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The <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">CD8<\/jats:styled-content><jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell response is vigorous, polyclonal and multispecific in acutely infected patients who successfully clear the virus and relatively weak and narrowly focused in chronically infected patients. The immunological basis for this dichotomy is unclear. A recent study using <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> transgenic mice and <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell receptor transgenic mice suggests that intrahepatic antigen presentation by <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> positive hepatocytes suppresses <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">CD8<\/jats:styled-content><jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell responses through a co\u2010inhibitory molecule, programmed cell death 1 (<jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\u20101). In contrast, antigen presentation by activated professional antigen\u2010presenting cells induces functional differentiation of <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">CD8<\/jats:styled-content><jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells. These findings suggest that the outcome of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell priming is largely dependent on the nature of antigen\u2010presenting cells. Another study suggests that the timing of <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">CD4<\/jats:styled-content><jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell priming regulates the magnitude of the <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">CD8<\/jats:styled-content><jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell response. Other factors that could regulate <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>\u2010specific cellular immune responses are high viral loads, mutational epitope inactivation, <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell receptor antagonism and infection of immunologically privileged tissues. However, these pathways become apparent only in the setting of an ineffective cellular immune response, which is therefore the fundamental underlying cause. Understanding the cellular and molecular mechanisms by which <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> evades host immune responses will eventually help develop new immunotherapeutic strategies designed to terminate chronic <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> infection.<\/jats:p>","DOI":"10.1111\/hepr.12439","type":"journal-article","created":{"date-parts":[[2014,10,21]],"date-time":"2014-10-21T04:13:50Z","timestamp":1413864830000},"page":"179-189","source":"Crossref","is-referenced-by-count":46,"title":["Immunobiology of hepatitis <scp>B<\/scp> virus infection"],"prefix":"10.1111","volume":"45","author":[{"given":"Masanori","family":"Isogawa","sequence":"first","affiliation":[{"name":"Department of Virology and Liver Unit Nagoya City University Graduate School of Medical Science  Nagoya Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuhito","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Department of Virology and Liver Unit Nagoya City University Graduate School of Medical Science  Nagoya Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,11,26]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra031087"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)64980-2"},{"key":"e_1_2_10_4_1","doi-asserted-by":"crossref","first-page":"6158","DOI":"10.1128\/jvi.69.10.6158-6169.1995","article-title":"V. 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