ArticlePLoS pathogens2014
Amphipathic α-helices in apolipoproteins are crucial to the formation of infectious hepatitis C virus particles.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 84 citations in OpenAlex.
- HVJ-E links Apolipoprotein d to antitumor effects.Journal for immunotherapy of cancer · 2025Article
- Determinants of susceptibility to SARS-CoV-2 infection in murine ACE2.Journal of virology · 2025Article
- Impaired ApoB secretion triggers enhanced secretion of ApoE to maintain triglyceride homeostasis in hepatoma cells.Journal of lipid research · 2025Article
- Autoantibodies to apolipoprotein A-I in hepatitis C virus infection: a role in disease progression?Frontiers in immunology · 2025Article
- Effects of the subtypes of apolipoprotein E on immune inhibition and prognosis in patients with Hepatocellular Carcinoma.Journal of cancer research and clinical oncology · 2024Article
- Comparative pathogenicity of SARS-CoV-2 Omicron subvariants including BA.1, BA.2, and BA.5.Communications biology · 2023Article
- Endosomal egress and intercellular transmission of hepatic ApoE-containing lipoproteins and its exploitation by the hepatitis C virus.PLoS pathogens · 2023Article
- Mechanism of the Regulation of Plasma Cholesterol Levels by PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Role of Vitamin D in Liver Disease and Complications of Advanced Chronic Liver Disease.International journal of molecular sciences · 2022Review
- Secretory glycoprotein NS1 plays a crucial role in the particle formation of flaviviruses.PLoS pathogens · 2022Article
- Hepatitis C virus induces oxidation and degradation of apolipoprotein B to enhance lipid accumulation and promote viral production.PLoS pathogens · 2021Article
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- Is HSD17B13 Genetic Variant a Protector for Liver Dysfunction? Future Perspective as a Potential Therapeutic Target.Journal of personalized medicine · 2021Review
- Hepatitis C Virus Uses Host Lipids to Its Own Advantage.Metabolites · 2021Review
- HCV Assembly and Egress via Modifications in Host Lipid Metabolic Systems.Cold Spring Harbor perspectives in medicine · 2021Review
- Dysregulation of Ephrin receptor and PPAR signaling pathways in neural progenitor cells infected by Zika virus.Emerging microbes & infections · 2020Article
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- The ATGL lipase cooperates with ABHD5 to mobilize lipids for hepatitis C virus assembly.PLoS pathogens · 2020Article
- Review
- Adenomatous polyposis coli-binding protein end-binding 1 promotes hepatocellular carcinoma growth and metastasis.PloS one · 2020Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein B (ApoB) and ApoE have been shown to participate in the particle formation and the tissue tropism of hepatitis C virus (HCV), but their precise roles remain uncertain. Here we show that amphipathic α-helices in the apolipoproteins participate in the HCV particle formation by using zinc finger nucleases-mediated apolipoprotein B (ApoB) and/or ApoE gene knockout Huh7 cells. Although Huh7 cells deficient in either ApoB or ApoE gene exhibited slight reduction of particles formation, knockout of both ApoB and ApoE genes in Huh7 (DKO) cells severely impaired the formation of infectious HCV particles, suggesting that ApoB and ApoE have redundant roles in the formation of infectious HCV particles. cDNA microarray analyses revealed that ApoB and ApoE are dominantly expressed in Huh7 cells, in contrast to the high level expression of all of the exchangeable apolipoproteins, including ApoA1, ApoA2, ApoC1, ApoC2 and ApoC3 in human liver tissues. The exogenous expression of not only ApoE, but also other exchangeable apolipoproteins rescued the infectious particle formation of HCV in DKO cells. In addition, expression of these apolipoproteins facilitated the formation of infectious particles of genotype 1b and 3a chimeric viruses. Furthermore, expression of amphipathic α-helices in the exchangeable apolipoproteins facilitated the particle formation in DKO cells through an interaction with viral particles. These results suggest that amphipathic α-helices in the exchangeable apolipoproteins play crucial roles in the infectious particle formation of HCV and provide clues to the understanding of life cycle of HCV and the development of novel anti-HCV therapeutics targeting for viral assembly.
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