Enhanced host immune responses in presence of HCV facilitate HBV clearance in coinfection

Liu, Shuhui; Zhao, Kaitao; Su, Xi; Gao, Xiaoxiao; Yao, Yongxuan; Kong, Ranran; Wang, Yun; Wu, Chunchen; Lu, Mengji; Chen, Xinwen; Pei, Rongjuan

doi:10.1016/j.virs.2022.04.001

Cited by 3 publications

(1 citation statement)

References 55 publications

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“…The samples of liver tissues were subjected to IHC and H&E staining as previously described 24 . Intrahepatic HBc and Flag‐RBM24 were detected using an anti‐HBc antibody (Gene Tech; GB058629) and an anti‐Flag antibody (Sigma‐Aldrich; F1804), respectively.…”

Section: Methodsmentioning

confidence: 99%

RNA‐binding motif protein 24 inhibits HBV replication in vivo

Yao

Chen

Huang

et al. 2023

Journal of Medical Virology

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Despite the extensive use of effective vaccines and antiviral drugs, chronic hepatitis B virus (HBV) infection continues to pose a serious threat to global public health. Therapies with novel mechanisms of action against HBV are being explored for achieving a functional cure. In this study, five murine models of HBV replication were used to investigate the inhibitory effect of RNA binding motif protein 24 (RBM24) on HBV replication. The findings revealed that RBM24 serves as a host restriction factor and suppresses HBV replication in vivo. The transient overexpression of RBM24 in hydrodynamics‐based mouse models of HBV replication driven by the CMV or HBV promoters suppressed HBV replication. Additionally, the ectopic expression of RBM24 decreased viral accumulation and the levels of HBV covalently closed circular DNA (cccDNA) in an rcccDNA mouse model. The liver‐directed transduction of adeno‐associated viruses (AAV)‐RBM24 mediated the stable hepatic expression of RBM24 in pAAV‐HBV1.2 and HBV/tg mouse models, and markedly reduced the levels of HBV cccDNA and other viral indicators. Altogether, these findings revealed that RBM24 inhibits the replication of HBV in vivo, and RBM24 may be a potential therapeutic target for combating HBV infections.

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Section: Methodsmentioning

confidence: 99%

RNA‐binding motif protein 24 inhibits HBV replication in vivo

Yao

Chen

Huang

et al. 2023

Journal of Medical Virology

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Oncogenic viruses, cancer biology, and innate immunity

White

Wu²,

Damania³

2022

Current Opinion in Immunology

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Co-infection with hepatitis B and C viruses: current state of the problem

Volynets,

Khavkin

2024

ECG

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Co-infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) is a complex clinical disease with an estimated worldwide prevalence of 1-15%. The transmission routes for HCV and HBV are similar. During co-infection, four serological profiles are observed: codominant, HCV dominant, HBV dominant and non-replicative. Although both HBV and HCV replicate in hepatocytes, their life cycles are quite different. Viral replication in co-infected cells is characterized by the dominance of HCV replication over HBV replication. Three theories of interaction between HCV and HBV are discussed. There are no established recommendations for the treatment of HBV/HCV co-infection. Treatment of chronic hepatitis C without HBV suppression increases the risk of HBV reactivation. In the review, we evaluate studies of both direct-acting antivirals and interferon-based therapies. Screening and prevention of co-infection are important to prevent serious HBV reactivation.

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Enhanced host immune responses in presence of HCV facilitate HBV clearance in coinfection

Cited by 3 publications

References 55 publications

RNA‐binding motif protein 24 inhibits HBV replication in vivo

RNA‐binding motif protein 24 inhibits HBV replication in vivo

Oncogenic viruses, cancer biology, and innate immunity

Co-infection with hepatitis B and C viruses: current state of the problem

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