Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/66450
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dc.contributor.authorTanaka, Y.
dc.contributor.authorSanchez, L.V.
dc.contributor.authorSugiyama, M.
dc.contributor.authorSakamoto, T.
dc.contributor.authorKurbanov, F.
dc.contributor.authorTatematsu, K.
dc.contributor.authorRoman, S.
dc.contributor.authorTakahashi, S.
dc.contributor.authorShirai, T.
dc.contributor.authorPanduro-Cerda, Arturo
dc.contributor.authorMizokami, M.
dc.date.accessioned2015-11-19T18:51:19Z-
dc.date.available2015-11-19T18:51:19Z-
dc.date.issued2008
dc.identifier.urihttp://hdl.handle.net/20.500.12104/66450-
dc.description.abstractAccumulated evidence indicated that hepatitis B virus genotype G (HBV/G) is present exclusively in coinfection with other HBV genotypes. In Mexico, HBV/G from 6 men who had sex with men were coinfected with HBV/H. Phylogenetically complete genomes of the 6 Mexican HBV/G strains were closely related to previous ones from the US/Europe. Using uPA/SCID mice with human hepatocytes, monoinfection with HBV/G did not result in detectable HBV DNA in serum, whereas superinfection with HBV/G at week 10 inoculated HBV/H when HBV/H DNA was elevated to > 107 copies/mL has enhanced the replication of HBV/G. The HBV/G was enhanced in another 3 inoculated with a serum passage containing HBV/G with a trace of HBV/H. Coinfection of mice with HBV/G and H induced fibrosis in the liver. In conclusion, the replication of HBV/G can be enhanced remarkably when it is coinfected with HBV/H. Coinfection with HBV/G may be directly cytopathic in immunosuppressive conditions. © 2008 Elsevier Inc. All rights reserved.
dc.titleCharacteristics of hepatitis B virus genotype G coinfected with genotype H in chimeric mice carrying human hepatocytes
dc.typeArticle
dc.identifier.doi10.1016/j.virol.2008.04.001
dc.relation.ispartofjournalVirology
dc.relation.ispartofvolume376
dc.relation.ispartofissue2
dc.relation.ispartofpage408
dc.relation.ispartofpage415
dc.subject.keywordChimeric mice; Fibrosis; HBV genotype G; HBV genotype H; MSM; Replication
dc.contributor.affiliationTanaka, Y., Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan; Sanchez, L.V., Department of Molecular Biology in Medicine, Old Civil Hospital of Belen, University of Guadalajara, Guadalajara, Jalisco, Mexico; Sugiyama, M., Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan; Sakamoto, T., Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan; Kurbanov, F., Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan; Tatematsu, K., Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan; Roman, S., Department of Molecular Biology in Medicine, Old Civil Hospital of Belen, University of Guadalajara, Guadalajara, Jalisco, Mexico; Takahashi, S., Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Shirai, T., Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Panduro, A., Department of Molecular Biology in Medicine, Old Civil Hospital of Belen, University of Guadalajara, Guadalajara, Jalisco, Mexico; Mizokami, M., Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan
dc.contributor.affiliationPanduro-Cerda, Arturo., Universidad de Guadalajara
dc.relation.isReferencedByScopus
dc.relation.isReferencedByWOS
dc.identifier.urlhttp://www.scopus.com/inward/record.url?eid=2-s2.0-44649156317&partnerID=40&md5=f88b17a0f07fafea9b42b615a50ec5b1
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