There is an A33-dependent mechanism for the incorporation of B5-GFP into vaccinia virus extracellular enveloped virions
There is an A33-dependent mechanism for the incorporation of B5-GFP into vaccinia virus extracellular enveloped virions
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DOI：
10.1016/j.virol.2010.03.017
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发表时间：
2010-06-20
期刊：
影响因子：
3.7
通讯作者：
Ward, Brian M.
中科院分区：
文献类型：
--
作者：
Chan, Winnie M.;Ward, Brian M.
正痘病毒产生两种抗原上不同的感染性病毒粒子，细胞内成熟病毒粒子和细胞外病毒粒子（EV）。A33和B5存在于EV上，而不在细胞内成熟病毒粒子上。为了研究A33的功能，我们构建了一种缺失A33R并表达B5R-GFP的重组病毒（vB5R-GFP/Delta A33R）。将vB5R-GFP/Delta A33R与类似病毒（v Delta A33R）进行比较，发现在存在A33R时不明显的感染性EV产生的额外缺陷。对这些重组体的表征表明，在缺乏A33的情况下产生的EV具有无法检测到的B5-GFP水平。两种重组体释放的EV量相似，但感染性不同。尽管由vB5R-GFP/Delta A33R产生的EV不含B5，但由这些重组体产生的病毒粒子能够结合细胞的数量大致相同。这些结果表明，在缺乏A33的情况下，B5的细胞质尾部有助于其进入子代病毒粒子的包膜。(C) 2010爱思唯尔公司版权所有。
Orthopoxviruses produce two, antigenically distinct, infectious virions, intracellular mature virions and extracellular virions (EV). A33 and B5 are found on EV but not on intracellular mature virions. To investigate the function of A33, a recombinant virus that has A33R deleted and expresses B5R-GFP (vB5R-GFP/Delta A33R) was generated. A comparison of vB5R-GFP/Delta A33R to an analogous virus (v Delta A33R) revealed an additional defect in infectious EV production that was not apparent when A33R was present. Characterization of these recombinants revealed that EV produced in the absence of A33 had undetectable levels of B5-GFP. Both recombinants released similar amounts of EV but there were differences in their infectivity. Approximately equal numbers of virions produced by these recombinants were able to bind cells even though EV produced by vB5R-GFP/Delta A33R do not contain B5. These results suggest that in the absence of A33, the cytoplasmic tail of B5 contributes to its incorporation into the envelope of progeny Virions. (C) 2010 Elsevier Inc. All rights reserved.