Human coronaviruses: viral and cellular factors involved in neuroinvasiveness and neuropathogenesis.
Human coronaviruses: viral and cellular factors involved in neuroinvasiveness and neuropathogenesis.
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DOI：
10.1016/j.virusres.2014.09.011
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发表时间：
2014-12-19
期刊：
影响因子：
5
通讯作者：
Talbot PJ
中科院分区：
文献类型：
--
作者：
Desforges M;Le Coupanec A;Stodola JK;Meessen-Pinard M;Talbot PJ
人类冠状病毒（HCoV）对小鼠和人类都具有天然的神经侵入性。跨神经元途径和血液途径都可能使病毒侵入中枢神经系统。神经元感染导致兴奋性毒性、神经变性和细胞死亡。HCoV可能与人类神经系统疾病有关。在感染人类的各种呼吸道病毒中，冠状病毒是重要的病原体，通常感染上呼吸道，主要与普通感冒有关。然而，在更脆弱的人群中，如新生儿、婴儿、老年人和免疫功能低下的个体，这些机会性病原体也可影响下呼吸道，导致肺炎、哮喘加重和各种类型的呼吸窘迫综合征。自20世纪60年代以来，人类冠状病毒对呼吸道的影响已经明确确立。然而，近三十年来，科学文献中报告的数据也表明，就像对其他人类病毒的描述一样，冠状病毒具有神经侵入能力，因为它们可以从呼吸道传播到中枢神经系统（CNS）。一旦到达那里，中枢神经系统细胞的感染（嗜神经性）可能导致人类健康问题，如脑炎和长期神经系统疾病。神经侵入性冠状病毒可能会损害中枢神经系统，因为宿主免疫反应可能与易感个体的自身免疫有关（病毒诱导的神经免疫病理）和/或病毒复制，直接诱导中枢神经系统细胞损伤（病毒诱导的神经病理）。鉴于所有这些特性，有人认为这些机会性人类呼吸道病原体可能与触发或加剧病因尚不清楚的神经系统疾病有关。在此，我们提出宿主和病毒因子参与调节与人类冠状病毒感染中枢神经系统相关的可能致病过程，我们试图破译病毒和宿主靶细胞之间复杂的相互作用，以表征它们在病毒生命周期中的作用以及细胞对病毒入侵的反应能力。
Human coronavirus (HCoV) are naturally neuroinvasive in both mice and humans. Both transneuronal and hematogenous route may allow virus invasion of the CNS. Infection of neurons leads to excitotoxicity, neurodegeneration and cell-death. HCoV are potentially associated with human neurological disorders. Among the various respiratory viruses infecting human beings, coronaviruses are important pathogens, which usually infect the upper respiratory tract, where they are mainly associated with common colds. However, in more vulnerable populations, such as newborns, infants, the elderly and immune-compromised individuals, these opportunistic pathogens can also affect the lower respiratory tract, leading to pneumonia, exacerbations of asthma, and various types of respiratory distress syndrome. The respiratory involvement of human coronaviruses has been clearly established since the 1960s. Nevertheless, for almost three decades now, data reported in the scientific literature has also demonstrated that, like it was described for other human viruses, coronaviruses have neuroinvasive capacities since they can spread from the respiratory tract to the central nervous system (CNS). Once there, infection of CNS cells (neurotropism) could lead to human health problems, such as encephalitis and long-term neurological diseases. Neuroinvasive coronaviruses could damage the CNS as a result of misdirected host immune responses that could be associated with autoimmunity in susceptible individuals (virus-induced neuroimmunopathology) and/or viral replication, which directly induces damage to CNS cells (virus-induced neuropathology). Given all these properties, it has been suggested that these opportunistic human respiratory pathogens could be associated with the triggering or the exacerbation of neurologic diseases for which the etiology remains poorly understood. Herein, we present host and viral factors that participate in the regulation of the possible pathogenic processes associated with CNS infection by human coronaviruses and we try to decipher the intricate interplay between virus and host target cells in order to characterize their role in the virus life cycle as well as in the capacity of the cell to respond to viral invasion.
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DOI：
10.1016/j.clim.2007.02.002
发表时间：
2007-06
期刊：
Clinical immunology (Orlando, Fla.)
影响因子：
--
作者：
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通讯作者：
Talbot PJ
影响因子：
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影响因子：
5.4
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影响因子：
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影响因子：
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作者：
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