Search

Human T lymphotropic virus 1 (HTLV-1) is a retrovirus associated with inflammatory diseases, including HTLV-1-associated myelopathy (HAM), and host genetic factors may be involved in disease evolution. The forkhead Box P3 (FOXP3) transcription factor is linked to homeostasis of the immune system, and the presence of polymorphisms in the promoter region of the FOXP3 gene should reflect its expression levels and consequent activation of regulatory T cells, which may contribute to severe inflammatory disorders, such as HAM. This study evaluated the rs2232365 polymorphism (−924 A/G) located in the promoter region of the FOXP3 gene and its association with HAM. Forty DNA samples from asymptomatic carriers and 25 samples from HAM patients were used, in addition to 130 control samples. The polymorphism was genotyped by conducting real-time polymerase chain reaction (PCR) (quantitative PCR [qPCR]) on extracted DNA. The proviral loads (PVLs) and CD4+ and CD8+ T lymphocyte counts were determined by qPCR and FACSCalibur flow cytometry, respectively. The PVLs, CD4+ T lymphocyte concentrations, and tumor necrosis factor-α dosages were considered predictive factors of the clinical profiles of HTLV-1 infection, all of which had higher levels in the HAM group. Carriers of the GG genotype for the polymorphism rs2232365 had high PVLs and CD4+ T lymphocyte concentrations. [ABSTRACT FROM AUTHOR]

Purpose: FOXP3 gene rs2232365 A/G and the rs3761548 A/C polymorphisms were associated with immune system-related diseases such as Hepatitis B virus (HBV) infection. The function of Treg cells which act as immune-suppressors in the control of HBV-related liver inflammation may be affected by these polymorphisms. The aim of the present study was to evaluate the association between these polymorphisms with HBV infection phases. Materials and Methods: The current study examined the FOXP3 gene polymorphisms in 116 patients with immune-active hepatitis B phase and in 116 individuals with inactive hepatitis B phase by a real-time polymerase chain reaction (RT-PCR). Results: In females, the A allele and AA genotype of rs2232365 polymorphism was not statistically significant although it increased 1.28- and 1.67-fold immune-active HBV risk. Although the G allele of rs2232365 polymorphism increased 1.69-fold immune active HBV risk, it was not statistically significant in males, either. Likewise, the rs3761548 polymorphism could not reach a statistically significant value in males and females, either. Conclusion: This research is to demonstrate the relation between phases of HBV infection and polymorphisms of the FOXP3 gene in the Turkish population. The results of this study showed that there is no effect of these polymorphisms on the immune-active phase of HBV, even though it increased immune-active HBV.

Purpose: FOXP3 gene rs2232365 A/G and the rs3761548 A/C polymorphisms were associated with immune system-related diseases such as Hepatitis B virus (HBV) infection. The function of Treg cells which act as immune-suppressors in the control of HBV-related liver inflammation may be affected by these polymorphisms. The aim of the present study was to evaluate the association between these polymorphisms with HBV infection phases. Materials and Methods: The current study examined the FOXP3 gene polymorphisms in 116 patients with immune-active hepatitis B phase and in 116 individuals with inactive hepatitis B phase by a real-time polymerase chain reaction (RT-PCR). Results: In females, the A allele and AA genotype of rs2232365 polymorphism was not statistically significant although it increased 1.28- and 1.67-fold immune-active HBV risk. Although the G allele of rs2232365 polymorphism increased 1.69-fold immune active HBV risk, it was not statistically significant in males, either. Likewise, the rs3761548 polymorphism could not reach a statistically significant value in males and females, either. Conclusion: This research is to demonstrate the relation between phases of HBV infection and polymorphisms of the FOXP3 gene in the Turkish population. The results of this study showed that there is no effect of these polymorphisms on the immune-active phase of HBV, even though it increased immune-active HBV. [ABSTRACT FROM AUTHOR]