详细记录  
题名: Human immunopathogenesis of severe acute respiratory syndrome (SARS)
作者:Mark J. Cameron, Jesus F. Bermejo-Martin, Ali Danesh, Matthew P. Muller and David J. Kelvin
来源:Virus Research[IF=2.562], In Press, Corrected Proof, Available online 19 March 2007,
URL :http://dx.doi.org/10.1016/j.virusres.2007.02.014
日期:070415
摘要: Mark J. Camerona, b, , Jesus F. Bermejo-Martinc, , Ali Danesha, b, , Matthew P. Mullerb, d, and David J. Kelvina, b, ,

aUniversity Health Network, MaRS Centre, 101 College Street, Toronto, Ontario M5G 1L7, Canada
bUniversity of Toronto, 1 King s College Circle, Toronto, Ontario M5S 1A8, Canada
cUniversity of Valladolid, Ramn y Cajal 7, Valladolid 47005, Spain
dMount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada

Available online 19 March 2007.

Summary

Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host. 19.

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