THE SPI-1 GENE OF RABBITPOX VIRUS DETERMINES HOST-RANGE AND IS REQUIRED FOR HEMORRHAGIC POCK FORMATION
THE SPI-1 GENE OF RABBITPOX VIRUS DETERMINES HOST-RANGE AND IS REQUIRED FOR HEMORRHAGIC POCK FORMATION
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DOI：
10.1006/viro.1994.1347
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发表时间：
1994-07-01
期刊：
影响因子：
3.7
通讯作者：
MOYER, RW
中科院分区：
文献类型：
--
作者：
ALI, AN;TURNER, PC;MOYER, RW
野生型兔痘病毒（RPV）和牛痘病毒（CPV）在感染2日龄鸡胚的鸡绒毛膜尿囊膜（CAM）后产生红色出血性病变或小袋。然而，在这两种病毒的野生型（wt）群体中，以约1%的频率自发出现白色、非出血性麻袋变异，反映了病毒DNA末端的复杂缺失/重排。RPV白痘突变体的一个亚群不能在猪肾（PK-15）细胞上形成斑块，被称为宿主范围（hr）突变体。在CPV的病例中，白斑的形成与SPI-2 （crmA）基因的突变有关。我们发现，5个自发性RPV白痘宿主突变体（RPV mu hr8sm、RPV mu hr23、RPV mu hr28、RPV mu hr30和RPV mu hr31）均含有一个SPI-2 （crmA）基因并表达crmA蛋白，但缺乏一个功能性的SPI-1基因。另外两种自发性RPV白痘突变体，RPV mu 9和RPV mu 12，它们在PK-15细胞上形成斑块（非宿主突变体），含有并表达一个SPI-1基因，但缺乏一个功能性的SPI-2基因。靶向破坏wtRPV的SPI-1或SPI-2基因，而只破坏wtCPV的SPI-2基因，都会产生产生白痘的突变体。RPV Delta SPI-1突变体不能在PK-15或人类A549细胞上形成斑块，而RPV Delta SPI-2突变体具有正常的宿主范围。与wtCPV相比，CPV Delta SPI-1和CPV Delta SPI-2突变体的宿主范围没有变化。在两种病毒之间观察到的这些表型差异可能反映了高度保守的SPI-1或SPI-2基因之间的小序列差异或其他剩余基因提供的总体表型。(C) 1994学术出版社，Inc.
Wild-type rabbitpox virus (RPV) and cowpox virus (CPV) produce red hemorrhagic lesions or pocks upon infection of the chicken chorioallantoic membrane (CAM) of ii-day-old embryonated chicken eggs. However, white, nonhemorrhagic pock variants arise spontaneously within wild-type (wt) populations of either virus at a frequency of about 1%, reflective of complex deletions/rearrangements in the termini of the viral DNA. A subpopulation of the RPV white-pock mutants fail to plaque on pig kidney (PK-15) cells and are referred to as host-range (hr) mutants. In the case of CPV, white-pock formation has been linked to mutations in the SPI-2 (crmA) gene. We show that five spontaneous RPV white-pock host-range mutants (RPV mu hr8sm, RPV mu hr23, RPV mu hr28, RPV mu hr30, and RPV mu hr31) each contain a SPI-2 (crmA) gene and express the crmA protein but lack instead a functional SPI-1 gene. Two other spontaneous RPV white-pock mutants, RPV mu 9 and RPV mu 12, which plaque on PK-15 cells (nonhost-range mutants) contain and express a SPI-1 gene but lack instead a functional SPI-2 gene. Targeted disruption of either the SPI-1 or SPI-2 genes of wtRPV, but only the SPI-2 gene of wtCPV, generates mutants which produce white pocks. The RPV Delta SPI-1 mutant fails to plaque on PK-15 or human A549 cells, whereas the RPV Delta SPI-2 mutant has a normal host range. No changes in host range compared to wtCPV for either the CPV Delta SPI-1 or CPV Delta SPI-2 mutants were noted. These differences in phenotypes observed between the two viruses may be reflective of either small sequence variations between the highly conserved SPI-1 or SPI-2 genes or the aggregate phenotypes provided by the other remaining genes. (C) 1994 Academic Press, Inc.