CHARACTERIZATION OF 2 AVIAN REOVIRUSES THAT EXHIBIT STRAIN-SPECIFIC QUANTITATIVE DIFFERENCES IN THEIR SYNCYTIUM-INDUCING AND PATHOGENIC CAPABILITIES

Citation
R. Duncan et K. Sullivan, CHARACTERIZATION OF 2 AVIAN REOVIRUSES THAT EXHIBIT STRAIN-SPECIFIC QUANTITATIVE DIFFERENCES IN THEIR SYNCYTIUM-INDUCING AND PATHOGENIC CAPABILITIES, Virology (New York, N.Y. Print), 250(2), 1998, pp. 263-272
Citations number
51
Categorie Soggetti
Virology
ISSN journal
00426822
Volume
250
Issue
2
Year of publication
1998
Pages
263 - 272
Database
ISI
SICI code
0042-6822(1998)250:2<263:CO2ART>2.0.ZU;2-T
Abstract
We previously proposed that the conservation of the nonessential syncy tium-inducing phenotype among all reported avian reovirus (ARV) isolat es may reflect a mechanism for enhanced virus dissemination in vivo, w hich in turn could contribute to the natural pathogenicity of ARV. Dir ect testing of this hypothesis has been hampered by the lack of availa ble virus strains with defined differences in their fusion-inducing ca pability. We now report on the characterization of two ARV strains, AR V-176 and ARV-138, that exhibited strain-specific differences in their fusogenic properties, which correlated with their pathogenic potentia l in embryonated eggs. Moreover, both virus strains possessed similar replicative abilities in cell culture, suggesting that the weakly fuso genic ARV-138 virus is specifically inhibited in its syncytium-inducin g ability. To test the use of these viruses for reassortant studies ai med at assessing the role of cell fusion in viral pathogenesis, a prel iminary genetic analysis was undertaken using a monoreassortant that c ontained nine genome segments from the parental ARV-138 virus and the S1 genome segment from the highly fusogenic and pathogenic ARV-176 par ental virus. The monoreassortant possessed the full fusogenic potentia l of the ARV-176 parental virus and displayed enhanced embryo pathogen icity, providing the first genetic evidence implicating the ARV S1 gen ome segment in both syncytium formation and viral pathogenesis. (C) 19 98 Academic Press