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An official publication of the Middle-Eastern Association for Cancer Research
Clinical Cancer Investigation Journal
ISSN Print: 2278-1668, Online: 2278-0513
ARTICLE
Year: 2022   |   Volume: 11   |   Issue: 1 S   |   Paper ID: CCLS220170

The relationship between the regulatory tat gene and the Foxp3 gene expression level in HIV-infected individuals with AIDS


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Abstract

A major factor in the pathogenesis and progression of AIDS as an acquired immunodeficiency is a defect in immune responses through improved regulatory and inhibitory functions that can be used as one of the goals of immunotherapy in the treatment of these patients. An increase in the Foxp3 transcription factor as a marker of Treg and as a suppressor molecule of the immune system is directly related to T-cell activity regulation and the HIV disease progression. Their association with the progression and prognosis of HIV malignancies has been demonstrated in separate studies. This study aimed to investigate the relationship between the expression levels of the regulatory tat gene and Foxp3 in HIV patients.

Methods: This study examined peripheral blood mononuclear cells (PBMCs) from 46 imprisoned HIV-positive patients and 46 normal individuals (as controls). The expression levels of Foxp3 and tat viral genes were evaluated using the Real-Time PCR technique.

Results: The expression of the Foxp3 gene significantly (P < 0.05) increased in the samples of HIV patients, particularly those treated with HARRT drugs. The expression of tat viral gene increased significantly in patients undergoing HARRT treatment compared to those not using the drug. A direct and partial correlation was observed between the expression levels of Foxp3 and tat viral genes in individuals undergoing treatment.

Conclusion: An increase in the expression of Foxp3 as a key marker of Treg and the increased expression of the tat viral gene as an inducer of Treg seem to be useful in the more accurate examination of prognosis, particularly in individuals undergoing treatment.

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ISSN Print: 2278-1668, Online: 2278-0513