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Published on: April 1, 2019
Nitric Oxide Synthase 2 (NOS2) Gene Polymorphisms Association With Risk of Pulmonary Tuberculosis (PTB): A
Ebrahim Alijani1, Mahboobeh Sabeti Akbar-Abad2,3, Hossein Shahriari1
1Clinical Immunology Research Center, Zahedan University of Medical Sciences, Zahedan, Iran, zaums.ac.ir.
Background:
Pulmonary tuberculosis (PTB) remains a significant global health challenge, necessitating a deeper understanding of genetic factors influencing susceptibility. This study investigates the association between five specific polymorphisms in the nitric oxide synthase 2 (NOS2) genes (rs7215373, rs2297518, rs2274894, rs1800482, and rs9282799) and the risk of developing PTB.
Methods:
Utilizing a case-control design, we analyzed genetic samples from 150 PTB patients and 150 matched healthy controls. Genotyping was conducted using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) methods. Statistical analyses, including logistic regression and Hardy-Weinberg equilibrium tests, were performed to assess the associations between NOS2 polymorphisms and PTB risk.
Results:
Our findings indicate that the rs7215373 and rs2274894 polymorphisms had no significant association with the risk of PTB. rs2297518 in the allelic model significantly reduced the risk by 0.50 against the occurrence of PTB (p = 0.041). rs1800482 polymorphism in the Codominant 2 (p = 0.041), recessive (p = 0.043), and allelic (p = 0.007) models reduced the risk of PTB by 0.85, 0.80, and 0.75, respectively. However, our results in examining the rs9282799 polymorphism showed that, contrary to previous results, the Codominant 1 (p = 0.009), dominant (p = 0.005), overdominant (p = 0.012), and allelic (p = 0.004) models increased the risk of PTB by 3.80, 3.75, 3.78, and 3.49, respectively.
Conclusion:
These results suggest that specific NOS2 gene polymorphisms may play a role in modulating the immune response to Mycobacterium tuberculosis, highlighting their potential as biomarkers for PTB risk assessment. Further research is warranted to elucidate the underlying mechanisms and to explore the implications for targeted prevention strategies in high-risk populations.
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