是否有证据支持猿猴多瘤病毒 SV40 VP4 病毒孔蛋白的存在？
Does the Evidence Support the Existence of the Simian Polyomavirus SV40 Vp4 Viroporin?
机构信息
University Hospital of North Norway, Department of Microbiology and Infection Control, Tromsø, Norway
UiT The Arctic University of Norway, Department of Clinical Medicine, Metabolic and Renal Research Group, Tromsø, Norway.
出版信息
mSphere. 2020 Mar 18;5(2):e00019-20. doi: 10.1128/mSphere.00019-20.
The simian polyomavirus SV40 was reported to express Vp4, an N-terminally truncated form of the minor capsid proteins Vp2 and Vp3. Since a missense mutation of the putative Vp4 start codon (Vp2M228I) was found to give reduced progeny release and delayed lysis, Vp4 was claimed to be a viroporin. However, two independent research groups, including our own, were unable to replicate these findings. In contrast, we found no Vp4 expression in SV40-infected cells and no reduction in progeny release for Vp4-deficient virus, and finally, we found that the single amino acid substitution unavoidably introduced into the overlapping Vp2/Vp3 genes during Vp4 mutagenesis reduced early steps but not virus release. Remarkably, the existence of the viroporin Vp4 still seems to be widely accepted, which presumably is preventing important research on polyomavirus release. With this perspective, we will review and comment on the most important experiments that led to the disputed announcement of the viroporin Vp4.
猴多瘤病毒 SV40 被报道表达 Vp4，这是次要衣壳蛋白 Vp2 和 Vp3 的 N 端截断形式。由于假定的 Vp4 起始密码子（Vp2M228I）的错义突变导致后代释放减少和延迟裂解，因此 Vp4 被认为是一种病毒孔蛋白。然而，包括我们自己在内的两个独立研究小组无法复制这些发现。相反，我们在 SV40 感染的细胞中没有发现 Vp4 的表达，也没有发现 Vp4 缺失病毒的后代释放减少，最后，我们发现，在 Vp4 诱变过程中不可避免地引入到重叠的 Vp2/Vp3 基因中的单个氨基酸取代减少了早期步骤，但没有减少病毒释放。值得注意的是，病毒孔蛋白 Vp4 的存在似乎仍然被广泛接受，这大概是阻碍了对多瘤病毒释放的重要研究。从这个角度出发，我们将回顾和评论导致有争议的病毒孔蛋白 Vp4 声明的最重要的实验。
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