Genetic reassortment among viruses causing hantavirus pulmonary syndrome.

Autor: Rodriguez LL; Special Pathogens Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA., Owens JH, Peters CJ, Nichol ST
Jazyk: angličtina
Zdroj: Virology [Virology] 1998 Mar 01; Vol. 242 (1), pp. 99-106.
DOI: 10.1006/viro.1997.8990
Abstrakt: In order to determine the frequency and characteristics of reassortment among viruses causing hantavirus pulmonary syndrome (HPS), mixed infections were initiated in tissue culture by using two closely related strains of Sin Nombre virus, CC107 (from eastern California) and NMR11 (from New Mexico), which share the same species of rodent host in nature, the deer mouse (Peromyscus maniculatus). Potential reassortant virus plaques were screened by multiplex RT-PCR, using primers specific for individual genome segments of each strain. Reassortant viruses involving the M and S segments and, to a lesser extent, the L segment were detected in 8.5% of 294 progeny plaques tested. In addition, approximately 30% of the progeny virus plaques appeared to contain S or M segments originating from both parental virus strains, i.e., they were diploid. Most of these diploid virus genotypes were not stable, becoming either reassortant or parental virus strains upon plaque-to-plaque virus passage. In contrast to the results above, only one virus reassortant and four diploids were observed among 163 progeny virus plaques from mixed infections between Sin Nombre virus NMR11 and the genetically more distant Black Creek Canal virus, an HPS-causing virus from Florida, which has the cotton rat (Sigmodon hispidus) as its natural host.
Databáze: MEDLINE