ArticleJournal of biomedical science2022
Hepatitis B virus suppresses complement C9 synthesis by limiting the availability of transcription factor USF-1 and inhibits formation of membrane attack complex: implications in disease pathogenesis.
Article in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- DNA methylation-mediated suppression of endocytosis confers resistance to duck hepatitis A virus type 3.Microbiology spectrum · 2026Article
- Clinical significance and mutation analysis of HBsAg and Anti-HBs coexistence in Chronic Hepatitis B.Virus research · 2026Article
- Mechanistic insight into complement C3 regulation during chronic HBV infection: effect on viral persistence and host immune response.Journal of biomedical science · 2026Article
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- Hepatocyte nuclear factor 4α is a critical factor for the production of complement components in the liver.In vitro cellular & developmental biology. Animal · 2024Article
- Hepatitis B Virus Increases SphK1-S1P Synthesis by Promoting the Availability of the Transcription Factor USF1.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Hepatitis B Virus Status and Clinical Outcomes in IgA Nephropathy.Kidney international reports · 2024Article
- Virus hijacking of host epigenetic machinery to impair immune response.Journal of virology · 2023Review
- Immune response and treatment targets of chronic hepatitis B virus infection: innate and adaptive immunity.Frontiers in cellular and infection microbiology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe complement system functions primarily as a first-line host defense against invading microbes, including viruses. However, the interaction of Hepatitis B virus (HBV) with the complement-components during chronic HBV infection remains largely unknown. We investigated the mechanism by which HBV inhibits the formation of cytolytic complement membrane-attack complex (MAC) and studied its impact on MAC-mediated microbicidal activity and disease pathogenesis.
methodsBlood/liver tissues were collected from chronically HBV-infected patients and controls. HepG2
resultsAmong the MAC components (C5b-C9), significant reduction was noted in the expression of C9, the major constituent of MAC, in HBV-infected HepG2
conclusionCollectively, HBX suppressed C9 transcription by restricting the availability of USF-1 through hypermethylation of USF-1-promoter and consequently hinder the formation and lytic functions of MAC. Early therapy is needed for both CHB and IT to normalize the aberrant complement profile and contain viral and bacterial infection and limit disease progression.
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Registered trials
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