伊朗儿童胃肠炎中人腺病毒的分子患病率和基因型分布。

IF 0.7 4区 医学 Q4 PATHOLOGY
Fetal and Pediatric Pathology Pub Date : 2023-12-01 Epub Date: 2023-11-22 DOI:10.1080/15513815.2023.2262576
Abdulhussain Kadhim Jwaziri, Mohammad Hadi Karbalaie Niya, Pegah Khales, Atefeh Kachooei, Milad Sabaei, Soheil Rahmani Fard, Ahmad Tavakoli
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引用次数: 0

摘要

目的:测定伊朗5岁以下儿童胃肠炎中人类腺病毒(HAdV)的分子流行率和基因型分布。结果:15例(15%)标本中检出HAdV DNA。在24-60岁年龄组中观察到HAdV的患病率最高和最低 月(n = 6.40%)和7-12 月(n = 2.13.3%)(p = 对9份HAdV阳性标本进行测序,其中4株为2型,5株为41型。在测序的样本中,我们只发现了2型和41型。我们的研究结果表明,除了40型和41型的HAdV外,2型HAdV也可能在引起儿童肠胃炎中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular Prevalence and Genotype Distribution of Human Adenovirus in Iranian Children with Gastroenteritis.

Objective: We determined the molecular prevalence and genotype distribution of human adenovirus (HAdV) among children under five years of age with gastroenteritis in Iran.

Methods: One hundred stool samples from children hospitalized were tested by PCR for adenovirus, and some of the positive samples were sequenced to determine the specific genotype.

Results: HAdV DNA was found in 15 samples (15%). The highest and the lowest prevalence of HAdV was observed in the age groups 24-60 months (n = 6; 40%) and 7-12 months (n = 2; 13.3%), respectively (p = 0.01). Nine HAdV-positive samples were sequenced, of which four isolates were HAdV type 2 and five isolates were HAdV type 41.

Conclusion: HAdV was most common in the 24-60-month-old children. Of the samples sequenced, we found only types 2 and 41. Our results show that in addition to HAdV types 40 and 41, HAdV type 2 may also play a role in causing gastroenteritis in children.

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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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