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目的了解晚期黄疸新生儿人巨细胞病毒(HCMV)感染状况,探讨HCMV US3基因多态性与致病性之间的关系。方法应用巢式PCR法检测2010年1～6月在本院新生儿科就诊的79例晚期黄疸新生儿样本HCMV US3基因,阳性标本结果进行双向DNA测序,通过BioEdit、DNAstar、GeneDoc等软件进行序列分析。结果 79例晚期黄疸新生儿中20例HCMV US3基因PCR扩增阳性,阳性率25.3%。以Towne作为参考株,序列比对分析显示,20株临床分离株US3的ORF长度均与参考株相同,为561bp,编码186个氨基酸蛋白。US3核酸变异比较普遍,变异主要集中在序列的N端,大部分是同义突变,US3氨基酸序列高度保守,仅几个位点在少数分离株中存在变异。未发现US3基因多态性与临床致病性的联系。结论 HCMV感染是导致新生儿晚期黄疸的重要原因之一。20株临床分离株HCMV US3基因编码的氨基酸序列比较保守,但仍存在一定的多态性。未发现不同临床分离株US3基因多态性与HCMV引起的新生儿晚期黄疸的联系。
Objective To understand the status of cytomegalovirus (HCMV) infection in neonatal jaundice and to explore the relationship between HCMV US3 gene polymorphism and pathogenicity. Methods Nested PCR was used to detect HCMV US3 gene in 79 neonatal jaundice neonates from January 2010 to June 2010 in our hospital. The positive samples were sequenced by two-dimensional DNA sequencing and sequenced by BioEdit, DNAstar, GeneDoc and other softwares . Results In 79 cases of neonatal jaundice, 20 cases of HCMV US3 gene were positive for PCR amplification, the positive rate was 25.3%. Using Towne as a reference strain, sequence alignment analysis showed that the ORF length of the 20 clinical isolates, US3, was 561 bp, encoding a protein of 186 amino acids. The variation of US3 nucleic acid is more common. The variation mainly concentrates on the N terminus of the sequence, most of which are synonymous mutations. The amino acid sequence of US3 is highly conserved. Only a few loci have variation in a few isolates. No association between US3 gene polymorphism and clinical pathogenicity was found. Conclusion HCMV infection is one of the important causes of neonatal jaundice. The amino acid sequences of 20 strains of clinical isolates HCMV US3 were conservative, but some polymorphisms still existed. No clinical isolates US3 gene polymorphism associated with HCMV induced neonatal jaundice.