Exploring the immunogenic properties of SARS-CoV-2 structural proteins: PAMP:TLR signaling in the mediation of the neuroinflammatory and neurologic sequelae of COVID-19.
Exploring the immunogenic properties of SARS-CoV-2 structural proteins: PAMP:TLR signaling in the mediation of the neuroinflammatory and neurologic sequelae of COVID-19.
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DOI：
10.1016/j.bbi.2023.04.009
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发表时间：
2023-07
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严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）在感染的急性期和急性期后（PASC; SARS-CoV-2感染的急性期后后遗症）产生一系列神经系统和神经精神症状。神经炎症过程被认为是这些症状的病因学中的关键因素。已经提出了支持脑中炎症事件发展的几种机制，包括SARS-CoV-2嗜神经性和外周炎症反应（即，细胞因子风暴）感染，这可能会通过免疫到大脑的信号通路产生神经炎症。在这篇综述中，我们探讨了支持结构蛋白（例如，来自SARS-CoV-2病毒粒子的刺突和刺突S1亚基）作为病原体相关分子模式（PAMP）起作用，以通过经典的Toll样受体（TLR）炎症途径在外周和/或脑中引发促炎免疫应答。我们认为SARS-CoV-2结构蛋白可能直接在大脑中产生炎症过程，独立于和/或除了外周促炎作用，这可能会在COVID-19的神经/神经精神症状的发展中发挥因果作用。
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) produces an array of neurologic and neuropsychiatric symptoms in the acute and post-acute phase of infection (PASC; post-acute sequelae of SARS-CoV-2 infection). Neuroinflammatory processes are considered key factors in the etiology of these symptoms. Several mechanisms underpinning the development of inflammatory events in the brain have been proposed including SARS-CoV-2 neurotropism and peripheral inflammatory responses (i.e., cytokine storm) to infection, which might produce neuroinflammation via immune-to-brain signaling pathways. In this review, we explore evidence in support of an alternate mechanism whereby structural proteins (e.g., spike and spike S1 subunit) derived from SARS-CoV-2 virions function as pathogen-associated molecular patterns (PAMPs) to elicit proinflammatory immune responses in the periphery and/or brain via classical Toll-Like Receptor (TLR) inflammatory pathways. We propose that SARS-CoV-2 structural proteins might directly produce inflammatory processes in brain independent of and/or in addition to peripheral proinflammatory effects, which might converge to play a causal role in the development of neurologic/neuropsychiatric symptoms in COVID-19.
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