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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

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 determi...

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Autores principales: Song, Lihua, Zhou, Yusen, He, Jun, Zhu, Hong, Huang, Rutong, Mao, Panyong, Duan, Qing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Birkhäuser-Verlag 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7088624/
https://www.ncbi.nlm.nih.gov/pubmed/18810628
http://dx.doi.org/10.1007/s11262-008-0283-4
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author Song, Lihua
Zhou, Yusen
He, Jun
Zhu, Hong
Huang, Rutong
Mao, Panyong
Duan, Qing
author_facet Song, Lihua
Zhou, Yusen
He, Jun
Zhu, Hong
Huang, Rutong
Mao, Panyong
Duan, Qing
author_sort Song, Lihua
collection PubMed
description 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.
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spelling pubmed-70886242020-03-23 Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates Song, Lihua Zhou, Yusen He, Jun Zhu, Hong Huang, Rutong Mao, Panyong Duan, Qing Virus Genes Article 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. Birkhäuser-Verlag 2008-09-23 2008 /pmc/articles/PMC7088624/ /pubmed/18810628 http://dx.doi.org/10.1007/s11262-008-0283-4 Text en © Springer Science+Business Media, LLC 2008 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
Song, Lihua
Zhou, Yusen
He, Jun
Zhu, Hong
Huang, Rutong
Mao, Panyong
Duan, Qing
Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates
title Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates
title_full Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates
title_fullStr Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates
title_full_unstemmed Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates
title_short Comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus S1 genes from six new serotype 2 human isolates
title_sort comparative sequence analyses of a new mammalian reovirus genome and the mammalian reovirus s1 genes from six new serotype 2 human isolates
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7088624/
https://www.ncbi.nlm.nih.gov/pubmed/18810628
http://dx.doi.org/10.1007/s11262-008-0283-4
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