{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu Q"],"funding":["U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences","NIDCR NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research","U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)","NIAID NIH HHS","U.S. Department of Health & Human Services | NIH | National Cancer Institute","NCI NIH HHS","NIGMS NIH HHS","Division of Intramural Research, National Institute of Allergy and Infectious Diseases"],"pagination":["1501-1520"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12337130"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(6)"],"pubmed_abstract":["Mitochondrial dynamics are pivotal for host immune responses upon infection, yet how viruses manipulate these processes to impair host defence and enhance viral fitness remains unclear. Here we show that Kaposi's sarcoma-associated herpesvirus (KSHV), an oncogenic virus also known as human herpesvirus 8, encodes Bcl-2 (vBcl-2), which reprogrammes mitochondrial architecture. It binds with NM23-H2, a host nucleoside diphosphate (NDP) kinase, to stimulate GTP loading of the dynamin-related protein (DRP1) GTPase, which triggers mitochondrial fission, inhibits mitochondrial antiviral signalling protein (MAVS) aggregation and impairs interferon responses in cell lines. An NM23-H2-binding-defective vBcl-2 mutant fails to evoke fission, leading to defective virion assembly due to activated MAVS-IF"],"journal":["Nature microbiology"],"pubmed_title":["Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production."],"pmcid":["PMC12337130"],"funding_grant_id":["R01 CA251275","R21 DE028256","R01 AI181758","R35 GM119721","R01 CA262631","R01 CA140964","R35GM119721","R01 CA238457"],"pubmed_authors":["Zheng Z","Cassel J","Pangilinan C","Altieri DC","Shen D","Liu Q","Guo S","Zhang L","McElroy R","Machhar JS","Kossenkov AV","Song J","Liang C","Gao SJ","Murphy ME","Guo H","Jung JU","Liang J","Lieberman PM","Salvino JM","Mansoori B","Zhu Q","Feng P","Liang Q"],"additional_accession":[]},"is_claimable":false,"name":"Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production.","description":"Mitochondrial dynamics are pivotal for host immune responses upon infection, yet how viruses manipulate these processes to impair host defence and enhance viral fitness remains unclear. Here we show that Kaposi's sarcoma-associated herpesvirus (KSHV), an oncogenic virus also known as human herpesvirus 8, encodes Bcl-2 (vBcl-2), which reprogrammes mitochondrial architecture. It binds with NM23-H2, a host nucleoside diphosphate (NDP) kinase, to stimulate GTP loading of the dynamin-related protein (DRP1) GTPase, which triggers mitochondrial fission, inhibits mitochondrial antiviral signalling protein (MAVS) aggregation and impairs interferon responses in cell lines. An NM23-H2-binding-defective vBcl-2 mutant fails to evoke fission, leading to defective virion assembly due to activated MAVS-IF","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jun","modification":"2026-05-29T16:34:18.046Z","creation":"2026-04-08T05:24:11.824Z"},"accession":"S-EPMC12337130","cross_references":{"pubmed":["40404827"],"doi":["10.1038/s41564-025-02018-3"]}}