title: Virus-neuron interactions in the mouse brain infected with Japanese encephalitis virus.
abstract: The virus-host interactions between Japanese encephalitis (JE) virus and mouse brain neurons were analyzed by electron microscopy. JE virus replicated exclusively in the rough endoplasmic reticulum (RER) of neurons. In the early phase of infection, the perikaryon of infected neurons had relatively normal-looking lamellar RER whose cisternae showed focal dilations containing progeny virions and characteristic endoplasmic reticulum (ER) vesicles. The reticular RER, consisted of rows of ribosomes surrounding irregular-shaped, membrane-unbounded cisternae and resembled that observed in JE-virus-infected PC12 cells, were also seen adjacent to the lamellar RER. The appearance of the reticular RER indicated that RER morphogenesis occurred in infected neurons in association with the viral replication. The fine network of Golgi apparatus was extensively obliterated by fragmentation and dissolution of the Golgi membranes and their replacement by the electron-lucent material. As the infection progressed, the lamellar RER was increasingly replaced by the hypertrophic RER which had diffusely dilated cisternae containing multiple progeny virions and ER vesicles. The Golgi apparatus, at this stage, was seen as coarse, localized Golgi complexes near the hypertrophic RER. In the later phase of infection, RER of infected neurons showed a degenerative change, with the cystically dilated cisternae being filled with ER vesicles and virions. Small, localized Golgi complexes frequently showed vesiculation, vacuolation, and dispersion. The present study, therefore, indicated that during the viral replication the normal lamellar RER which synthesized neuronal secretory and membrane proteins was replaced by the hypertrophic RER which synthesized the viral proteins. The hypertrophic RER eventually degenerated into cystic RER whose cisternae were filled with viral products. The constant degenerative change which occurred in the Golgi apparatus during the viral replication suggested that some of the viral proteins transported from RER to the Golgi apparatus were harmful to the Golgi apparatus and that increasing damage to the Golgi apparatus during the viral replication played the principal role in the pathogenesis of JE-virus-infected neurons in the central nervous system.
authors.affiliation: Department of Ultrastructural Pathology, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
authors.forename: T
authors.initials: T
authors.lastname: Hase
mesh_terms: D000818:Animals; D001921:Brain / Q000382:microbiology* / Q000648:ultrastructure; D004664:Encephalitis Virus, Japanese / Q000502:physiology*; D004672:Encephalitis, Japanese / Q000382:microbiology / Q000473:pathology*; D004721:Endoplasmic Reticulum / Q000382:microbiology / Q000648:ultrastructure; D006056:Golgi Apparatus / Q000648:ultrastructure; D051379:Mice; D008813:Mice, Inbred ICR; D008854:Microscopy, Electron; D009474:Neurons / Q000382:microbiology* / Q000648:ultrastructure; D014764:Viral Proteins / Q000378:metabolism; D014779:Virus Replication
chemical_list: D014764:Viral Proteins