Bioscience reports · 2019
Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis.
СтатьяМетаанализПоддержка исследования: вне правительства СШАСистематический обзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhou Peiru, Xie Yufei, Yan Zhimin, Liu Xiaosong, Hua Hong
Аннотация
OBJECTIVES: To investigate the association between dectin-1 gene single nucleotide polymorphisms (SNPs) and susceptibility to fungal infection (FI).
METHODS: Databases were searched electronically and manually to identify case-control studies concerning dectin-1 SNPs and FI, which were published up to 12 November 2018. The Newcastle-Ottawa Quality Assessment Scale was used to determine the study quality and bias. The SNP frequencies of the B (the variant or minor allele) and A (the wild or major allele) alleles of the dectin-1 gene in both cases and controls were analyzed with regard to FI susceptibility.
RESULTS: Eight high-quality studies were included in the review. Systemic review of the included studies demonstrated that dectin-1 SNPs rs3901533 and rs7309123 might be associated with susceptibility to invasive pulmonary aspergillosis infection; moreover, rs16910527 SNP can possibly increase the susceptibility to oropharyngeal candidiasis in HIV-positive patients. The meta-analysis identified significant associations between dectin-1 SNPs and overall FI risk in the homozygote model (pooled odds ratio (OR) 1.77, P=0.04). When classified by subtypes, significant associations were also found for deep FI in the homozygote model (pooled OR 2.46, P=0.01) and the recessive model (pooled OR 2.85, P=0.002). There appeared to be no significant association between dectin-1 SNPs and superficial FI.
CONCLUSION: Systemic review of the included studies suggested that dectin-1 SNPs rs3901533, rs7309123, and rs16910527 might play a role in FI susceptibility. The meta-analysis provided convincing evidence that dectin-1 SNPs might have an important role in FI susceptibility, especially for deep FI.
METHODS: Databases were searched electronically and manually to identify case-control studies concerning dectin-1 SNPs and FI, which were published up to 12 November 2018. The Newcastle-Ottawa Quality Assessment Scale was used to determine the study quality and bias. The SNP frequencies of the B (the variant or minor allele) and A (the wild or major allele) alleles of the dectin-1 gene in both cases and controls were analyzed with regard to FI susceptibility.
RESULTS: Eight high-quality studies were included in the review. Systemic review of the included studies demonstrated that dectin-1 SNPs rs3901533 and rs7309123 might be associated with susceptibility to invasive pulmonary aspergillosis infection; moreover, rs16910527 SNP can possibly increase the susceptibility to oropharyngeal candidiasis in HIV-positive patients. The meta-analysis identified significant associations between dectin-1 SNPs and overall FI risk in the homozygote model (pooled odds ratio (OR) 1.77, P=0.04). When classified by subtypes, significant associations were also found for deep FI in the homozygote model (pooled OR 2.46, P=0.01) and the recessive model (pooled OR 2.85, P=0.002). There appeared to be no significant association between dectin-1 SNPs and superficial FI.
CONCLUSION: Systemic review of the included studies suggested that dectin-1 SNPs rs3901533, rs7309123, and rs16910527 might play a role in FI susceptibility. The meta-analysis provided convincing evidence that dectin-1 SNPs might have an important role in FI susceptibility, especially for deep FI.