Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.
Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.
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DOI：
10.1016/j.virol.2015.06.006
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发表时间：
2015-10
期刊：
影响因子：
3.7
通讯作者：
Feuer R
中科院分区：
文献类型：
--
作者：
Sin J;Mangale V;Thienphrapa W;Gottlieb RA;Feuer R
柯萨奇病毒（CV）是相对常见的病毒，与许多严重的人类疾病有关，包括心肌炎和脑膜脑炎。这些病毒被认为具有溶细胞性，但可以在某些宿主组织内持续较长时间，需要逃避宿主免疫反应并大大降低复制率。作为小核糖核酸病毒科的一员，CV 历来被认为是无包膜病毒，尽管最近的证据表明 CV 和其他小核糖核酸病毒会劫持宿主膜并获得包膜。获得包膜可能会给 CV 病毒体带来明显的好处，例如对中和抗体的抵抗力和有效的非裂解性病毒传播。 CV 对宿主中的祖细胞表现出独特的趋向性，这可能有助于解释年轻宿主对感染的易感性以及成人慢性疾病的形成。 CV 还被证明可以利用自噬来最大限度地提高病毒复制并协助靶细胞进行非常规释放。在本文中，我们回顾了在阐明病毒在宿主细胞内复制和传播、确定向性决定因素以及确定病毒逃避宿主免疫反应的策略方面的最新进展。此外，我们将强调尚未解答的问题，并提供有关 CV 发病机制的未来观点。
Coxsackieviruses (CVs) are relatively common viruses associated with a number of serious human diseases, including myocarditis and meningo-encephalitis. These viruses are considered cytolytic yet can persist for extended periods of time within certain host tissues requiring evasion from the host immune response and a greatly reduced rate of replication. A member of Picornaviridae family, CVs have been historically considered non-enveloped viruses – although recent evidence suggest that CV and other picornaviruses hijack host membranes and acquire an envelope. Acquisition of an envelope might provide distinct benefits to CV virions, such as resistance to neutralizing antibodies and efficient nonlytic viral spread. CV exhibits a unique tropism for progenitor cells in the host which may help to explain the susceptibility of the young host to infection and the establishment of chronic disease in adults. CVs have also been shown to exploit autophagy to maximize viral replication and assist in unconventional release from target cells. In this article, we review recent progress in clarifying virus replication and dissemination within the host cell, identifying determinants of tropism, and defining strategies utilized by the virus to evade the host immune response. Also, we will highlight unanswered questions and provide future perspectives regarding the potential mechanisms of CV pathogenesis.