{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang H"],"funding":["Guangzhou Basic and Applied Basic Research Program","Science and Technology Planning Project of Guangdong Province"],"pagination":["2148-2167"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12459367"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(10)"],"pubmed_abstract":["Ebola virus disease (EVD) caused by <i>Zaire</i> Ebolavirus (EBOV) infection is a major threat to public health in Africa and even worldwide, due to its extremely high mortality rate. However, there are still no effective antiviral therapies that can completely cure EVD. A comprehensive understanding of virus-host interactions would be beneficial for developing new antiviral agents. Here, we showed that CXCR4-induced macroautophagy/autophagy and was internalized to endosomes by interacting with glycoprotein (GP) on viral particles during EBOV infection; this promoted the EBOV attachment and entry, which was reduced by CXCR4 antagonist and neutralizing antibody. We also found that CXCR4 increased EBOV replication by downregulating cytotoxic GP to promote viral fitness instead of influencing"],"journal":["Autophagy"],"pubmed_title":["Dual roles of CXCR4 (C-X-C motif chemokine receptor 4) in promoting entry of ebolavirus and targeting excessive glycoprotein for reticulophagic degradation to facilitate viral fitness."],"pmcid":["PMC12459367"],"funding_grant_id":["2021B1212040017","No. 2024A04J4559"],"pubmed_authors":["Li X","Qian J","Li J","Liu L","Long Z","Huang H","Fan L","Lu J","Shi W","Yan H","Wang J"],"additional_accession":[]},"is_claimable":false,"name":"Dual roles of CXCR4 (C-X-C motif chemokine receptor 4) in promoting entry of ebolavirus and targeting excessive glycoprotein for reticulophagic degradation to facilitate viral fitness.","description":"Ebola virus disease (EVD) caused by <i>Zaire</i> Ebolavirus (EBOV) infection is a major threat to public health in Africa and even worldwide, due to its extremely high mortality rate. However, there are still no effective antiviral therapies that can completely cure EVD. A comprehensive understanding of virus-host interactions would be beneficial for developing new antiviral agents. Here, we showed that CXCR4-induced macroautophagy/autophagy and was internalized to endosomes by interacting with glycoprotein (GP) on viral particles during EBOV infection; this promoted the EBOV attachment and entry, which was reduced by CXCR4 antagonist and neutralizing antibody. We also found that CXCR4 increased EBOV replication by downregulating cytotoxic GP to promote viral fitness instead of influencing","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-03T19:33:07.541Z","creation":"2026-04-30T03:12:15.12Z"},"accession":"S-EPMC12459367","cross_references":{"pubmed":["40223186"],"doi":["10.1080/15548627.2025.2492877"]}}