Link between MnSOD Ala16Val (rs4880) polymorphism and asthma risk is insignificant from sequential meta-analysis.

The mitochondrial manganese superoxide dismutase (MnSOD) enzyme protects lungs against oxidative stress by neutralizing the free radical superoxide produced in the respiratory function. This has relevance to asthma. Therefore, it is of interest to describe the potential effect of MnSOD Ala16Val genetic polymorphism to asthma risk.

ACE deletion allele is associated with susceptibility to SARS-CoV-2 infection and mortality rate: An epidemiological study in the Asian population.

Background: Severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) is believed to have emerged from Wuhan, China, and spreads over 215 countries worldwide. The spike protein of SARS-CoV-2 binds to angiotensin-converting enzyme-2 (ACE-2) receptors and enter the host cells. Several reports have been highlighted the importance of ACE-2 on the pathogenesis of COVID-19.

Association of MBL-2 gene polymorphisms with systemic lupus erythematosus: an updated meta-analysis and trial sequential analysis.

Objectives: Mannose-binding lectin (MBL), an essential innate immune molecule, enhances the opsonization process and activates the complement system. Genetic variations at the promoter and coding region of the MBL-2 gene have been associated with susceptibility to systemic lupus erythematosus (SLE); however, reports remained inconsistent. The present study performs a meta-analysis of published peer-reviewed articles to draw a definitive conclusion.

TNF-α promoter polymorphisms (G-238A and G-308A) are associated with susceptibility to Systemic Lupus Erythematosus (SLE) and P. falciparum malaria: a study in malaria endemic area.

Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine associated with autoimmune and infectious diseases. Importance of TNF-α in P. falciparum malaria and systemic lupus erythematosus (SLE) have been demonstrated.

Pharmacogenetic association between gene polymorphisms and isoniazid induced hepatotoxicity: trial sequence meta-analysis as evidence.

Hepatotoxicity is a severe problem generally faced by tuberculosis (TB) patients. It is a well-known adverse reaction due to anti-TB drugs in TB patients undergoing long-term treatment. The studies published previously have explored the connection of N-acetyltransferase 2 () gene polymorphisms with isoniazid-induced hepatotoxicity, but the results obtained were inconsistent and inconclusive.

Association between vitamin D receptor polymorphisms and systemic lupus erythematosus in an Indian cohort.

Aim: Systemic lupus erythematosus (SLE) is an autoimmune disorder with various clinical manifestations. Susceptibility to development of SLE has been linked to several factors, such as genetic, environmental and hormonal. Vitamin D appears to have a regulatory role on disease manifestation and activity.

A Meta-analysis of MBL2 Polymorphisms and Tuberculosis Risk.

MBL2 gene encodes mannose-binding lectin, is a member of innate immune system. Earlier studies revealed that MBL2 gene variants, rs1800451, rs1800450, rs5030737, rs7096206, rs11003125 and rs7095891 are associated with impaired serum level and susceptibility to TB, but their results are inconsistent. A meta-analysis was performed by including 22 studies (7095 TB-patients and 7662 controls) and data were analyzed with respect to associations between alleles, genotypes and minor allele carriers to evaluate the potential association between MBL2 polymorphisms and TB risk.

Heterozygous mutants of TIRAP (S180L) polymorphism protect adult patients with Plasmodium falciparum infection against severe disease and mortality.

Toll-interleukin-1 receptor domain containing adapter protein (TIRAP) plays a crucial role in TLR2 and TLR4 signaling pathways. Glycosylphospatidylinositol (GPI), considered a toxin molecule of Plasmodium falciparum, interacts with TLR2 and 4 to induce an immune inflammatory response. A single nucleotide polymorphism at coding region of TIRAP (S180L) has been reported to influence TLRs signaling.