Journal
JOURNAL OF VIROLOGY
Volume 74, Issue 20, Pages 9792-9796Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.20.9792-9796.2000
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Funding
- NCI NIH HHS [R37 CA040489, R37-CA40489] Funding Source: Medline
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Following antigen recognition, hepatitis B virus (HBV)-specific cytotoxic T lymphocytes (CTL) induce a necroinflammatory liver disease in HBV-transgenic mice. An early event in this process is CTL-dependent activation of apoptosis in a small fraction of HBV-positive hepatocytes. Here we show that cytoplasmic HBV nucleocapsids and their cargo of replicative DNA intermediates survive CTL-induced apoptosis of hepatocytes in vitro. These results suggest that destruction of infected cells per se is not sufficient to destroy the replicating HBV genome in infected tissue and that other events in addition to this process are required for viral clearance to occur.
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