Coronaviruses post-SARS: update on replication and pathogenesis.
Coronaviruses post-SARS: update on replication and pathogenesis.
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DOI：
10.1038/nrmicro2147
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发表时间：
2009-06
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冠状病毒是一种正链RNA病毒，可引起人类、家畜和伴侣动物的疾病。它们最臭名昭著的是在2002-2003年引起严重急性呼吸系统综合征（SARS）爆发。所有冠状病毒都遵循相同的基本复制策略。所有冠状病毒编码15或16个复制酶相关蛋白，4或5个结构蛋白和1-8个组特异性或辅助蛋白。许多复制酶蛋白在双膜囊泡（DMV）和来自内质网的网状膜网络中组装成复制机制。冠状病毒很容易跨物种传播。当SARS冠状病毒从蝙蝠跨越物种到达中间宿主（如果子狸），然后到达人类时，就说明了这一现象。这也解释了包括人类在内的大量物种感染与牛冠状病毒密切相关的病毒的原因。在许多冠状病毒感染中，疾病严重程度在病毒清除期间增加，这表明宿主免疫反应既是保护性的，也是致病性的。此外，免疫应答的特定方面的抑制导致较不严重的疾病和较少的组织破坏，而不减少病毒清除的动力学。像所有成功的病毒一样，冠状病毒已经进化出被动和主动机制来逃避干扰素反应。DMV中的复制可能会使双链RNA无法到达细胞传感器，从而导致先天免疫反应的被动逃避。冠状病毒在2002-2003年SARS爆发期间获得了突出地位，但有许多不同的冠状病毒感染人类和动物。Perlman和Netland描述了冠状病毒的生物学，包括它们的复制，宿主免疫反应和种间传播。虽然冠状病毒在近60年前首次被发现，但直到2003年，当其中一个成员被确定为严重急性呼吸系统综合征的病原体时，它们才声名狼借。以前已知这些病毒是家畜和伴侣动物的呼吸道和肠道感染的重要病原体，并导致约15%的普通感冒病例。本文综述了冠状病毒复制机制、与宿主免疫反应的相互作用以及疾病发病机制的最新进展。它还强调了最近发现的许多新型冠状病毒以及该病毒家族跨越物种障碍的倾向。
Coronaviruses are positive strand RNA viruses that cause disease in humans, and domestic and companion animals. They are most notorious for causing severe acute respiratory syndrome (SARS) outbreaks in 2002–2003. All coronaviruses follow the same basic strategy of replication. All coronaviruses encode 15 or 16 replicase related proteins, 4 or 5 structural proteins and 1–8 group-specific or accessory proteins. Many of the replicase proteins are assembled into replication machinery in double-membrane vesicles (DMVs) and on a reticular network of membranes that are derived from the endoplasmic reticulum. Coronaviruses are readily transmitted across species. This phenomenon was illustrated when the SARS-coronavirus crossed species from bats to intermediate hosts, such as palm civets, and then to humans. It also explains the large number of species, including humans, that are infected with viruses closely related to bovine coronavirus. In many coronavirus infections, disease severity increases during virus clearance, suggesting that the host immune response is both protective and pathogenic. Furthermore, inhibition of specific aspects of the immune response results in less severe disease and less tissue destruction, without diminishing the kinetics of virus clearance. Like all successful viruses, coronaviruses have evolved both passive and active mechanisms to evade the interferon response. Replication in DMVs may contribute to passive evasion of the innate immune response by making double-stranded RNA inaccessible to cellular sensors. Coronaviruses gained prominence during the SARS outbreaks of 2002–2003, but there are many different coronaviruses that infect humans and animals. Perlman and Netland describe the biology of the coronaviruses, including their replication, host immune response and interspecies transmission. Although coronaviruses were first identified nearly 60 years ago, they only received notoriety in 2003 when one of their members was identified as the aetiological agent of severe acute respiratory syndrome. Previously these viruses were known to be important agents of respiratory and enteric infections of domestic and companion animals and to cause approximately 15% of all cases of the common cold. This Review focuses on recent advances in our understanding of the mechanisms of coronavirus replication, interactions with the host immune response and disease pathogenesis. It also highlights the recent identification of numerous novel coronaviruses and the propensity of this virus family to cross species barriers.
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