Innate immune control of West Nile virus infection

被引:37
作者
Arjona, Alvaro [1 ,2 ]
Wang, Penghua [1 ]
Montgomery, Ruth R. [3 ]
Fikrig, Erol [1 ,4 ]
机构
[1] Yale Univ, Sch Med, Sect Infect Dis, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Thomson Reuters IP & Sci, New Haven, CT USA
[3] Yale Univ, Sch Med, Sect Rheumatol, New Haven, CT USA
[4] Howard Hughes Med Inst, Chevy Chase, MD USA
关键词
TOLL-LIKE RECEPTOR-3; DISEASE-VECTOR MOSQUITOS; ANTIGEN-PRESENTING CELLS; DOUBLE-STRANDED-RNA; DENDRITIC CELLS; ANTIVIRAL RESPONSE; ANOPHELES-GAMBIAE; AEDES-AEGYPTI; ENCEPHALITIS-VIRUS; IN-VITRO;
D O I
10.1111/j.1462-5822.2011.01649.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
West Nile virus (WNV), from the Flaviviridae family, is a re-emerging zoonotic pathogen of medical importance. In humans, WNV infection may cause life-threatening meningoencephalitis or long-term neurologic sequelae. WNV is transmitted by Culex spp. mosquitoes and both the arthropod vector and the mammalian host are equipped with antiviral innate immune mechanisms sharing a common phylogeny. As far as the current evidence is able to demonstrate, mosquitoes primarily rely on RNA interference, Toll, Imd and JAK-STAT signalling pathways for limiting viral infection, while mammals are provided with these and other more complex antiviral mechanisms involving antiviral effectors, inflammatory mediators, and cellular responses triggered by highly specialized pathogen detection mechanisms that often resemble their invertebrate ancestry. This mini-review summarizes our current understanding of how the innate immune systems of the vector and the mammalian host react to WNV infection and shape its pathogenesis.
引用
收藏
页码:1648 / 1658
页数:11
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