This study assessed the relationship between the quality of HIV care and treatment literacy on antiretroviral therapy (ART) adherence and viral suppression among female sex workers (FSWs) living with HIV (n = 211) in Santo Domingo, Dominican Republic. Multivariable logistic regression results indicate better patient-provider communication (AOR 1.04; 95% CI 1.01-1.07) and respectful treatment (AOR 2.17; 95% CI 1.09-4.32) increase the odds of viral suppression, while higher costs reduce both the odds of ART adherence (AOR 0.57, 95% CI 0.34- 0.95) and being virally suppressed (AOR 0.59, 95% CI 0.41-0.85). Greater treatment literacy was associated with an increased odds of ART adherence (AOR 4.15 for understanding of viral load; 95% CI 1.50-11.52) and viral suppression (AOR 2.75 for understanding of CD4 count; 95% CI 1.31-5.80). Findings support investments in treatment education, effective and respectful patient-provider communication, dignified care, and cost-support for associated HIV care costs to facilitate FSWs' pathway towards viral suppression.
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http://dx.doi.org/10.1007/s10461-022-03647-z | DOI Listing |
Viruses
December 2024
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
Achieving the precise targeting of lentiviral vectors (LVs) to specific cell populations is crucial for effective gene therapy, particularly in cancer treatment where the modulation of the tumor microenvironment can enhance anti-tumor immunity. Programmed cell death protein 1 (PD-1) is overexpressed on activated tumor-infiltrating T lymphocytes, including regulatory T cells that suppress immune responses via FOXP3 expression. We developed PD1-targeted LVs by incorporating the anti-PD1 nanobody nb102c3 into receptor-blinded measles virus H and VSV-G glycoproteins.
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December 2024
Department of Microbiology, Virology, and Immunology, I. Horbachevsky Ternopil National Medical University, 46001 Ternopil, Ukraine.
Metformin, a widely used antidiabetic medication, has emerged as a promising broad-spectrum antiviral agent due to its ability to modulate cellular pathways essential for viral replication. By activating AMPK, metformin depletes cellular energy reserves that viruses rely on, effectively limiting the replication of pathogens such as influenza, HIV, SARS-CoV-2, HBV, and HCV. Its role in inhibiting the mTOR pathway, crucial for viral protein synthesis and reactivation, is particularly significant in managing infections caused by HIV, CMV, and EBV.
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December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
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November 2024
Institute of Virology, Faculty of Veterinary Medicine, Justus-Liebig-University Giessen, Schubertstrasse 81, 35392 Giessen, Germany.
Some viruses can suppress superinfections of their host cells by related or different virus species. The phenomenon of superinfection exclusion can be caused by inhibiting virus attachment, receptor binding and entry, by replication interference, or competition for host cell resources. Blocking attachment and entry not only prevents unproductive double infections but also stops newly produced virions from re-entering the cell post-exocytosis.
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November 2024
Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.
The host enzyme heparanase (HPSE) facilitates the release of herpes simplex virus type 2 (HSV-2) from target cells by cleaving the viral attachment receptor heparan sulfate (HS) from infected cell surfaces. HPSE 2, an isoform of HPSE, binds to but does not possess the enzymatic activity needed to cleave cell surface HS. Our study demonstrates that HSV-2 infection significantly elevates HPSE 2 protein levels, impacting two distinct stages of viral replication.
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