Year: 2025
Type: article
Study design: Observational Study
Abstract: Although ART leads to viral suppression, people living with HIV (PLWH) still face an increased risk of comorbidities, such as cancer. The HIV-1 Tat protein may contribute to the promotion of chronic inflammation, oxidative stress, and genomic instability. While the presence of anti-Tat antibodies has been associated with slower disease progression, their potential role in modulating DNA damage remains unclear. Assess the effect of anti-Tat antibodies on cytotoxic and DNA damage in PLWH. A cross-sectional study was conducted in 178 PLWH. Serum anti-Tat IgG antibodies were measured using enzyme-linked immunosorbent assay (ELISA). Cytotoxicity and DNA damage were assessed via serum 8-hydroxy-2′-deoxyguanosine (8-OHdG) and nuclear anomalies (Micronucleus cytome assay) in 2000 buccal cells. Statistical significance was considered at p < 0.05. Anti-Tat antibodies were found in 24.2% of participants. Positive individuals had lower CD4+ T cell counts (p = 0.045) and higher levels of pyknosis (p = 0.0001). No differences in 8-OHdG were found, but 8-OHdG correlated positively with CD4+ counts (rho = 0.334, p = 0.006). Pyknosis negatively correlated with CD4+ counts (rho = −0.272, p = 0.027). Anti-Tat antibodies may not prevent DNA damage but could be related to cytotoxic effects in PLWH.
DOI: 10.3390/ijms26157229
Authors: Juan Ernesto Gutiérrez-Sevilla, Jorge Gaona-Bernal, Gracia Viviana González-Enríquez, Martha Escoto-Delgadillo, Guillermo Moisés Zúñiga-González, Belinda Claudia Gómez-Meda, Silvia Gabriela Luévano-Gómez, Alma Minerva Pérez-Ríos, Maribel Ávila-Morán, Víctor Eduardo García-Arias, Jessica Paloma Torres-Ríos, Jhonathan Cárdenas-Bedoya, Blanca Miriam Torres-Mendoza
Institutions: Mexican Social Security Institute, Universidad de Guadalajara
Language: English
Topic: HIV Research and Treatment
Subfield: Virology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,499
Award: G1775824999
OpenAlex ID: W4412694265
