ApaI VDR Polymorphism as a Risk Factor of Treatment Failure in Chronic Hepatitis C Patients
Noora Hassan Hezam Al-Aqmer1*, Zain Aamir2, Muhammad Farooq Hanif3, Soumble Zulfiqar4, Sibgha Zulfiqar1, Mateen Izhar5 and Abdul Rauf Shakoori4*
1Department of Physiology, Shaikh Zayed Postgraduate Medical Institute, Shaikh Zayed Medical Complex, Lahore, Pakistan
2Primary and Secondary Healthcare Department, Lahore, Pakistan
3Gastroenterology and Hepatology, Pakistan Kidney and Liver Institute and Research Center, Lahore, Pakistan
4School of Biological Sciences, University of the Punjab, Lahore, Pakistan
5Department of Microbiology, Shaikh Zayed Postgraduate Medical Institute, Shaikh Zayed Medical Complex, Lahore, Pakistan
* Corresponding author: arshakoori.sbs@pu.edu.pk, drnooraalaqmer@gmail.com
Fig. 1.
RFLP pattern of ApaI VDR polymorphism (rs7975232) in 2% agarose gel showing homozygous wild AA genotype with a band of 744 bp (Lanes# 6, 9, 10, and 11), heterozygous Aa genotype with the bands 744, 527, and 217 bp (Lanes# 3, 4, 7, and 8), and homozygous mutant aa genotypes with the bands 527 and 217 bp (Lanes# 1, 2, and 5).