Restriction of avian reovirus in primary chicken embryo tendon cells.
Upon infection of the gastrointestinal tract, some avian reovirus strains spread to multiple organs of their natural hosts, chickens, and establish persistent infections. One manifestation of chronic infection is the development of arthritis in the tendons of the chickens. In order to study events associated with persistent infections in the tendon, primary cultures of chick embryo tendon (CET) cells were infected with avian reovirus. The CET cells supported a noncytopathic infection for at least 16 days, shedding lower amounts of progeny virus than a permissive cell culture, chick embryo fibroblasts (CEF). The virus from the CET cells was predominantly cell-associated unlike virus from the CEF cells. Initiation of infection was much slower in CET cells as indicated by fewer cells expressing antigen or exporting virus over the first 48 hr. However, most CET cells gained these abilities over the course of infection. Initial events in virus infection, binding, and penetration were not impaired in tendon cells but transcription of single-strand RNA was delayed and double-strand RNA production was clearly inhibited. The CET cells supported efficient replication of another avian virus, Newcastle disease virus, suggesting that restriction for avian reovirus is virus specific, in addition to being tissue specific.
Huang
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Department of Immunology/Microbiology, Rush Medical College, Chicago, Illinois 60612.
D000818:Animals; D001483:Base Sequence; D002478:Cells, Cultured; D002642:Chick Embryo; D003588:Cytopathogenic Effect, Viral; D005347:Fibroblasts / Q000166:cytology / Q000821:virology; D008969:Molecular Sequence Data; D009522:Newcastle disease virus / Q000502:physiology; D012367:RNA, Viral / Q000096:biosynthesis; D012087:Reoviridae / Q000502:physiology* / Q000648:ultrastructure; D013710:Tendons / Q000166:cytology / Q000821:virology*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
D012367:RNA, Viral; D014764:Viral Proteins