| First Author | Song L | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 3 | Pages | e92678 |
| PubMed ID | 24664247 | Mgi Jnum | J:291636 |
| Mgi Id | MGI:6245682 | Doi | 10.1371/journal.pone.0092678 |
| Citation | Song L, et al. (2014) Multi-organ lesions in suckling mice infected with SARS-associated mammalian reovirus linked with apoptosis induced by viral proteins mu1 and sigma1. PLoS One 9(3):e92678 |
| abstractText | We reported the isolation and characterization of a novel mammalian reassortant reovirus BYD1 that may have played an accomplice role with SARS-coronavirus during the 2003 SARS pandemic. The pathogenic mechanism of this novel reovirus is unknown. Reovirus pathogenicity has been associated with virus-induced apoptosis in cultured cells and in vivo. The reovirus outer capsid protein mu1 is recognized as the primary determinant of reovirus-induced apoptosis. Here, we investigated the apoptosis induced by BYD1, its outer capsid protein mu1, and its cell-attachment protein sigma1 to understand the pathogenesis of BYD1. We also investigated BYD1 caused systemic complications in suckling mice. Under electron microscopy, BYD1-infected cells showed characteristics typical of apoptosis. Notably, ectopically expressed mu1 and sigma1 induced similar pathological apoptosis, independent of BYD1 infection, in host cells in which they were expressed, which suggests that mu1 and sigma1 are both apoptotic virulence factors. Consistent with previous reports of reovirus pathogenicity, suckling mice intracranially inoculated with BYD1 developed central nerve damage, myocarditis, and pneumonia. Collectively, our data suggest that BYD1 mu1- and sigma1-induced apoptosis is involved in the multi-organ lesions in a suckling mouse BYD1 infection model. |
