Inflammatory markers associated with male genital Schistosomiasis and HIV co-Infection.
Schistosomiasis is a diseases caused by a water-borne parasitic trematode of different species of the genus Schistosoma. Male genital schistosomiasis is an infection caused by Schistosoma haematobium species which releases eggs into the reproductive tissues of the bladder. The released eggs cause granuloma lesions that induce an inflammatory response that include activation of CD4+ immune cells in the genitals leading to expression of receptors required by the HIV virus to attach and gain access into other cells. The prevalence of schistosomiasis and human immunodeficiency virus (HIV) are geographically concurrent and co-infection can have a higher unrecognized risk for progression and acquisition of the virus. In this study assessing CD4+ counts and the HIV viral load of infected individuals is important to know the impact that male genital schistosomiasis has on HIV progression. Assessing genetic variability of the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) and anti-inflammatory cytokine interleukin 10 (IL-10) in male individuals is a key factor in determining if there is an increased risk of HIV progression and transmission during co-infection. Samples (138) were collected from male of reproductive ages that are residing in Ngundu, Masvingo province. Individuals were initially screened for S. haematobium infection by urine filtration techniques and egg counts using a light microscope. Human immunodeficiency virus infection was determined by information from OI clinics and diagnosis was done voluntarily by serology using HIV rapid kits. The CD4+ counts in plasma and seminal viral loads were quantified using cell flow cytometry pre- and post-treatment with praziquantel. Cytokine levels in plasma were determined using ELISA methods. Extracted DNA from blood was used to detect single nucleotide polymorphisms of promoter sites -308 G/A of TNF-α and IL 10 G/A at position -1082 using Amplification Refractory Mutation System Polymerase Chain Reaction (ARMS-PCR). Plasma and seminal viral load decreased and CD4+ counts increased post treatment to prove the unknown impact of male genital schistosomiasis on HIV progression. The higher the infection intensity of male genital schistosomiasis, the higher the levels of TNF-α (P=0.51). Single nucleotide polymorphisms of the promoter site -308A/G TNF-α dominant A allele had the lowest frequency (11%) in the population but had the highest mean concentration levels (p=0.345). Interleukin 10 promoter position -1082 dominant G allele associated with the highest cytokine production had highest frequency but the cytokine levels were notably not different (p=0.44). Human immunodeficiency virus infected only individuals had lower TNF-α levels than MGS and HIV co-infected individuals as a result of MGS infection causing a continuous inflammatory environment therefore indirectly adding in HIV replication and progression. The levels of the TNF-α in circulation had an effect in the CD4+ counts showing that continuous inflammation as a result of male genital schistosomiasis infection has an effect on HIV infected individuals. Extended inflammatory condition as a result of schistosomiasis infection indirectly activates latent HIV thereby increasing progression. The results showed that male genital schistosomiasis infection has an effect on the viral loads and CD4+ counts of HIV infected individuals. The study on host immuno-genetics of IL-10 and TNF-α for schistosomiasis and HIV co-infection did not have a significant effect on the cytokine levels. However an increase or decrease in particular cytokine levels as a result of genotypic trends may contribute to understanding the underlying mechanisms driving transmission and progression in areas prevalent with co-infection.
Additional Citation InformationChoto, E.T. (2016) Inflammatory Markers Associated with Male Genital Schistosomiasis and HIV Co-Infection. (Unpublished thesis). University of Zimbabwe.
Male genital schistosomiasis
human immunodeficiency virus