SARS-CoV INFLAMMATORY RESPONSE

An innate immune response against SARS-CoV infection is triggered by the recognition of pathogen-associated molecular patterns (PAMPs, dsRNA) by pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs). Activated receptors recruit adaptor proteins, which trigger the activation of multiple kinases, ultimately activating transcription factors including interferon regulatory factor3 (IRF3) and nuclear factor kappa- light-chain-enhancer of activated B cells (NF-κB). NF-kB promotes the production of type I interferons (IFN-I), which are released and bind the IFN-α/β receptor (IFNAR) expressed on the surface of other cells. This inflammatory response to SARS-CoV infection represents the first line defense against the virus. Coronaviruses interfere with several steps of the immune response, including RNA sensing, type I IFN production and IFN dependent signaling.

针对严重急性呼吸综合征冠状病毒（SARS-CoV）感染的固有免疫应答，可通过模式识别受体（pattern recognition receptors，PRRs）识别作为病原体相关分子模式（pathogen-associated molecular patterns，PAMPs）的双链RNA（dsRNA）而触发，这类受体包括Toll样受体（Toll-like receptors，TLRs）与RIG-I样受体（RIG-I-like receptors，RLRs）。激活的受体会招募衔接蛋白，进而激活多种激酶，最终激活包括干扰素调节因子3（interferon regulatory factor 3，IRF3）与核因子κB（nuclear factor kappa-light-chain-enhancer of activated B cells，NF-κB）在内的转录因子。核因子κB可促进I型干扰素（type I interferons，IFN-I）的合成与释放，后者可结合其他细胞表面表达的IFN-α/β受体（IFN-α/β receptor，IFNAR）。这种针对SARS-CoV感染的炎症应答是机体抵御病毒的第一道防线。冠状病毒可干扰固有免疫应答的多个环节，包括RNA感知、I型干扰素合成以及干扰素依赖性信号通路。