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Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates.

ABSTRACT: We previously described isolation of a potentially new mammalian reovirus, designated BYD1, which can cause clinical symptoms similar to that of severe acute respiratory syndrome (SARS) in guinea pigs and macaques, from throat swabs of one SARS patient of Beijing, in 2003. For this study, we determined the genome sequences of BYD1 and the S1 gene sequences of other five mammalian reovirus isolates (BLD, JP, and BYL were isolated from different SARS patients during the outbreak, 302I and 302II were isolated from fecal specimens of two children of Beijing in 1982) to allow molecular comparison with other previously reported mammalian reoviruses (MRVs). Comparative analyses of the BYD1 genome with those of three prototype mammalian reovirus strains demonstrated that BYD1 is a novel reassortant virus, with its S1 gene segment coming from a previously unidentified serotype 2 isolate and other nine segments coming from ancestors of homologous T1L and T3D segments, which supports the hypothesis that mammalian reovirus gene segments reassort in nature. Further analyses of the S1 segments of the six isolates showed that all the isolates are novel serotype 2 MRVs based on their S1 gene sequences, which are markedly different from those of all previously reported, and the S1 genes of the four new isolates share more than 99% identity with each other, proving that they diverged from a common ancestor most recently, and the S1 genes of the four new isolates share about 65% identity with those of the two strains isolated in 1982.

SUBMITTER: Song L

PROVIDER: S-EPMC7088624 | biostudies-literature | 2008 Dec

REPOSITORIES: biostudies-literature

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Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates.

Song Lihua L Zhou Yusen Y He Jun J Zhu Hong H Huang Rutong R Mao Panyong P Duan Qing Q

Virus genes 20080923 3

We previously described isolation of a potentially new mammalian reovirus, designated BYD1, which can cause clinical symptoms similar to that of severe acute respiratory syndrome (SARS) in guinea pigs and macaques, from throat swabs of one SARS patient of Beijing, in 2003. For this study, we determined the genome sequences of BYD1 and the S1 gene sequences of other five mammalian reovirus isolates (BLD, JP, and BYL were isolated from different SARS patients during the outbreak, 302I and 302II we ...[more]

PMID: 18810628

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Project description:UnlabelledReceptors expressed on the host cell surface adhere viruses to target cells and serve as determinants of viral tropism. Several viruses bind cell surface glycans to facilitate entry, but the contribution of specific glycan moieties to viral disease is incompletely understood. Reovirus provides a tractable experimental model for studies of viral neuropathogenesis. In newborn mice, serotype 1 (T1) reovirus causes hydrocephalus, whereas serotype 3 (T3) reovirus causes encephalitis. T1 and T3 reoviruses engage distinct glycans, suggesting that glycan-binding capacity contributes to these differences in pathogenesis. Using structure-guided mutagenesis, we engineered a mutant T1 reovirus incapable of binding the T1 reovirus-specific glycan receptor, GM2. The mutant virus induced substantially less hydrocephalus than wild-type virus, an effect phenocopied by wild-type virus infection of GM2-deficient mice. In comparison to wild-type virus, yields of mutant virus were diminished in cultured ependymal cells, the cell type that lines the brain ventricles. These findings suggest that GM2 engagement targets reovirus to ependymal cells in mice and illuminate the function of glycan engagement in reovirus serotype-dependent disease.ImportanceReceptor utilization strongly influences viral disease, often dictating host range and target cell selection. Different reovirus serotypes bind to different glycans, but a precise function for these molecules in pathogenesis is unknown. We used type 1 (T1) reovirus deficient in binding the GM2 glycan and mice lacking GM2 to pinpoint a role for glycan engagement in hydrocephalus caused by T1 reovirus. This work indicates that engagement of a specific glycan can lead to infection of specific cells in the host and consequent disease at that site. Since reovirus is being developed as a vaccine vector and oncolytic agent, understanding reovirus-glycan interactions may allow manipulation of reovirus glycan-binding properties for therapeutic applications.

Dataset Information

Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates.

Publications

Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates.

Similar Datasets

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