Journal
VIRUSES-BASEL
Volume 14, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/v14020373
Keywords
hepatitis B virus; cellular FLIP (c-FLIP); viral FLIP (v-FLIP); HBx; innate immune system
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Funding
- National Research Foundation of Korea (NRF) - Korea government [NRF-2020R1A2C3010511, 2021M3A9I2080488, NRF-2021M3A9H3017086]
- Korea National Institute of Health [2021-ER1801-00]
- Korea Health Promotion Institute [2021-ER1801-00] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2021M3A9I2080488] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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This review provides a comprehensive overview of the interplay between HBx and c-FLIP in HBV replication and carcinogenesis. The strategies adopted by HBV to establish chronic infection are described, as well as the conventional roles of c-FLIP in apoptosis and viral replication.
During viral evolution and adaptation, many viruses have utilized host cellular factors and machinery as their partners. HBx, as a multifunctional viral protein encoded by the hepatitis B virus (HBV), promotes HBV replication and greatly contributes to the development of HBV-associated hepatocellular carcinoma (HCC). HBx interacts with several host factors in order to regulate HBV replication and evolve carcinogenesis. The cellular FADD-like IL-1 beta-converting enzyme (FLICE)-like inhibitory protein (c-FLIP) is a major factor that functions in a variety of cellular pathways and specifically in apoptosis. It has been shown that the interaction between HBx and c-FLIP determines HBV fate. In this review, we provide a comprehensive and detailed overview of the interplay between c-FLIP and HBV in various environmental circumstances. We describe strategies adapted by HBV to establish its chronic infection. We also summarize the conventional roles of c-FLIP and highlight the functional outcome of the interaction between c-FLIP and HBV or other viruses in viral replication and the innate immune system.
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