ArticleThe Journal of biological chemistry2012
Transient activation of the PI3K-AKT pathway by hepatitis C virus to enhance viral entry.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 101 citations in OpenAlex.
- Reciprocal control of viral infection and phosphoinositide dynamics.FEBS letters · 2026Review
- The PI3K/Akt Pathway in Herpesvirus Biology: A Double-Edged Sword in Host-Virus Interactions.Microorganisms · 2026Review
- Loss of Akt3 enhances antiviral immunity while disrupting corneal homeostasis during ocular HSV-1 infection.Frontiers in immunology · 2026Article
- A novel comprehensive strategy for research on wine-processed mechanism of corni fructus guided by variation in the chemical components and network analysis.BMC complementary medicine and therapies · 2025Article
- CD81 Aggravates Ovarian Cancer Progression via p-Cresyl Sulfate-Mediated Mitophagy in Tim4Journal of cellular and molecular medicine · 2025Article
- The CXCL8/MAPK/hnRNP-K axis enables susceptibility to infection by EV-D68, rhinovirus, and influenza virus in vitro.Nature communications · 2025Article
- Multi-protomics analysis identified host cellular pathways perturbed by tick-borne encephalitis virus infection.Nature communications · 2024Article
- A conserved role for AKT in the replication of emerging flaviviruses in vertebrates and vectors.Virus research · 2024Article
- Article
- Live and let die: signaling AKTivation and UPRegulation dynamics in SARS-CoVs infection and cancer.Cell death & disease · 2022Review
- The HCV Envelope Glycoprotein Down-Modulates NF-κB Signalling and Associates With Stimulation of the Host Endoplasmic Reticulum Stress Pathway.Frontiers in immunology · 2022Article
- Article
- Chandipura virus dysregulates the expression of hsa-miR-21-5p to activate NF-κB in human microglial cells.Journal of biomedical science · 2021Article
- Akt Interacts with Usutu Virus Polymerase, and Its Activity Modulates Viral Replication.Pathogens (Basel, Switzerland) · 2021Article
- Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021Review
- Epigenetic Mechanisms Involved in HCV-Induced Hepatocellular Carcinoma (HCC).Frontiers in oncology · 2021Review
- Akt Phosphorylation of Hepatitis C Virus NS5B Regulates Polymerase Activity and Hepatitis C Virus Infection.Frontiers in microbiology · 2021Article
- Inhibitory Effect of PIK-24 on Respiratory Syncytial Virus Entry by Blocking Phosphatidylinositol-3 Kinase Signaling.Antimicrobial agents and chemotherapy · 2020Article
- Siniperca chuatsi rhabdovirus (SCRV) induces autophagy via PI3K/Akt-mTOR pathway in CPB cells.Fish & shellfish immunology · 2020Article
- The machinery for endocytosis of epidermal growth factor receptor coordinates the transport of incoming hepatitis B virus to the endosomal network.The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The PI3K-AKT signaling pathway plays an important role in cell growth and metabolism. Here we report that hepatitis C virus (HCV) transiently activates the PI3K-AKT pathway. This activation was observed as early as 15 min postinfection, peaked by 30 min, and became undetectable at 24 h postinfection. The activation of AKT could also be mediated by UV-inactivated HCV, HCV pseudoparticle, and the ectodomain of the HCV E2 envelope protein. Because antibodies directed against CD81 and claudin-1, but not antibodies directed against scavenger receptor class B type I or occludin, could also activate AKT, the interaction between HCV E2 and its two co-receptors CD81 and claudin-1 probably triggered the activation of AKT. This activation of AKT by HCV was important for HCV infectivity, because the silencing of AKT by siRNA or the treatment of cells with its inhibitors or with the inhibitor of its upstream regulator PI3K significantly inhibited HCV infection, whereas the expression of constitutively active AKT enhanced HCV infection. The PI3K-AKT pathway is probably involved in HCV entry, because the inhibition of this pathway could inhibit the entry of HCV pseudoparticle but not the VSV pseudoparticle into cells. Furthermore, the treatment of cells with the AKT inhibitor AKT-V prior to HCV infection inhibited HCV infection, whereas the treatment after HCV infection had no obvious effect. Taken together, our studies indicated that HCV transiently activates the PI3K-AKT pathway to facilitate its entry. These results provide important information for understanding HCV replication and pathogenesis and raised the possibility of targeting this cellular pathway to treat HCV patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.