Division of Pediatric Gastroenterology, Department of Pediatrics, Taipei Medical University-Shuang Ho Hospital, Taipei.
Molecular Infectious Disease Research Center, Chang Gung Memorial Hospital, Taoyuan.
Medicine (Baltimore). 2021 Mar 26;100(12):e25123. doi: 10.1097/MD.0000000000025123.
Human norovirus (NoV) is the leading cause of acute gastroenteritis and the rapid transmission of NoV renders infection control problematic. Our study aimed to investigate viral shedding in gastroenteritis in children caused by variants of emerging norovirus strains infections.We used RNA-dependent RNA polymerase (RdRp) sequencing to measure NoV genome copies in stool to understand the relationship between the clinical manifestations and viral shedding in hospitalized patients. The near full-length NoV genome sequence was amplified via reverse transcription-polymerase chain reaction (RT-PCR) and NoV recombination was analyzed using the Recombination Analysis Tool (RAT).From January 2015 to March 2018, 77 fecal specimens were collected from hospitalized pediatric patients with confirmed NoV gastroenteritis. The NoV genotypes were GII.4 (n = 22), non-GII.4 (n = 14), GII.4 Sydney (n = 21), and GII.P16-GII.2 (n = 20). Viral load increased from days 2 to 9 from the illness onset, resulting in an irregular plateau without peaks. After day 9, the viral load declined gradually and most viral shedding in feces ceased by day 15. The average viral load was highest in GII.4 Sydney followed by GII.P16-GII.2 infections and lowest in non-GII.4 infections. GII.4 unclassified infections showed the longest viral shedding time, followed by GII.4 Sydney infections, GII.P16-GII.2 recombinant infection resulted in the shortest duration. NoVs evolved to form a group of GII.P16-GII.2 variants during the 2017 to 2018 period.The viral load and shedding period and was different in variants of NoV infections in children. High mutation rate of emerging and re-emerging variants was observed to an enhanced epidemic risk rendering continuous surveillance.
人类诺如病毒(NoV)是急性胃肠炎的主要原因,诺如病毒的快速传播使得感染控制成为一个问题。我们的研究旨在调查由新兴诺如病毒株变异引起的儿童胃肠炎中的病毒脱落情况。我们使用 RNA 依赖性 RNA 聚合酶(RdRp)测序来测量粪便中的 NoV 基因组拷贝数,以了解住院患者的临床表现与病毒脱落之间的关系。通过逆转录-聚合酶链反应(RT-PCR)扩增近全长 NoV 基因组序列,并使用重组分析工具(RAT)分析 NoV 重组。从 2015 年 1 月到 2018 年 3 月,从确诊为诺如病毒胃肠炎的住院儿科患者中收集了 77 份粪便标本。诺如病毒基因型为 GII.4(n=22)、非 GII.4(n=14)、GII.4 Sydney(n=21)和 GII.P16-GII.2(n=20)。病毒载量从发病第 2 天到第 9 天增加,导致无峰的不规则平台。第 9 天后,病毒载量逐渐下降,第 15 天粪便中大部分病毒脱落停止。GII.4 Sydney 感染的平均病毒载量最高,其次是 GII.P16-GII.2 感染,非 GII.4 感染的病毒载量最低。未分类的 GII.4 感染表现出最长的病毒脱落时间,其次是 GII.4 Sydney 感染,GII.P16-GII.2 重组感染导致最短的持续时间。在 2017 年至 2018 年期间,NoV 进化形成了一组 GII.P16-GII.2 变体。儿童中不同诺如病毒变异株的病毒载量、脱落期和时间不同。新兴和重新出现的变异体的高突变率增加了流行风险,需要持续监测。