title: Innate immunity in viral encephalitis: role of C5.
abstract: The complement system is a critical component of both the innate and acquired immune systems. It is important in host defense against viruses, bacteria, and fungi for opsonization and for lysis of pathogens. However, activated complement can also cause tissue damage. There is compelling evidence that complement factors are presented in the central nervous system (CNS). Complement activation (by any of the three pathways: classical, alternate, and lectin) can lead to inflammation and tissue damage, while at the same time may also restrict certain pathogens in the CNS. C5a is formed by proteolytic cleavage C5. C5a is considered the most potent proinflammatory mediator, often called an anaphylotoxin. In this communication, we examine the roles of C5 (C5a) in vesicular stomatitis virus (VSV)-induced encephalitis. We found that C5a is produced during VSV infection, but C5-deficient mice had similar pathology as their controls. We concluded that C5 is not a critical factor in mediating the host response during VSV encephalitis.
authors.affiliation: Department of Biology, New York University, New York 10003-6688, USA.
authors.forename: Nannan
authors.initials: N
authors.lastname: Chen
authors.forename: Carol Shoshkes
authors.initials: CS
authors.lastname: Reiss
mesh_terms: D000818:Animals; D016466:CHO Cells; D002490:Central Nervous System / Q000276:immunology; D015936:Complement C5a / Q000276:immunology*; D006224:Cricetinae; D004195:Disease Models, Animal; D018792:Encephalitis, Viral / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009569:Nitric Oxide / Q000096:biosynthesis; D018353:Rhabdoviridae Infections / Q000453:epidemiology / Q000276:immunology*; D014721:Vesicular stomatitis Indiana virus / Q000276:immunology*
chemical_list: D009569:Nitric Oxide; D015936:Complement C5a