POLYMERASE CHAIN-REACTION DETECTION OF SMALL ROUND-STRUCTURED VIRUSES FROM 2 RELATED HOSPITAL OUTBREAKS OF GASTROENTERITIS USING INOSINE-CONTAINING PRIMERS
POLYMERASE CHAIN-REACTION DETECTION OF SMALL ROUND-STRUCTURED VIRUSES FROM 2 RELATED HOSPITAL OUTBREAKS OF GASTROENTERITIS USING INOSINE-CONTAINING PRIMERS
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DOI：
10.1002/jmv.1890450215
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发表时间：
1995-02-01
影响因子：
12.7
通讯作者：
CLARKE, IN
中科院分区：
文献类型：
--
作者：
GREEN, SM;LAMBDEN, PR;CLARKE, IN
在英国发生的两起胃肠炎爆发，分别发生在利明顿和南安普顿医院，相隔9天。两次暴发的临床和流行病学特征均为小圆结构病毒（SRSV）感染，迅速出现腹泻和/或恶心和呕吐，并通过继发传播传播暴发。免疫电镜（EM）观察到SRSV颗粒在60%的粪便样品从两次爆发，没有其他病原体被检测到。第二次暴发的指示病例是一名患者，他在第一次暴发期间从利明顿医院出院后因腹泻和呕吐入院。用聚合酶链反应（PCR）技术对这两次暴发疫情进行了鉴定，以确定这两次暴发疫情是由同一株SRSV引起的。设计了一对含肌苷的PCR引物，用于扩增SRSV基因组I和II的RNA聚合酶区。使用组II引物的PCR实现了较高的检出率为SRSVs粪便样品（68%的样品阳性，从两个爆发）比免疫EM。使用组I引物或使用常规简并PCR引物未检测到SRSV。两次爆发的PCR扩增产物的核苷酸序列是相同的，为单一SRSV毒株的参与提供了分子流行病学证据。将该病毒的RNA聚合酶区域与遗传组I（69.4-75.0%氨基酸同一性）和遗传组II（88.9-100%氨基酸和77.1-88.1%核苷酸同一性）SRSV的相应区域进行比较，表明致病性SRSV是遗传组II的独特成员。(C)1995 Wiley-Liss，Inc.
Two outbreaks of gastroenteritis in the UK which occurred nine days apart at Lymington and Southampton hospitals were investigated. The clinical and epidemiological features of both outbreaks were characteristic of small round-structured virus (SRSV) infection with rapid onset of diarrhoea and/or nausea and vomiting and propagation of the outbreaks by secondary spread. SRSV particles were observed by immune electron microscopy (EM) in 60% of faecal samples from both outbreaks and no other pathogens were detected. The index case for the second outbreak was a patient who was admitted with diarrhoea and vomiting after being discharged from Lymington hospital during the first outbreak. The possibility that the two outbreaks were caused by the same strain of SRSV was investigated by the polymerase chain reaction (PCR). New inosine-containing PCR primers were designed to amplify the RNA polymerase region of SRSV cDNA from genetic groups I and II. The PCR using the group II primers achieved a higher detection rate for SRSVs in faecal samples (68% of samples positive from both outbreaks) than immune EM. SRSVs were not detected using the group I primers or using conventional degenerate PCR primers. The nucleotide sequences of PCR amplicons from both outbreaks were identical providing molecular epidemiological evidence for the involvement of a single SRSV strain. Comparison of the RNA polymerase region of this virus with the equivalent regions of genetic group I (69.4-75.0% amino acid identity) and genetic group II (88.9-100% amino acid and 77.1-88.1% nucleotide identity) SRSVs revealed that the causative SRSV was a distinct member of genetic group II. (C) 1995 Wiley-Liss, Inc.