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dc.contributor.authorCiupe, Stanca M.en_US
dc.contributor.authorHews, Sarahen_US
dc.date.accessioned2018-10-26T14:38:31Z
dc.date.available2018-10-26T14:38:31Z
dc.date.issued2012-07-02en_US
dc.identifier.othere39591en_US
dc.identifier.urihttp://hdl.handle.net/10919/85535
dc.description.abstractWe develop mathematical models for the role of hepatitis B e-antigen in creating immunological tolerance during hepatitis B virus infection and propose mechanisms for hepatitis B e-antigen clearance, subsequent emergence of a potent cellular immune response, and the effect of these on liver damage. We investigate the dynamics of virus-immune cells interactions, and derive parameter regimes that allow for viral persistence. We modify the model to account for mechanisms responsible for hepatitis B e-antigen loss, such as seroconversion and virus mutations that lead to emergence of cellular immune response to the mutant virus. Our models demonstrate that either seroconversion or mutations can induce immune activation and that instantaneous loss of e-antigen by either mechanism is associated with least liver damage and is therefore more beneficial for disease outcomes.en_US
dc.format.mimetypeapplication/pdfen_US
dc.language.isoen_USen_US
dc.publisherPLOSen_US
dc.rightsCreative Commons Attribution 4.0 Internationalen_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0en_US
dc.titleMathematical Models of E-Antigen Mediated Immune Tolerance and Activation following Prenatal HBV Infectionen_US
dc.typeArticle - Refereeden_US
dc.description.versionPeer Revieweden_US
dc.title.serialPLOS ONEen_US
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0039591en_US
dc.identifier.volume7en_US
dc.identifier.issue7en_US
dc.type.dcmitypeTexten_US
dc.identifier.pmid22768303en_US
dc.identifier.eissn1932-6203en_US


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Creative Commons Attribution 4.0 International
License: Creative Commons Attribution 4.0 International