Human papillomavirus and herpes simplex virus infections in patients with mucocutaneous lesions can be linked to host TBX-21 gene polymorphism

Abstract

Background and objective: Human papillomavirus (HPV) and herpes simplex-2 (HSV-2) are the common cause of genital lesions in women. The variation in host genetic makeup can determine the consequence of a viral infection in that host. T-bet gene polymorphism has been associated with the incidence of several types of infections. This study investigates the impact of T-bet polymorphism on the incidence of HPV and HSV in genital lesions. Methods: 215 women, including 71 HPV infected, 72 HSV-2 infected, and 72 controls were enrolled. Viral genotyping was done on genital swab samples using Realtime PCR. In all participants, the extracted DNA from blood was tested for T-bet gene variation at Ch17.rs17244587 G>A site using ARMS-PCR. ELISA was done to participants sera to detect HSV-1 IgM. Results: Genotyping of HPV infection revealed that (73.0%) were at low risk. Most individuals (72.5%) were homozygous GG, while (20.9%) were heterozygous AG and (6.5%) were homozygous AA, of which 92.8% were HSV-2 infected patients. None of 18 (8.4%) HSV-1-IgM positive women were homozygous AA. Conclusion: T-bet gene allele A appears to be linked with more incidence of HSV-2 in genital lesions, but such influence was not observed for HPV genotypes and HSV-1. Keywords: HPV genotypes; HSV-2 infection; Genital lesion; T-bet polymorphism.

E -Selectin is associated with stable angina and myocardial infarction in a sample of Kurdish population

“…Hence, a number of studies have demonstrated that mutations resulted in glycine to arginine in the transmembrane molecules, of which E-selectin is a member, is associated with the majority of relevant diseases [28,29]. Indeed, there is a solid evidence that such highly charged mutations can lead to misfolding of transmembrane proteins and subsequently cause protein dysfunction [30,31]. In a very similar study Zhao et al, studied SNPs in the same region namely exon 4 of E-selectin.…”