| ORIGINAL ARTICLE
|Year : 2015 | Volume
| Issue : 1 | Page : 16-20
Tumour necrosis factor-alpha promoter polymorphism and its association with viral dilated cardiomyopathy in Indian population: A pilot study
B Mishra1, M Sharma1, S Sarkar1, A Bahl2, UN Saikia3, RK Ratho1
1 Department of Virology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Cardiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
3 Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Purpose: Tumour necrosis factor-α (TNF-α), a pro-inflammatory cytokine has been implicated in the pathophysiology of several viral infections. TNF-α promoter gene polymorphism is thus believed to play the modulating role in this disease pathogenesis. Several studies have shown the increased level of TNF-α in dilated cardiomyopathy (DCM). However, the role of the TNF-α promoter polymorphism is yet to be delineated in this regard. The present study for the first time tried to explore the association of TNF-α gene polymorphism with DCM of viral aetiology.
Materials and Methods: Eighteen histopathologically proven DCM cases with viral genome positivity and 17 healthy controls were genotyped using polymerase chain reaction of TNF-α promoter gene followed by restriction fragment length polymorphism to determine the SNPs of -238G/A, -308G/A, -857C/T and -863C/A. Results: Of the 18 DCM cases 4 (22.2%) were positive for adenovirus (AdV), 2 (11.1%) for enterovirus (EV) and 12 (66.7%) had co-infection. Six of the 18 DCM cases (35.3%) had -238G/A polymorphism, and 10 (55.5%) had -863 homozygous AA genotype. The association of these polymorphisms was statistically significant as compared to controls (P < 0.05). Conclusions: The present pilot study suggests the possible association of TNFα -238G/A and -863C/A polymorphism with DCM of viral aetiology.
Department of Virology, Postgraduate Institute of Medical Education and Research, Chandigarh
Source of Support: None, Conflict of Interest: None
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