A Fas Gene Polymorphism Influences Herpes Simplex Virus Type 2 Infection in South African Women
2010 (English)In: Journal of Medical Virology, ISSN 0146-6615, E-ISSN 1096-9071, Vol. 82, no 12, 2082-2086 p.Article in journal (Refereed) Published
Herpes simplex virus type 2 (HSV-2) is a common sexually transmitted infection (STI) worldwide that causes genital infection. Among several factors responsible, host genetic factors may play an important role in susceptibility to HSV-2 infection. Apoptosis is a vital mechanism in eliminating virus-infected cells and controlling viral infections. Apoptosis can be regulated and triggered by the interaction between Fas and Fas Ligand (FasL). Polymorphisms in genes encoding Fas and FasL might result in altered apoptosis and contribute in susceptibility to viral infections. Two polymorphisms in Fas gene (FasR-1377G > A, FasR-670A > G) and one in FasL gene (FasL-844T > C) have been well studied and associated with different diseases. These polymorphisms were investigated in 407 South African women of black African and mixed-ancestry origin to determine if they were associated with HSV-2 seropositivity. Two hundred sixty-five women were HSV-2 infected and 142 were non-infected. HSV-2 was detected using HerpeSelect ELISA test and genotyping was performed using TaqMan assay. FasR-1377A allele showed a statistically significant association (P = 0.008) with reduced risk of HSV-2 infection. Analyzing the FasR haplotypes also showed a statistically significant association (P = 0.0001) with FasR-1377/FasR-670 AG haplotype and reduced risk of HSV-2 infection. There was no significant association found with FasR-670A > G and FasL-844T > C polymorphisms and risk of HSV-2 infection. This is, to our knowledge, the first time a non-HLA genetic link with HSV-2 infection has been reported.
Place, publisher, year, edition, pages
2010. Vol. 82, no 12, 2082-2086 p.
fas, polymorphism, HSV, apoptosis
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-134110DOI: 10.1002/jmv.21926ISI: 000283628700013OAI: oai:DiVA.org:uu-134110DiVA: diva2:374263