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dc.contributor.authorPfaender, Stephanie
dc.contributor.authorWalter, Stephanie
dc.contributor.authorGrabski, Elena
dc.contributor.authorTodt, Daniel
dc.contributor.authorBruening, Janina
dc.contributor.authorRomero-Brey, Inés
dc.contributor.authorGather, Theresa
dc.contributor.authorBrown, Richard J P
dc.contributor.authorHahn, Kerstin
dc.contributor.authorPuff, Christina
dc.contributor.authorPfankuche, Vanessa M
dc.contributor.authorHansmann, Florian
dc.contributor.authorPostel, Alexander
dc.contributor.authorBecher, Paul
dc.contributor.authorThiel, Volker
dc.contributor.authorKalinke, Ulrich
dc.contributor.authorWagner, Bettina
dc.contributor.authorBartenschlager, Ralf
dc.contributor.authorBaumgärtner, Wolfgang
dc.contributor.authorFeige, Karsten
dc.contributor.authorPietschmann, Thomas
dc.contributor.authorCavalleri, Jessika M V
dc.contributor.authorSteinmann, Eike
dc.date.accessioned2017-07-13T11:52:32Z
dc.date.available2017-07-13T11:52:32Z
dc.date.issued2017-03-21
dc.identifier.citationImmune protection against reinfection with nonprimate hepacivirus. 2017, 114 (12):E2430-E2439 Proc. Natl. Acad. Sci. U.S.A.en
dc.identifier.issn1091-6490
dc.identifier.pmid28275093
dc.identifier.doi10.1073/pnas.1619380114
dc.identifier.urihttp://hdl.handle.net/10033/621010
dc.description.abstractHepatitis C virus (HCV) displays a restricted host species tropism and only humans and chimpanzees are susceptible to infection. A robust immunocompetent animal model is still lacking, hampering mechanistic analysis of virus pathogenesis, immune control, and prophylactic vaccine development. The closest homolog of HCV is the equine nonprimate hepacivirus (NPHV), which shares similar features with HCV and thus represents an animal model to study hepacivirus infections in their natural hosts. We aimed to dissect equine immune responses after experimental NPHV infection and conducted challenge experiments to investigate immune protection against secondary NPHV infections. Horses were i.v. injected with NPHV containing plasma. Flow cytometric analysis was used to monitor immune cell frequencies and activation status. All infected horses became viremic after 1 or 2 wk and viremia could be detected in two horses for several weeks followed by a delayed seroconversion and viral clearance. Histopathological examinations of liver biopsies revealed mild, periportally accentuated infiltrations of lymphocytes, macrophages, and plasma cells with some horses displaying subclinical signs of hepatitis. Following viral challenge, an activation of equine immune responses was observed. Importantly, after a primary NPHV infection, horses were protected against rechallenge with the homologous as well as a distinct isolate with only minute amounts of circulating virus being detectable.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleImmune protection against reinfection with nonprimate hepacivirus.en
dc.typeArticleen
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infectionsforschung GmbH, Feodor-Lynen-Str. 7, 30625 Hannover, Germany.en
dc.identifier.journalProceedings of the National Academy of Sciences of the United States of Americaen
refterms.dateFOA2018-06-13T04:23:48Z
html.description.abstractHepatitis C virus (HCV) displays a restricted host species tropism and only humans and chimpanzees are susceptible to infection. A robust immunocompetent animal model is still lacking, hampering mechanistic analysis of virus pathogenesis, immune control, and prophylactic vaccine development. The closest homolog of HCV is the equine nonprimate hepacivirus (NPHV), which shares similar features with HCV and thus represents an animal model to study hepacivirus infections in their natural hosts. We aimed to dissect equine immune responses after experimental NPHV infection and conducted challenge experiments to investigate immune protection against secondary NPHV infections. Horses were i.v. injected with NPHV containing plasma. Flow cytometric analysis was used to monitor immune cell frequencies and activation status. All infected horses became viremic after 1 or 2 wk and viremia could be detected in two horses for several weeks followed by a delayed seroconversion and viral clearance. Histopathological examinations of liver biopsies revealed mild, periportally accentuated infiltrations of lymphocytes, macrophages, and plasma cells with some horses displaying subclinical signs of hepatitis. Following viral challenge, an activation of equine immune responses was observed. Importantly, after a primary NPHV infection, horses were protected against rechallenge with the homologous as well as a distinct isolate with only minute amounts of circulating virus being detectable.


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