TIM22 and TIM29 inhibit HBV replication by up-regulating SRSF1 expression
© 2024 Wiley Periodicals LLC..
Hepatitis B virus (HBV) infection is a serious global health problem. After the viruses infect the human body, the host can respond to the virus infection by coordinating various cellular responses, in which mitochondria play an important role. Evidence has shown that mitochondrial proteins are involved in host antiviral responses. In this study, we found that the overexpression of TIM22 and TIM29, the members of the inner membrane translocase TIM22 complex, significantly reduced the level of intracellular HBV DNA and RNA and secreted HBV surface antigens and E antigen. The effects of TIM22 and TIM29 on HBV replication and transcription is attributed to the reduction of core promoter activity mediated by the increased expression of SRSF1 which acts as a suppressor of HBV replication. This study provides new evidence for the critical role of mitochondria in the resistance of HBV infection and new targets for the development of treatment against HBV infection.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:96 |
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Enthalten in: |
Journal of medical virology - 96(2024), 2 vom: 06. Feb., Seite e29439 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Guo, Lin [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 05.02.2024 Date Revised 05.02.2024 published: Print Citation Status MEDLINE |
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doi: |
10.1002/jmv.29439 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM367844141 |
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520 | |a Hepatitis B virus (HBV) infection is a serious global health problem. After the viruses infect the human body, the host can respond to the virus infection by coordinating various cellular responses, in which mitochondria play an important role. Evidence has shown that mitochondrial proteins are involved in host antiviral responses. In this study, we found that the overexpression of TIM22 and TIM29, the members of the inner membrane translocase TIM22 complex, significantly reduced the level of intracellular HBV DNA and RNA and secreted HBV surface antigens and E antigen. The effects of TIM22 and TIM29 on HBV replication and transcription is attributed to the reduction of core promoter activity mediated by the increased expression of SRSF1 which acts as a suppressor of HBV replication. This study provides new evidence for the critical role of mitochondria in the resistance of HBV infection and new targets for the development of treatment against HBV infection | ||
650 | 4 | |a Journal Article | |
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650 | 4 | |a TIM29 | |
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650 | 7 | |a Serine-Arginine Splicing Factors |2 NLM | |
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650 | 7 | |a TIMM29 protein, human |2 NLM | |
650 | 7 | |a Mitochondrial Precursor Protein Import Complex Proteins |2 NLM | |
700 | 1 | |a Liu, Jia-Jun |e verfasserin |4 aut | |
700 | 1 | |a Long, Shao-Yuan |e verfasserin |4 aut | |
700 | 1 | |a Wang, Pei-Yun |e verfasserin |4 aut | |
700 | 1 | |a Li, Shan |e verfasserin |4 aut | |
700 | 1 | |a Wang, Jin-Lan |e verfasserin |4 aut | |
700 | 1 | |a Wei, Xia-Fei |e verfasserin |4 aut | |
700 | 1 | |a Li, Jie |e verfasserin |4 aut | |
700 | 1 | |a Lei, Ling |e verfasserin |4 aut | |
700 | 1 | |a Huang, Ai-Long |e verfasserin |4 aut | |
700 | 1 | |a Hu, Jie-Li |e verfasserin |4 aut | |
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