MODIFICATION OF DISCRETE NUCLEAR DOMAINS INDUCED BY HERPES-SIMPLEX VIRUS TYPE-1 IMMEDIATE-EARLY GENE-1 PRODUCT (ICP0)
MODIFICATION OF DISCRETE NUCLEAR DOMAINS INDUCED BY HERPES-SIMPLEX VIRUS TYPE-1 IMMEDIATE-EARLY GENE-1 PRODUCT (ICP0)
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DOI：
10.1099/0022-1317-74-12-2679
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发表时间：
1993-12-01
影响因子：
3.8
通讯作者：
SPIVACK, JG
中科院分区：
文献类型：
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作者：
MAUL, GG;GULDNER, HH;SPIVACK, JG
单纯疱疹病毒1型（HSV-1）感染的结果取决于宿主和病毒因素的相互作用。在裂解感染期间，HSV-1导致离散核结构域（ND 10）的免疫荧光染色丧失。这种宿主ND 10染色的消除发生在仅允许HSV-1立即早期病毒基因表达的条件下。Western印迹分析表明，ND 10染色的损失是由于ND 10重新分布，而不是蛋白质降解或周转。当检测所有HSV-1立即早期基因的缺失突变体时，仅感染立即早期基因1产物（ICP 0）缺失突变体d11403不能消除ND 10抗原染色。此外，ICP 0与ND 10抗原短暂共定位，之后ND 10抗原变得不可检测。在d11403感染的后期，宿主ND 10抗原保留在病毒诱导的结构中，这在野生型HSV-1感染期间从未观察到。这些结果表明，ICP 0可能直接参与宿主核结构域的修饰。用表达ICP 0的腺病毒重组体感染表明，在不存在其他HSV-1蛋白的情况下，ICP 0足以改变位于ND 10的宿主抗原的核分布。我们推测ICP 0在病毒复制过程中的反式激活功能可能是通过替换介导的。修饰或重组核宿主因子。
The outcome of herpes simplex virus type 1 (HSV-1) infection depends upon the interplay of both host and viral factors. During lytic infection, HSV-1 causes a loss of immunofluorescent staining of discrete nuclear domains (ND10). This elimination of the host's ND10 staining occurs under conditions that allow only HSV-1 immediate early viral gene expression. Western blot analysis indicates that the loss of ND10 staining is due to ND10 redistribution, rather than protein degradation or turnover. When deletion mutants of all of the HSV-1 immediate early genes were tested, only infection with an immediate early gene 1 product (ICP0) deletion mutant, d11403, was unable to eliminate ND10 antigen staining. Also, ICP0 transiently colocalized with ND10 antigens, after which ND10 antigens became undetectable. At late times during infection with d11403, the host ND10 antigens were retained in virus-induced structures which were never observed during wild-type HSV-1 infection. These results suggested that ICP0 may be directly involved in the modification of the host nuclear domain. Infection with an adenovirus recombinant that expressed ICP0 demonstrated that in the absence of other HSV-1 proteins ICP0 was sufficient for the change in nuclear distribution of host antigens located at ND10. We postulate that the trans-activation function of ICP0 during viral replication may be mediated by replacing. modifying or reorganizing nuclear host factors.