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Dec 2025 DOI 10.14302/issn.2324-7339.jcrhap-25-5515
Rao AnaghaCorresponding author
Background Peripheral neuropathy (PN) is a common and debilitating complication in people living with HIV (PLHIV). While HIV itself contributes to neuropathy, certain antiretroviral therapy (ART) drugs, particularly nucleoside reverse transcriptase inhibitors (NRTIs) such as stavudine (d4T) and zidovudine (AZT), are known for their neurotoxic effects. Objectives To evaluate the impact of ART on HIV-associated peripheral neuropathy (HIV-PN) and to determine whether certain ART regimens increase the risk or severity of neuropathy. Materials and Methods A cross-sectional study was conducted among 158 HIV-positive patients. Neuropathy was diagnosed using clinical criteria, Total Neuropathy Score (TNS), and nerve conduction studies (NCS). Patients were grouped based on their ART regimen, and statistical analysis was performed to assess the association between ART type and peripheral neuropathy severity. Results It was noted that patients on older NRTIs (stavudine, zidovudine) had significantly higher rates of peripheral neuropathy (p=0.002) and tenofovir-based regimens were associated with lower peripheral neuropathy prevalence (p=0.01). There was a significant correlation between the duration of ART exposure and peripheral neuropathy severity (p<0.001), suggesting a cumulative neurotoxic effect. Conclusion Older ART regimens, particularly stavudine and zidovudine, significantly contribute to HIV-PN. The study supports the WHO recommendation to phase out neurotoxic ART and highlights the importance of early ART regimen optimisation to prevent long-term neurological complications.
Nov 2019 DOI 10.14302/issn.2324-7339.jcrhap-19-3070
Sharma BechanCorresponding author Department of Biochemistry, Faculty of Science, University of Allahabad, Allahabad-211002, UP, India.
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.