cccDNA
肝细胞癌
医学
乙型肝炎病毒
乙型肝炎
病毒学
免疫学
病毒
免疫系统
癌症研究
乙型肝炎表面抗原
作者
Nevin Varghese,Amry Majeed,Suraj Nyalakonda,Tina Boortalary,Dina Halegoua‐De Marzio,Hie‐Won Hann
出处
期刊:Cancers
[MDPI AG]
日期:2024-02-14
卷期号:16 (4): 777-777
标识
DOI:10.3390/cancers16040777
摘要
Chronic hepatitis B virus (HBV) infection is the largest global cause of hepatocellular carcinoma (HCC). Current HBV treatment options include pegylated interferon-alpha and nucleos(t)ide analogues (NAs), which have been shown to be effective in reducing HBV DNA levels to become undetectable. However, the literature has shown that some patients have persistent risk of developing HCC. The mechanism in which this occurs has not been fully elucidated. However, it has been discovered that HBV's covalently closed circular DNA (cccDNA) integrates into the critical HCC driver genes in hepatocytes upon initial infection; additionally, these are not targets of current NA therapies. Some studies suggest that HBV undergoes compartmentalization in peripheral blood mononuclear cells that serve as a sanctuary for replication during antiviral therapy. The aim of this review is to expand on how patients with HBV may develop HCC despite years of HBV viral suppression and carry worse prognosis than treatment-naive HBV patients who develop HCC. Furthermore, HCC recurrence after initial surgical or locoregional treatment in this setting may cause carcinogenic cells to behave more aggressively during treatment. Curative novel therapies which target the life cycle of HBV, modulate host immune response, and inhibit HBV RNA translation are being investigated.
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