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Infection and drug resistance

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Background Mannose-binding lectin (MBL) or mannose-binding protein (MBP), encoded by MBL2 gene and secreted by the liver, activates complement system through lectin pathway in innate immunity against the host's infection. Conflictingly, a number of MBL2 variants, rs1800450 (A>B), rs1800451 (A>C), rs5030737 (A>D), rs7096206 (Y>X), rs11003125 (H>L), and rs7095891 (P>Q) allele, have been found to be associated with compromised serum levels and pulmonary tuberculosis (PTB) susceptibility. The present meta-analysis study was performed to evaluate the potential association of these MBL2 gene variants with PTB susceptibility. Materials and methods A quantitative synthesis was performed on PubMed (Medline), EMBASE, and Google Scholar web database searches. A meta-analysis was performed to calculate the pooled odds ratios and 95% CIs for all the genetic models. Results A total of 14 eligible studies were included to analyze their pooled data for associations between alleles, genotypes, and minor allele carriers. The statistical analysis revealed the significant reduced PTB risk with homozygous variant genotype of rs1800451 polymorphism (CC vs AA: P=0.043; OR =0.828, 95% CI =0.689-0.994). Contrary to this, the variant allele of rs5030737 polymorphism showed association with increased PTB risk (D vs A: P=0.026; OR =1.563, 95% CI =1.054-2.317). However, the other genetic models of rs1800450 (A>B), rs7096206 (Y>X), and rs11003125 (H>L) MBL2 gene polymorphisms did not divulge any association with PTB susceptibility. Conclusion The current meta-analysis concludes that rs1800451 (A>C) and rs5030737 (A>D) polymorphisms of MBL2 gene play a significant role in PTB susceptibility. Further, well-designed epidemiological studies with larger sample size including consideration of environmental factors are warranted for the future.


Dove Medical Press Ltd.



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Computer Sciences | Life Sciences


MBL2; PTB; mannose-binding lectin; meta-analysis; polymorphism; pulmonary tuberculosis

Creative Commons License

Creative Commons Attribution-Noncommercial 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

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