (NJ) isolates from the 1982-1983 epizootic in the United States (US) were compared with three laboratory adapted strains of vesicular stomatitis virus (VSV): NJ Hazelhurst, NJ Ogden and Indiana San Juan. Successive undiluted passages showed that the virulent isolates did not readily exhibit 'autointerference' because they did not readily generate and amplify DI particles. Viral RNA synthesis of isolates that were exposed to homotypic or heterotypic DI particles generated from the laboratory strains showed that the isolates were totally resistant to the heterotypic DI particle and partially resistant to the homotypic DI particle. In contrast, Indiana San Juan and NJ Ogden were inhibited by hetero- or homotypic DI particles. NJ Hazelhurst more closely resembled the isolates. This demonstrates that virulence of VSV in its natural setting may be related to a number of factors, including the slower generation and amplification of endogenous DI particles, as well as the increased resistance of the virus to some pre-existing DI particles.

Defective Viruses↗

Immunoprecipitating human antigens associated with vesicular stomatitis virus grown in HeLa cells.

Vesicular stomatitis virus (VSV) preparations made in HeLa cells, VSV(HeLa), appeared to contain non-viral structural proteins. This was suggested by neutralization of the virus with homologous and heterologous antisera made against VSV prepared in different cells. Antisera against uninfected HeLa cells failed to neutralize VSV(HeLa) but did immunoprecipitate the virus in the presence of Staphylococcus aureus. These immunoprecipitated VSV(HeLa) retained their infectivity, despite the presence of antibody and bacteria. The anti-HeLa cell serum did not react with VSV grown in rodent cells nor did anti-Vero cells serum immunoprecipitate VSV(HeLa). When the anti-HeLa cell serum was absorbed with whole HeLa cells, it no longer specifically precipitated VSV(HeLa). Because over 98% of infectious VSV(HeLa) was neutralizable by anti-VSV serum and immunoprecipitable by anti-HeLa serum, these virions were called mosaics. Physical identification of HeLa cell determinants on the mosaics was accomplished by further purification and radioiodination followed by selective immunoprecipitations with antisera. Two to three major bands with molecular weights around 75,000 Da were identified as HeLa cell determinants associated with the mosaic VSV(HeLa).

Animals↗