Cellular resistance to arbovirus infection.
When an arbovirus enters an arthropod in an infected blood meal, several mechanisms may interact to affect its life cycle and ultimate transmissibility. Intrinsic absolute failure in the establishment of infection must be contrasted with infection that is successfully established but is variably modulated in its viral yield throughout the vector's life-span. Degrees of vertebrate host resistance make this modulation a central factor in determining whether an arthropod is an important vector in nature; moreover, human intervention that affects modulating mechanisms may become a basis for disease control. In the absence of evidence of real immune resistance to arbovirus infections in arthropods, other more primitive modulating mechanisms must be considered: interferonlike substances may be formed in arthropod cells; arthropod cells may "cure" themselves by a unique endophagocytic digestion of their virus burden; homologous interference with viral replicative processes may be mediated via wild or mutant viral RNA species acting to shut down further RNA synthesis; and homologous interference may be mediated by RNA of defective-interfering virus formed earlier in infection.
D000330:Aedes / Q000276:immunology / Q000382:microbiology; D000818:Animals; D001103:Arboviruses / Q000254:growth & development* / Q000276:immunology; D001181:Arthropods / Q000276:immunology / Q000382:microbiology*; D003465:Culex / Q000382:microbiology; D003673:Defective Viruses / Q000254:growth & development; D004663:Encephalitis Virus, Eastern Equine / Q000254:growth & development; D004665:Encephalitis Virus, St. Louis / Q000254:growth & development; D009154:Mutation; D012367:RNA, Viral / Q000096:biosynthesis; D014158:Transcription, Genetic; D014762:Viral Interference; D014779:Virus Replication
D012367:RNA, Viral