Mahalingam R, White T, Wellish M, Gilden D H, Soike K, Gray W L
Department of Neurology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
Virology. 2000 Sep 1;274(2):420-8. doi: 10.1006/viro.2000.0465.
Simian varicella virus (SVV) causes varicella (chickenpox) in nonhuman primates, becomes latent in cranial and dorsal root ganglia, and reactivates to produce zoster (shingles). Because the clinical and molecular features of SVV closely resemble those of varicella zoster virus (VZV) infection of humans, SVV infection of primates has served as an experimental model of VZV pathogenesis and latency. The SVV genome has been completely mapped, but attempts to clone the 3600-bp EcoRI fragment located at the leftward end of the virus genome have hitherto been unsuccessful. Herein, we report the cloning and the complete nucleotide sequence of this region. Comparison of the SVV and VZV sequences in this region revealed an 8-bp inverted repeat sequence flanking the unique long segment of the SVV genome; an 879-bp open-reading frame (ORF) A in SVV that is absent in VZV but has 42% amino acid identity to SVV ORF 4 and 49% to VZV ORF 4; a 342-bp ORF B in SVV with 35% amino acid identity to a 387-bp ORF located to the left of ORF 1 on the VZV genome; and a 303-bp ORF in SVV with 27% amino acid identity to VZV ORF 1. No homologue of VZV ORF 2 was detected. Transcripts specific for ORFs A and B were present in SVV-infected cells in culture and in acutely infected monkey ganglia. Overall, there are more than 2000 bp of DNA in the SVV genome that are absent in the VZV genome.
猴水痘病毒(SVV)可在非人灵长类动物中引起水痘,并潜伏于颅神经节和背根神经节,之后再激活引发带状疱疹。由于SVV的临床和分子特征与人类水痘带状疱疹病毒(VZV)感染极为相似,灵长类动物的SVV感染已成为VZV发病机制和潜伏的实验模型。SVV基因组已被完全定位,但此前试图克隆位于病毒基因组左端的3600 bp EcoRI片段均未成功。在此,我们报告该区域的克隆及完整核苷酸序列。该区域SVV和VZV序列的比较显示,SVV基因组独特长片段两侧有一个8 bp的反向重复序列;SVV中有一个879 bp的开放阅读框(ORF)A,VZV中没有,但与SVV的ORF 4有42%的氨基酸同一性,与VZV的ORF 4有49%的氨基酸同一性;SVV中有一个342 bp的ORF B,与VZV基因组中ORF 1左侧一个387 bp的ORF有35%的氨基酸同一性;SVV中有一个303 bp的ORF,与VZV的ORF 1有27%的氨基酸同一性。未检测到VZV ORF 2的同源物。在培养的SVV感染细胞和急性感染的猴神经节中存在ORF A和B的特异性转录本。总体而言,SVV基因组中有超过2000 bp的DNA在VZV基因组中不存在。