ArticleAutophagy2022
CCDC88A/GIV promotes HBV replication and progeny secretion via enhancing endosomal trafficking and blocking autophagic degradation.
Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Review
- Avian pathogenic Escherichia coli virulence protein Hcp2a induces incomplete autophagy in chicken HD11 cells.Poultry science · 2026Article
- Secretion of the HBV small surface antigen is driven by an ER autophagic pathway.Hepatology communications · 2026Article
- The microRNA (miRNA) signatures in different phases of the natural history of chronic hepatitis B virus infection.Scientific reports · 2026Article
- Role of autophagy in tumorigenesis and drug resistance: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Targeting GNG4 inhibits tumor progression and restores enzalutamide sensitivity in prostate cancer by suppressing autophagy.Cell death & disease · 2026Article
- Sindbis virus is suppressed in the yellow fever mosquitoAutophagy · 2025Article
- Mitochondrial respiratory chain regulates HBV clearance through dual modulation of lysosomal acidification.Emerging microbes & infections · 2025Article
- HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis.Virologica Sinica · 2025Review
- Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025Review
- Small Extracellular Vesicles Orchestrate Cisplatin-Induced Ototoxicity: Potential Biomarker and Targets Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GIV/Girdin Modulation of Microglial Activation in Ischemic Stroke: Impact of FTO-Mediated m6A Modification.Molecular neurobiology · 2025Article
- Hepatitis B surface antigen hijacks TANK-binding kinase 1 to suppress type I interferon and induce early autophagy.Cell death & disease · 2025Article
- Bridging the gap: investigating the role of phosphorylation at the serine 129 site of α-synuclein in VAPB-PTPIP51 interactions.Acta neuropathologica communications · 2025Article
- Dual-specificity tyrosine-regulated kinase 4 modulates the STAT3-FOS signaling axis to inhibit hepatitis B virus replicationInternational journal of biological sciences · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- Exosomes target HBV-host interactions to remodel the hepatic immune microenvironment.Journal of nanobiotechnology · 2024Review
- Interconnection of cellular autophagy and endosomal vesicle trafficking and its role in hepatitis B virus replication and release.Virologica Sinica · 2024Review
- Hepatitis B virus promotes its own replication by enhancing RAB5A-mediated dual activation of endosomal and autophagic vesicle pathways.Emerging microbes & infections · 2023Article
- CCDC50 promotes tumor growth through regulation of lysosome homeostasis.EMBO reports · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) particles are thought to be secreted from hepatocytes through multivesicular bodies (MVBs); however, the cellular trafficking mechanisms prior to this process remain elusive. It has been reported that CCDC88A/GIV expression, which is involved in multiple aspects of vesicular trafficking, changes dynamically at different phases of chronic HBV infection. In this study, we focused on the role of CCDC88A/GIV in HBV replication. In the liver tissues of chronically HBV-infected patients, HBV infection significantly enhanced CCDC88A/GIV expression, and increased endoplasmic reticulum (ER) stress and autophagosome formation without changing endosome formation. Additionally, colocalization of SHBsAg with early endosomes (~30.2%) far exceeded that with autophagosomes (~3.2%). In hepatoma cells, CCDC88A/GIV and its downstream proteins, DNM2 (dynamin 2; a CCDC88A/GIV effector), CLTC and RAB5A significantly enhanced HBV replication and endosome formation but inhibited autophagosome formation. Blocking endocytosis disrupted HBsAg trafficking to endosomes and caused its accumulation in the ER lumen, which triggered ER stress to initiate the unfolded protein response (UPR). Therefore, HBsAg trafficking into autophagosomes was increased, and the lysosomal activity and maturation, which was inhibited by HBV infection, were restored. Meanwhile, core particles were prevented from entering MVBs. CCDC88A/GIV and its other effector, GNAI3, decreased autophagic flux by enhancing the insulin-induced AKT-MTOR pathway, thereby inhibiting HBV antigens autophagic degradation. In conclusion, CCDC88A/GIV enhanced HBV replication by increasing endosomal trafficking and reducing autophagic degradation of HBV antigens, suggesting that CCDC88A/GIV-mediated endosomal trafficking plays an important role in HBV replication and progeny secretion.
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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 Socratic graph.