title: Increased mitochondrial functions in human glioblastoma cells persistently infected with measles virus.
abstract: Measles virus (MV) is known for its ability to cause an acute infection with a potential of development of persistent infection. However, knowledge of how viral genes and cellular factors interact to cause or maintain the persistent infection has remained unclear. We have previously reported the possible involvement of mitochondrial short chain enoyl-CoA hydratase (ECHS), which is localized at mitochondria, in the regulation of MV replication. In this study we found increased functions of mitochondria in MV-persistently infected cells compared with uninfected or acutely infected cells. Furthermore, impairment of mitochondrial functions by treatment with mitochondrial inhibitors such as ethidium bromide (EtBr) or carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) induced the cytopathic effects of extensive syncytial formation in persistently infected cells. These findings suggest that mitochondria are one of the subcellular organelles contributing to regulate persistent infection of MV. Recent studies showed mitochondria provide an integral platform for retinoic acid-inducible protein (RIG-I)-like cytosolic receptors (RLRs) signaling and participate in cellular innate antiviral immunity. Our findings not only reveal a role of mitochondria in RLR mediated antiviral signaling but also suggest that mitochondria contribute to the regulation of persistent viral infection.
authors.affiliation: Department of Microbiology and Immunology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. Electronic address: megumi@nms.ac.jp.
authors.forename: Megumi
authors.initials: M
authors.lastname: Takahashi
authors.forename: Alexander M
authors.initials: AM
authors.lastname: Wolf
authors.forename: Eiji
authors.initials: E
authors.lastname: Watari
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Norose
authors.forename: Shigeo
authors.initials: S
authors.lastname: Ohta
authors.forename: Hidemi
authors.initials: H
authors.lastname: Takahashi
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D005909:Glioblastoma / Q000235:genetics / Q000378:metabolism / Q000821:virology*; D006801:Humans; D008457:Measles / Q000235:genetics / Q000378:metabolism / Q000821:virology*; D008459:Measles virus / Q000187:drug effects / Q000502:physiology*; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D015854:Up-Regulation; D014779:Virus Replication / Q000187:drug effects
chemical_list: D000255:Adenosine Triphosphate
keywords: Measles virus; Mitochondria; Mitochondrial membrane potential; Oxidative stress condition; Persistent infection