Interference of Apoptosis by Hepatitis B Virus

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dc.contributor.authorLin, Shaoli
dc.contributor.authorZhang, Yan-Jin
dc.date.accessioned2023-11-28T15:58:26Z
dc.date.available2023-11-28T15:58:26Z
dc.date.issued2017-08-18
dc.description.abstractHepatitis B virus (HBV) causes liver diseases that have been a consistent problem for human health, leading to more than one million deaths every year worldwide. A large proportion of hepatocellular carcinoma (HCC) cases across the world are closely associated with chronic HBV infection. Apoptosis is a programmed cell death and is frequently altered in cancer development. HBV infection interferes with the apoptosis signaling to promote HCC progression and viral proliferation. The HBV-mediated alteration of apoptosis is achieved via interference with cellular signaling pathways and regulation of epigenetics. HBV X protein (HBX) plays a major role in the interference of apoptosis. There are conflicting reports on the HBV interference of apoptosis with the majority showing inhibition of and the rest reporting induction of apoptosis. In this review, we described recent studies on the mechanisms of the HBV interference with the apoptosis signaling during the virus infection and provided perspective.
dc.description.urihttps://doi.org/10.3390/v9080230
dc.identifierhttps://doi.org/10.13016/dspace/zc6n-2y5j
dc.identifier.citationLin, S.; Zhang, Y.-J. Interference of Apoptosis by Hepatitis B Virus. Viruses 2017, 9, 230.
dc.identifier.urihttp://hdl.handle.net/1903/31497
dc.language.isoen_US
dc.publisherMDPI
dc.relation.isAvailableAtCollege of Agriculture & Natural Resourcesen_us
dc.relation.isAvailableAtDepartment of Veterinary Medicineen_us
dc.relation.isAvailableAtDigital Repository at the University of Marylanden_us
dc.relation.isAvailableAtUniversity of Maryland (College Park, MD)en_us
dc.subjecthepatitis B virus (HBV)
dc.subjectapoptosis
dc.subjecthepatocellular carcinoma (HCC)
dc.subjectX protein
dc.titleInterference of Apoptosis by Hepatitis B Virus
dc.typeArticle
local.equitableAccessSubmissionNo

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