Maunula L, Von Bonsdorff C-H
HUCH Laboratory Diagnostics, Division of Virology, Haartmaninkatu 3, 00290 Helsinki, Finland.
J Clin Virol. 2005 Nov;34(3):186-94. doi: 10.1016/j.jcv.2005.03.004.
Outbreak investigation methods for enteric viruses were improved in 1990s when gene amplification techniques were established in viral laboratories.
The objective of the study was to determine the causative agents for Finnish viral gastroenteritis outbreaks. Our aim was also to further characterise the norovirus strains, reveal the temporal occurrence of norovirus (NV) genotypes and to study some epidemiological aspects concerning the outbreaks.
A total of 416 Finnish viral gastroenteritis outbreaks that occurred during 5 years (1998-2002), excluding those among hospitalised children, were investigated for enteric viruses. Stool samples were screened by electron microscopy as well as analyzed by specific noro- and astrovirus RT-PCR tests. Amplicon sequence analysis was used to find out norovirus genotypes.
Noroviruses caused 252 (60.6%) of the outbreaks; other viruses, astro- or rotavirus, caused four epidemics. Norovirus epidemics occurred in all kinds of settings, most often in hospitals (30.6%) and in restaurants and canteens (14.3%). Both NV genogroups were found every year, but NV GGII outbreaks always outnumbered those of GGI. All but one outbreak at hospitals and nursing homes were of genotype GII. Polymerase sequence analysis revealed a variety of NV genotypes; six GI and at least eight GII genotypes. The GI.3 Birmingham-like and GII.4 Bristol-like genotype appeared every year, whereas the other types were circulating for shorter periods or sporadically. During the study period the genotypes GII.4 (Bristol), GII.1 (Hawaii), an emerging genotype GIIb, and a new variant of GII.4 predominated in that order. Indication for rapid genetic changes in the genotype GII.4 was also noticed.
Noroviruses were the most prevalent causative agents in the outbreaks. Many NV genotypes were circulating, and a shift in the predominant genotypes was evident between epidemic seasons.
20世纪90年代,随着病毒实验室基因扩增技术的建立,肠道病毒的暴发调查方法得到了改进。
本研究的目的是确定芬兰病毒性肠胃炎暴发的病原体。我们的目标还包括进一步鉴定诺如病毒株,揭示诺如病毒(NV)基因型的时间分布,并研究与这些暴发相关的一些流行病学特征。
对1998年至2002年这5年间发生的416起芬兰病毒性肠胃炎暴发事件(不包括住院儿童中的暴发事件)进行肠道病毒调查。粪便样本通过电子显微镜进行筛查,并通过特异性诺如病毒和星状病毒RT-PCR检测进行分析。扩增子序列分析用于确定诺如病毒基因型。
诺如病毒导致了252起(60.6%)暴发事件;其他病毒,如星状病毒或轮状病毒,引发了4起疫情。诺如病毒疫情发生在各种场所,最常见于医院(30.6%)以及餐馆和食堂(14.3%)。每年都发现了两种NV基因组,但NV GGII暴发事件的数量总是超过GG I。除了医院和疗养院的一起暴发事件外,其他所有事件均为GII基因型。聚合酶序列分析揭示了多种NV基因型;6种GI基因型和至少8种GII基因型。GI.3伯明翰样和GII.4布里斯托样基因型每年都会出现,而其他类型的传播时间较短或呈散发性。在研究期间,GII.4(布里斯托)、GII.1(夏威夷)、一种新兴的GIIb基因型以及GII.4的一种新变体按此顺序占主导地位。还注意到GII.4基因型存在快速基因变化的迹象。
诺如病毒是暴发中最常见的病原体。许多NV基因型在传播,并且在流行季节之间,主要基因型明显发生了变化。