The association of host genes with specific sexually transmitted infections

Abstract

Sexually transmitted infections (STIs) are hazardous to human health worldwide. STIs have a direct influence on sexual and reproductive health and can increase the chances of HIV. Globally, more than 1 million STIs are acquired every day and the majority are asymptomatic. Approximately, 374 million cases of STIs have been reported annually. The most prevalent STIs include chlamydia, gonorrhoea, syphilis, and trichomoniasis. These STIs are caused by Chlamydia trachomatis, Neisseria gonorrhoeae, Treponema pallidum and Trichomonas vaginalis. The major factor that contributes to the susceptibility and prognosis of infectious diseases is genetic variation. Host genes play a huge role in STIs and immune response. The production of host factors is stimulated by a variety of bacteria, viruses and parasites and the host factors can play a role in increasing host vulnerability to infection and pathogen persistence. Genetic variation or polymorphisms within certain host genes can influence the course of pathogen infection and disease progression. Polymorphisms can contribute to changes in gene expression and or changes in the protein structure. which may either contribute to/or protect against infection. This review discusses the role of host genes in influencing the susceptibility of the most prevalent STIs caused by Chlamydia trachomatis, Trichomonas vaginalis, Treponema pallidum and Neisseria gonorrhoeae. We evaluate polymorphisms associated pathogen recognition signalling pathway of these diseases. These polymorphisms may be used as biomarkers to infer risk to specific STIs.

Genetic predictors for bacterial vaginosis in women living with and at risk for HIV infection

“…Though BV has been associated with risk for STIs, we were not able to address rates of concurrent STIs as longitudinal testing for STIs was not performed in the cohort, although baseline rates of chlamydia were low in one substudy and there were no differences in history of self‐reported STIs by BV status 23 . A few studies have documented polymorphisms in TLRs and cytokines (IL‐10, IL‐17) associated with chlamydia and gonorrhea, though these are distinct from the polymorphisms in our study, and reported from small studies with participants from distinct racial/ethnic groups without assessment for genetic ancestry 66,67 . We did not stratify our analysis by HIV status due to the low number of HIV‐negative participants in each group and similar rates of BV in participants with and without HIV have been documented previously in the cohort 23 .…”

“…23 A few studies have documented polymorphisms in TLRs and cytokines (IL-10, IL-17) associated with chlamydia and gonorrhea, though these are distinct from the polymorphisms in our study, and reported from small studies with participants from distinct racial/ethnic groups without assessment for genetic ancestry. 66,67 We did not stratify our analysis by HIV status due to the low number of HIV-negative participants in each group and similar rates of BV in participants with and without HIV have been documented previously in the cohort. 23 We did not have protein expression data to assess in relation to these polymorphisms, and this should be pursued in future studies to explore the functional consequences of these genetic alterations.…”