Document Type : Original Article
Authors
1
Infectious Disease Research Center, Avicenna Institute of Clinical Sciences, Hamadan University of Medical Sciences, Hamadan, Iran.
2
Department of Microbiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
3
Immunology Department, Faculty of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
4
Research Center for Health Sciences, Department of Epidemiology, School of Health, Hamadan University of Medical Sciences, Hamadan, Iran.
5
Autism Spectrum Disorders Research Center, Institute of Neuroscience and Mental Health, Hamadan University of Medical Sciences, Hamadan, Iran.
Abstract
Prior research has indicated a potential link between the miR-146a rs2910164 genetic
variant and an individual's susceptibility to pulmonary tuberculosis (TB). Nevertheless, the
evidence from various studies is contradictory and has not yielded a consensus. This meta-
analysis was therefore conducted to systematically assess the relationship between this
specific single nucleotide polymorphism (SNP) and the risk of developing tuberculosis.
A systematic literature search was performed utilizing the electronic databases PubMed,
Web of Science, Scopus, and ISI to capture all relevant publications available through April
2024. To ensure comprehensive coverage, the reference lists of retrieved full-text articles
were also manually scrutinized. For the quantitative synthesis, pooled odds ratios (ORs)
with their corresponding 95% confidence intervals (CIs) were computed to determine the
overall effect estimates. The chi-square (χ²) test and the I² statistic were applied to assess
and quantify heterogeneity. This meta-analysis included 6363 individuals (2904 TB patients
and 3459 healthy controls) from eight case–control studies. The pooled effect estimates
across all genetic inheritance models (e.g., dominant model: OR = 0.971, 95% CI: 0.884–
1.068) did not reveal a significant link between the rs2910164 polymorphism and
susceptibility to tuberculosis. The analysis revealed considerable heterogeneity across most
genetic models, as indicated by I² statistics exceeding 70%. Conversely, statistical tests
found no evidence of publication bias. The collective evidence from this analysis does not
support a significant association between the miR-146a rs2910164 G>C variant and
tuberculosis susceptibility. Confirmation of this null association necessitates future
validation in large-scale, rigorously designed studies.
Keywords