中文摘要：

背景人的 cytomegalovirus (HCMV ) 在 vivo 感染很多个机关和纸巾。不同症状和 HCMV 感染的织物向性也许源于基因多型性。包含至少 19 个开的读物框架(ORF )( 到 151 的表示 UL133 ) 的 DNA 的一个新区域在低经过的 HCMV 临床的种类， Toledo，和几其它被发现低经过临床孤立，然而并非在 HCMV 实验室种类在场， AD169。这些基因之一， UL143 ，被学习在 HCMV 探索 UL143 ORF 的顺序可变性临床孤立并且检验在基因可变性和 HCMV infection.Methods 的结果之间的可能的协会从怀疑的天生地 感染HCMV 的婴儿获得的种类的 UL143 基因被聚合酶链反应( PCR )和 sequenced.Results 放大种类的十九个序列被划分成 2 个主要的组， G1 ( n=16 )和 G2 ( n=3 )。所有与 Toledo 相比序列有框架移动变化。核苷酸多型性授与实质的氨基酸替换什么时候与 Toledo 相比。在 G1 的种类的所有 16 UL143 通常认为的蛋白质由于错误感觉变化有一个新 myristylation 地点和二个 PKC 地点的损失。没有有说服力的关系在 HCMV 疾病的存在之间被观察， UL 143 顺序 group.Conclusions HCMV-UL143 在低经过存在孤立。框架移动变化引起的顺序可变性在所有 HCMV 临床的种类被发现。没有明显的连接在 UL143 多型性和怀疑的先天的 HCMV 感染的结果之间被观察。

英文摘要：

Background Human cytomegalovirus （HCMV） infects a number of organs and tissues in vivo. The different symptoms and tissue tropisms of HCMV infection perhaps result from genetic polymorphism. A new region of DNA containing at least 19 open reading frames （ORFs） （denoted UL133 to 151） was found in the low-passage HCMV clinical strain, Toledo, and several other low-passage clinical isolates, but not present in the HCMV laboratory strain, AD169. One of these genes, UL143, was studied to explore the sequence variability of UL143 ORF in HCMV clinical isolates and examine the possible association between gcne variability and the outcome of HCMV infection. Methods The UL143 gone of the strains obtained from suspected congenitally HCMV-infectcd infants was amplified by polymerase chain reaction （PCR） and sequenced. Results Nineteen sequences of the strains were divided into 2 major groups, G1（n=16） and G2（n=3）. All of the sequences had frame-shift mutation compared to Toledo. Nucleotide polymorphisms conferred substantial amino acid substitutions when compared with Toledo. All 16 UL143 putative proteins of the strains in G1 had a new myristylation site and loss of two PKC sites owing to missense mutations. No convincing relationships were observed between the presence of HCMV disease and the UL143 sequence group. Conclusions HCMV-UL143 existed in low passage isolates. Sequence variability caused by frame -shift mutation was found in all HCMV clinical strains. No obvious linkage was observed between UL143 polymorphisms and the outcome of suspected congenital HCMV infection.