病毒感染对宿主TLRs模式识别与免疫应答信号的影响

Modulation of the Host Toll-like Receptor Signaling Pathways by Virus Infection

TLRs是一类古老的天然模式识别分子,通过识别病毒的PAMPs,活化依赖和非依赖于MyD88的信号通路,诱导IFNs、促炎性细胞因子和趋化因子等分子的释放和表达,清除病毒的感染;同时,病毒为了感染宿主,采用多种免疫逃避策略干扰机体TLRs的信号,尤其调节MyD88、NF-κB、TRIF和IRFs等重要信号分子,以逃避机体天然PRRs的监视、识别和清除。因此,本文重点以VACV、HCV和HIV为例,介绍病毒感染对宿主TLRs模式识别与免疫应答信号的调节,以进一步理解病毒与宿主相互作用的复杂性,为病毒病的有效防治提供理论依据。

Toll-like receptors （TLRs） are germline-encoded pattern recognition receptors （PRRs） that play a central role in host cell recognition and responses to virus infection, leading to the production of interferons（IFNs） and proinflammatory cytokines. In parallel, in order to establish an infection, viruses have to develop exclusively strategies to interfere with TLRs signaling, particularly some important adaptors activation such as MyD88, NF-kB, TRIF and IRFs, and suppress or escape host＇s antiviral immune response. In this paper, we review the latest findings on the various strategies used by viruses to modulate TLRs-mediated innate immune response, with special emphasis on immune evasion mechanism of VACV, HCV and HIV. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses hamper TLRs signaling and how to overcome viral infection.