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TGF-β Suppression of HBV RNA through AID-Dependent Recruitment of an RNA Exosome Complex
HBV is one of the causative factors of hepatocellular carcinoma. Recent studies have shown that the members of the APOBEC deaminase family are antiviral factors that suppress the replication of viruses, such as HIV-1 and HBV. APOBEC3G suppresses viral replication by either hypermutation of nascent DNA or inhibition of reverse transcription. Recent studies have been suggested that AID, another APOBEC family member, restricts viruses and retrotransposons that use reverse transcription for their replication. However, little is known about the antiviral mechanisms of AID. TGF-β is a pleiotropic cytokine involved in the suppression of HBV replication, but the mechanism underlying its anti-HBV activity is unclear. In this study, we found that AID plays a role in the anti-HBV activity of TGF-β. Further study revealed that AID physically associates with a viral RNP complex containing reverse transcriptase and recruits the RNA degradosome (RNA exosome) to the RNP complex to degrade the viral RNA. To the best of our knowledge, this study is the first to reveal a novel antiviral pathway in which AID triggers viral RNA degradation by tethering the RNA exosome to the viral reverse transcriptase/RNA complex. Viral RNA may be another target for APOBEC antiviral activity.
Vyšlo v časopise: TGF-β Suppression of HBV RNA through AID-Dependent Recruitment of an RNA Exosome Complex. PLoS Pathog 11(4): e32767. doi:10.1371/journal.ppat.1004780
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004780Souhrn
HBV is one of the causative factors of hepatocellular carcinoma. Recent studies have shown that the members of the APOBEC deaminase family are antiviral factors that suppress the replication of viruses, such as HIV-1 and HBV. APOBEC3G suppresses viral replication by either hypermutation of nascent DNA or inhibition of reverse transcription. Recent studies have been suggested that AID, another APOBEC family member, restricts viruses and retrotransposons that use reverse transcription for their replication. However, little is known about the antiviral mechanisms of AID. TGF-β is a pleiotropic cytokine involved in the suppression of HBV replication, but the mechanism underlying its anti-HBV activity is unclear. In this study, we found that AID plays a role in the anti-HBV activity of TGF-β. Further study revealed that AID physically associates with a viral RNP complex containing reverse transcriptase and recruits the RNA degradosome (RNA exosome) to the RNP complex to degrade the viral RNA. To the best of our knowledge, this study is the first to reveal a novel antiviral pathway in which AID triggers viral RNA degradation by tethering the RNA exosome to the viral reverse transcriptase/RNA complex. Viral RNA may be another target for APOBEC antiviral activity.
Zdroje
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Hygiena a epidemiológia Infekčné lekárstvo Laboratórium
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