Abstract
The telomeres existing at the end of the eukaryotic chromosome, play an important role in localization, pairing of homologous chromosomes during cell division and synapsis formation, while telomerase is involved in maintenance of the telomere length. The application of antiHIV-1 molecules particularly NRTIs have been shown to interfere with telomerase function thereby inducing aging processes. Since the application of these molecules has already indicated production of oxidative stress and toxicity in AIDS patients, their adverse impact on telomerase function may further worsen the situation. In addition, the negative influence of antiHIV-1 regimens on certain host factors involved in telomerase function may enhance aging. HAART changes the landscape of the disease by progressively decreasing the progression of HIV-1, but exerts prolonged adverse effects on the telomerase function. Though there is no exact information available on this issue, intensive efforts are needed to explore regulation of telomerase expression in HIV infected individuals and particularly those receiving antiretrovirals.
Highlights
Human Immunodeficiency Virus Type-1 (HIV-1) belongs to the retroviridae family and to the Lentivirus genus
The number of CD4+ T-lymphocyte cells
Kaposi sarcoma is the most common neoplasm occurring in persons with acquired immunodeficiency syndrome (AIDS); approximately 15 to 20% of AIDS patients develop this neoplasm, which only occurs in immune-competent individual[6]
Summary
Human Immunodeficiency Virus Type-1 (HIV-1) belongs to the retroviridae family and to the Lentivirus genus. The chemical agents which interfere in the normal biochemical function of the viral integrase, which catalyses the integration of proviral DNA (cDNA) into human genome include dolutegravir (DTG) and raltegravir (RAL) 3 The inhibitors of these two enzymes, have been found not to modulate or regulate the telomerase function. The TERT exhibits the ability to support a specific catalytic function i.e. RNA dependent RNA polymerization (RdRP)[6] It displays template independent terminal transferase activity[7]. The interactions between viral proteins and ARTs with the telomerase may induce immune deficiency in host and enhance level of oxidative stress in mitochondria which are associated with ageing This mini review article is an endeavour to present the updated and comprehensive information on the modulation of host telomerase activity by NRTIs/NNRTIs and induction of ageing processes there off
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