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排斥超感染病毒:一种快速病毒传播的机制。

Repulsion of superinfecting virions: a mechanism for rapid virus spread.

机构信息

Department of Virology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK.

出版信息

Science. 2010 Feb 12;327(5967):873-876. doi: 10.1126/science.1183173. Epub 2010 Jan 21.

DOI:10.1126/science.1183173
PMID:20093437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4202693/
Abstract

Viruses are thought to spread across susceptible cells through an iterative process of infection, replication, and release, so that the rate of spread is limited by replication kinetics. Here, we show that vaccinia virus spreads across one cell every 75 minutes, fourfold faster than its replication cycle would permit. To explain this phenomenon, we found that newly infected cells express two surface proteins that mark cells as infected and, via exploitation of cellular machinery, induce the repulsion of superinfecting virions away toward uninfected cells. Mechanistically, early expression of proteins A33 and A36 was critical for virion repulsion and rapid spread, and cells expressing these proteins repelled exogenous virions rapidly. Additional spreading mechanisms may exist for other viruses that also spread faster than predicted by replication kinetics.

摘要

病毒被认为通过感染、复制和释放的迭代过程在易感细胞中传播,因此传播速度受到复制动力学的限制。在这里,我们表明,牛痘病毒每 75 分钟跨越一个细胞传播,比其复制周期快四倍。为了解释这一现象,我们发现新感染的细胞表达两种表面蛋白,将细胞标记为感染细胞,并通过利用细胞机制,诱导超感染病毒粒子远离未感染细胞。从机制上讲,早期表达蛋白 A33 和 A36 对于病毒粒子的排斥和快速传播至关重要,并且表达这些蛋白的细胞能够迅速排斥外源性病毒粒子。对于其他传播速度超过复制动力学预测的病毒,可能存在其他传播机制。

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本文引用的文献

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Expression of the A56 and K2 proteins is sufficient to inhibit vaccinia virus entry and cell fusion.A56和K2蛋白的表达足以抑制痘苗病毒的进入和细胞融合。
J Virol. 2009 Feb;83(4):1546-54. doi: 10.1128/JVI.01684-08. Epub 2008 Nov 26.
2
Vaccinia virus morphogenesis and dissemination.痘苗病毒的形态发生与传播。
Trends Microbiol. 2008 Oct;16(10):472-9. doi: 10.1016/j.tim.2008.07.009. Epub 2008 Sep 12.
3
The vaccinia virus fusion inhibitor proteins SPI-3 (K2) and HA (A56) expressed by infected cells reduce the entry of superinfecting virus.受感染细胞表达的痘苗病毒融合抑制蛋白SPI-3(K2)和HA(A56)可减少超感染病毒的进入。
Virology. 2008 Oct 25;380(2):226-33. doi: 10.1016/j.virol.2008.07.020. Epub 2008 Aug 28.
4
Association of vaccinia virus fusion regulatory proteins with the multicomponent entry/fusion complex.痘苗病毒融合调节蛋白与多组分进入/融合复合体的关联
J Virol. 2007 Jun;81(12):6286-93. doi: 10.1128/JVI.00274-07. Epub 2007 Apr 4.
5
Interaction between vaccinia virus extracellular virus envelope A33 and B5 glycoproteins.痘苗病毒细胞外病毒包膜A33和B5糖蛋白之间的相互作用。
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6
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