Herpes simplex virus type 1 VP26 is not essential for replication in cell culture but influences production of infectious virus in the nervous system of infected mice
Herpes simplex virus type 1 VP26 is not essential for replication in cell culture but influences production of infectious virus in the nervous system of infected mice
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DOI：
10.1006/viro.1998.9230
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发表时间：
1998-07-20
期刊：
影响因子：
3.7
通讯作者：
Person, S
中科院分区：
文献类型：
--
作者：
Desai, P;DeLuca, NA;Person, S
VP26是1型单纯疱疹病毒最小的衣壳蛋白，由UL35开放阅读框编码。它位于衣壳外表面，与组成衣壳的苍鹭中的VP5以一对一的化学计量比相互作用。编码VP26基因的零突变被产生并转移到Kos基因组中。在Vero细胞上分离到重组病毒，表明VP26的缺失不是病毒在细胞培养中生长所必需的。命名为K Delta 26Z的VP26缺失突变体的特性证实了这一点。根据病毒爆发大小判断，K Delta 26Z感染的Vero细胞的病毒产量仅比野生型感染细胞减少两倍。对K Delta 26Z感染的细胞提取液进行沉降分析后，观察到三种衣壳类型(A、B和C)。除了没有VP26外，这些衣壳的组成与野生型衣壳相似。小鼠眼球模型被用来确定VP26是否在体内发挥主要作用。与野生型病毒相比，突变病毒在眼睛中的产量减少了两倍；然而，在三叉神经节中，突变病毒的产量减少了30-100倍。通过共培养试验确定的突变病毒的重新激活也减少了。为了确定VP26对衣壳易位的影响，将VP26零突变转移到一种特定胸苷激酶突变的病毒中，该突变本身被运输到三叉神经节，但其DNA不在三叉神经节中复制。使用定量聚合酶链式反应分析，在神经节中检测到的病毒基因组的数量在存在或不存在VP26的情况下是相似的。因此，VP26似乎没有帮助病毒衣壳从小鼠的眼睛转移到三叉神经节，但对三叉神经节中传染性病毒的产生是重要的。(C)1998年学术出版社。
VP26 is the smallest capsid protein of herpes simplex virus type 1 and is encoded by the UL35 open reading frame. It resides on the outer capsid surface, interacting with VP5 in a one to one stoichiometry in the herons that comprise capsids. A null mutation in the gene encoding VP26 was generated and transferred into the KOS genome. Recombinant viruses were isolated on Vero cells, which indicated that the absence of VP26 was not required for growth of the virus in cell culture. This was confirmed by the characterization of the VP26 null mutant, designated K Delta 26Z. The yield of virus from K Delta 26Z-infected Vero cells was decreased only twofold relative to wild-type-infected cells, as judged by the burst size. All three types of capsids (A, B, and C) were observed after sedimentation analysis of K Delta 26Z-infected cell extracts. These capsids were similar in composition to wild-type capsids except for the absence of VP26. The mouse ocular model was used to determine if VP26 played a major role in vivo. The yield of the mutant virus relative to wild-type virus was decreased twofold in the eye; however, the mutant virus yields were decreased 30- to 100-fold in the trigeminal ganglia. Reactivation of the mutant virus as determined by cocultivation assays was also reduced. To determine the effect of VP26 on capsid translocation, the VP26 null mutation was transferred into a virus specifiying a thymidine kinase mutation that by itself is transported to the trigeminal ganglia but whose DNA is not replicated in the ganglia. Using quantitative PCR assays the number of viral genomes detected in the ganglia was similar in the presence or the absence of VP26. Therefore, VP26 does not appear to aid in the translocation of the virus capsid from the mouse eye to the trigeminal ganglia but is important for infectious virus production in the ganglia. (C) 1998 Academic Press.