Autor(es): Morrison Thomas E, Simmons Jason D, Heise Mark T

Resumo: Alphaviruses such as Ross River virus (RRV) - chikungunya virus are mosquito-transmitted viruses that cause explosive epidemics of debilitating arthritis - myositis affecting millions of humans worldwide. Previous studies using a mouse model of RRV-induced disease demonstrated that viral infection results in a severe inflammatory arthritis - myositis - that complement component 3 (C3) contributes to the destructive phase of the inflammatory disease but not the recruitment of cellular infiltrates to the sites of RRV-induced inflammation. Here, we demonstrate that mice deficient in complement receptor 3 (CR3) (CD11b(-/-)), a signaling receptor activated by multiple lig-s including the C3 cleavage fragment iC3b, develop less-severe disease signs - decreased tissue destruction compared to RRV-infected wild-type mice. CR3 deficiency had no effect on viral replication, nor did it diminish the magnitude, kinetics, - composition of the cellular infiltrates at the sites of inflammation. However, the genetic absence of CR3 diminished the expression of specific proinflammatory - cytotoxic effectors, including S100A9/S100A8 - interleukin-6, within the inflamed tissues, suggesting that CR3-dependent signaling at the sites of inflammation contributes to tissue damage - severe disease.

Imprenta: Journal of Virology, v. 82, n. 22, p. 11263-11272, 2008

Identificador do objeto digital: 10.1128/JVI.01352-08

Descritores: Chikungunya virus - Biosynthesis ; Chikungunya virus - Cytopathology ; Chikungunya virus - Pathogenesis ; Chikungunya virus - Proteins ; Chikungunya virus - Cytokines ; Chikungunya virus - Inflammation ; Chikungunya virus - Viral infections ; Chikungunya Virus - Virus ; Chikungunya virus - Vaccine ; Chikungunya virus - Epidemic ; Chikungunya virus - Immunology ; Chikungunya virus - Public health

Data de publicação: 2008

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