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dc.contributor.authorCiupe, Stanca M.
dc.contributor.authorRibeiro, Ruy M.
dc.contributor.authorPerelson, Alan S.
dc.date.accessioned2018-11-19T18:38:15Z
dc.date.available2018-11-19T18:38:15Z
dc.date.issued2014-07
dc.identifier.issn1553-734X
dc.identifier.othere1003730
dc.identifier.urihttp://hdl.handle.net/10919/85910
dc.description.abstractHepatitis B is a DNA virus that infects liver cells and can cause both acute and chronic disease. It is believed that both viral and host factors are responsible for determining whether the infection is cleared or becomes chronic. Here we investigate the mechanism of protection by developing a mathematical model of the antibody response following hepatitis B virus (HBV) infection. We fitted the model to data from seven infected adults identified during acute infection and determined the ability of the virus to escape neutralization through overproduction of non-infectious subviral particles, which have HBs proteins on their surface, but do not contain nucleocapsid protein and viral nucleic acids. We showed that viral clearance can be achieved for high anti-HBV antibody levels, as in vaccinated individuals, when: (1) the rate of synthesis of hepatitis B subviral particles is slow; (2) the rate of synthesis of hepatitis B subviral particles is high but either anti-HBV antibody production is fast, the antibody affinity is high, or the levels of pre-existent HBV-specific antibody at the time of infection are high, as could be attained by vaccination. We further showed that viral clearance can be achieved for low equilibrium anti-HBV antibody levels, as in unvaccinated individuals, when a strong cellular immune response controls early infection.en_US
dc.description.sponsorshipSMC acknowledges support from NSF grant DMS-1214582. Portions of this work were performed under the auspices of the U.S. Department of Energy under contract DE-AC52-06NA25396 and supported by NIH grants P20-GM103452, AI028433 and OD011095. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
dc.format.mimetypeapplication/pdfen_US
dc.language.isoen_US
dc.publisherPLOS
dc.rightsCreative Commons Attribution 4.0 Internationalen_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0en_US
dc.subjectimmunodeficiency-virus type-1
dc.subjectcirculating immune-complexes
dc.subjectneutralizing antibodies
dc.subjectclearance rate
dc.subjecthiv-infection
dc.subjectdynamics
dc.subjectigg
dc.subjectkinetics
dc.subjecttherapy
dc.subjectplasma
dc.titleAntibody Responses during Hepatitis B Viral Infectionen_US
dc.typeArticle - Refereed
dc.title.serialPLOS Computational Biology
dc.identifier.doihttps://doi.org/10.1371/journal.pcbi.1003730
dc.identifier.volume10
dc.identifier.issue7
dc.type.dcmitypeTexten_US
dc.identifier.pmid25078553
dc.identifier.eissn1553-7358


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