西北亚马逊地区急性胃肠炎患儿和非急性胃肠炎患儿诺如病毒基因型的流行病学分析

IF 2.6 4区医学 Q3 INFECTIOUS DISEASES

Infection Genetics and Evolution Pub Date : 2025-07-27 DOI:10.1016/j.meegid.2025.105804

Yan Cardoso Pimenta , Glenda Maria Santos Moreira , Waldemar da Silva Souza , Alberto Ignacio Olivares Olivares , Lennart Svensson , José Paulo Gagliardi Leite , Johan Nordgren , Marcia Terezinha Baroni de Moraes

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引用次数: 0

摘要

诺如病毒在世界范围内引起急性胃肠炎（AGE），生活在低收入地区的年龄≤5 岁的儿童是最脆弱的。组织血型抗原（HBGA）被认为是人类诺如病毒的附着因子，特定基因型的易感性通常依赖于FUT2基因型介导的分泌物表型。本回顾性研究纳入734名年龄≤5 岁的AGE儿童(病例组；66 %,485/734)或非age组(对照组；34 %,249/734)，来自亚马逊雨林（巴西、委内瑞拉和圭亚那），在我们之前的研究中，87 %的儿童是阳性分泌物（641/734）。共40.2 % (88/219；GII)和14.6 % (7/48；诺瓦克病毒的GI)成功的基因,被:GII.1 (n = 5),GII.2 (n = 25),GII.4 (n = 32),GII.6 (n = 19),GII.7 (n = 5),GII.14 (n = 2),GI.2 (n = 1),GI.3 (n = 4)和GI.7 (n = 2)。大多数基因型GII诺如病毒，包括所有32个GII.4，在分泌物阳性儿童中检测到（94.3 %,83/88）。分泌阴性患儿仅检出基因型GII.2 （n = 2）、GII.6 （n = 3）、GII.2 （n = 1）和gii .7 （n = 1）。值得注意的是，主要的GII.4和GII.6与AGE没有显著相关(OR 1.1；95 % CI 0.5 ~ 2.4, P = 0.7,OR 1.4；95 % CI 0.5 ~ 4.0, P = 0.4)，而gi .2与AGE相关(OR 6.1；95 % CI 1.4 ~ 26.2, P = 0.01)。基因型gi1 .2和gi1 .4在所有年龄组中均有较高的检测频率。总之，在亚马逊地区传播的诺如病毒基因型有很大的多样性。只有GII.2基因型与AGE相关，而主要的GII.4基因型在AGE患儿和无AGE患儿中检测到的频率相似。

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Epidemiological profiles of norovirus genotypes in children with and without acute gastroenteritis from the northwestern Amazon region

Noroviruses causes acute gastroenteritis (AGE) worldwide, with children living in low-income areas aged ≤5 years being the most vulnerable. Histo-blood group antigens (HBGA) are recognized as attachment factors for human noroviruses and susceptibility of a given genotype is frequently dependent on the secretor phenotype mediated by FUT2 genotype. This retrospective study involved 734 children aged ≤5 years with AGE (cases group; 66 %, 485/734) or non-AGE (control group; 34 %, 249/734), from the Amazon rainforest (Brazil, Venezuela, and Guyana) and in our previous studies, 87 % of children were positive secretors (641/734). A total of 40.2 % (88/219; GII) and 14.6 % (7/48; GI) of noroviruses were successfully genotyped, being: GII.1 (n = 5), GII.2 (n = 25), GII.4 (n = 32), GII.6 (n = 19), GII.7 (n = 5), GII.14 (n = 2), GI.2 (n = 1), GI.3 (n = 4) and GI.7 (n = 2). Most genotyped GII norovirus including all 32 GII.4, were detected in secretor-positive children (94.3 %, 83/88). Only genotypes GII.2 (n = 2), GII.6 (n = 3), GI.2 (n = 1) and GI.7 (n = 1) were detected in secretor-negative children. Of note, the predominant GII.4 and the GII.6 were not significantly associated with AGE (OR 1.1; 95 % CI 0.5 to 2.4, P = 0.7 and OR 1.4; 95 % CI 0.5 to 4.0, P = 0.4, respectively), in contrast to GII.2 was associated with AGE (OR 6.1; 95 % CI 1.4 to 26.2, P = 0.01). Genotypes GII.2, and GII.4 were detected in all age groups at high frequencies. In conclusion a great diversity of norovirus genotypes circulating in the Amazon region. Only the GII.2 genotype was associated with AGE, while the predominant GII.4 was detected at similar frequencies in both children with AGE and children without AGE.

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来源期刊

Infection Genetics and Evolution 医学-传染病学

CiteScore

8.40

自引率

0.00%

发文量

215

审稿时长

82 days

期刊介绍： (aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID) Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance. However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors. Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases. Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .