A Functional Variant of  &lt;i&gt;CD40&lt;/i&gt; Modulates Clearance of Hepatitis B Virus in Hepatocytes via Regulation of the ANXA2/CD40/BST2 Axis

Chen, Jiaxuan; Chen, Haitao; Mai, Haoming; Lou, Shuang; Luo, Mengqi; Xie, Haisheng; Zhou, Bin; Hou, Jinlin; Jiang, Deke

doi:10.2139/ssrn.4022091

Cited by 1 publication

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“…Thus, the late triggering of the CD4+ T cell response would not be able to support the development of quantitatively and qualitatively effective CD8+ T cells, favoring viral persistence. Recent evidence also underlines the role of the JAK/STAT system and bone marrow stromal antigen 2 (BST2), a key gene for the production of IFN induced by cells that express CD40 [44]. Similar pathways are those involving cytotoxic T-lymphocyte associated antigen 4 (CTLA-4), T-cell immunoglobulin, and mucin domain-containing protein (Tim-3) [45][46][47][48], making the modulation of the adaptive immune system one of the major targets for future therapeutic approaches.…”

Section: Hbv and Host Immune Systemmentioning

confidence: 99%

HBV Infection and Host Interactions: The Role in Viral Persistence and Oncogenesis

Nevola

Beccia

Rosato³

et al. 2023

IJMS

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Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus–host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.

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