Diarrhoea-related morbidity is reduced by zinc supplementation in HIV-1-infected children. The mechanisms of this effect are largely undefined. We provide evidence for role for Tat (transactivating peptide produced by HIV-1) in the pathogenesis of diarrhoea in AIDS patients. In this study we showed that zinc, preventing Tat-induced fluid secretion, directly limits a specific mechanism of HIV-1-related diarrhoea. Our data support a 'zinc approach' in adjunct to specific antiretroviral therapy in HIV-1-infected children.
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http://dx.doi.org/10.1097/QAD.0b013e328011849a | DOI Listing |
Curr HIV Res
January 2025
Clinical Laboratory, The People's Hospital of Baoding, Baoding, Hebei, 071000, China.
Open Heart
November 2024
Department of Medicine, University of Cape Town, Observatory 7925, Republic of South Africa.
EClinicalMedicine
November 2024
School of Public Health, Shenzhen University Medical School, Shenzhen, China.
Background: Despite significant reductions in mother-to-child HIV-1 transmission risks due to the advancements and scale-up of antiretroviral therapy (ART), the global burden of HIV-1 drug resistance (HIVDR) in treatment-naive and treatment-experienced children and adolescents remains poorly understood. In this study, we conducted a systematic review and meta-analysis to estimate the prevalence of HIVDR in these populations globally, regionally, and at the country level.
Methods: We systematically searched PubMed, Embase, and Web of Science for studies reporting HIVDR in treatment-naive and treatment-experienced children and adolescents from inception to June 28, 2024.
HIV-1 envelope glycoproteins (Env) from primary HIV-1 isolates typically adopt a pretriggered "closed" conformation that resists to CD4-induced (CD4i) non-neutralizing antibodies (nnAbs) mediating antibody-dependent cellular cytotoxicity (ADCC). CD4-mimetic compounds (CD4mcs) "open-up" Env allowing binding of CD4i nnAbs, thereby sensitizing HIV-1-infected cells to ADCC. Two families of CD4i nnAbs, the anti-cluster A and anti-coreceptor binding site (CoRBS) Abs, are required to mediate ADCC in combination with the indane CD4mc BNM-III-170.
View Article and Find Full Text PDFBioorg Med Chem Lett
October 2024
State Key Laboratory of Biotherapy, Collaborative Innovation Center of Biotherapy and Cancer Center, West China Hospital of Sichuan University, Sichuan, Chengdu 610041, China. Electronic address:
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