The introduction of highly active anti-retroviral therapy (HAART) for Human Immunodeficiency Virus (HIV) infection has significantly improved the life expectancy of HIV positive patients. Hepatitis C virus (HCV) co-infection is common in HIV infected patients and is now a significant cause of morbidity and mortality. Optimal management and treatment of HCV in HIV infected patients is therefore essential. Interferon-alpha (IFN-alpha) and ribavirin is the mainstay of treatment for HCV infection in HIV infected people. The sustained virological response rate (SVR) with combination therapy is lower than that commonly observed in HCV mono-infected patients. This is, at least in part, due to the very high treatment drop out rates. Ribavirin in combination with HAART is associated with particular side effects such as mitochondrial toxicity. Therefore, vigilant monitoring of patients during therapy, in specialist centers is essential. Pegylated interferon (PEG-IFN) plus ribavirin is particularly promising as it is easier to administer and will probably become the treatment of choice for co-infected patients. A SVR is associated with genotype 2 and 3, in addition to a high CD4+ cell count and a low HCV load prior to therapy. The progression of HCV related liver disease in HIV positive patients is faster than in subjects with HCV infection alone. As a result, there is an increasing incidence of cirrhosis and end-stage liver disease in co-infected patients. Liver transplantation is being evaluated in many centers. To date the experiences are very limited but encouraging in term of survival rate.
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http://dx.doi.org/10.2174/1381612043384286 | DOI Listing |
EClinicalMedicine
December 2024
University of North Carolina Project-China, Guangzhou, China.
Background: Adolescents (10-19 years old) have poor outcomes across the prevention-to-treatment HIV care continuum, leading to significant mortality and morbidity. We conducted a systematic review and meta-analysis of interventions that documented HIV outcomes among adolescents in HIV high-burden countries.
Methods: We searched PubMed, EMBASE, Scopus, and the Cochrane Library for studies published between January 2015 and September 2024, assessing at least one HIV outcome along the prevention-to-care cascade, including PrEP uptake, HIV testing, awareness of HIV infections, ARV adherence, retention, and virological suppression.
Unlabelled: The persistence of HIV-1 reservoirs during combination anti-retroviral therapy (cART) leads to chronic immune activation and systemic inflammation in people with HIV (PWH), associating with a suboptimal immune reconstitution as well as an increased risk of non-AIDS events. This highlights the needs to develop novel therapy for HIV-1 related diseases in PWH. In this study, we assessed the therapeutic effect of CD24-Fc, a fusion protein with anti-inflammatory properties that interacts with danger-associated molecular patterns (DAMPs) and siglec-10, in chronic HIV-1 infection model using humanized mice undergoing suppressive cART.
View Article and Find Full Text PDFTo inhibit endocytic entry of some viruses, cells promote acidification of endosomes by expressing the short isoform of human nuclear receptor 7 (NCOA7) which increases activity of vacuolar ATPase (V-ATPase). While we found that HIV-1 infection of primary T cells led to acidification of endosomes, NCOA7 levels were only marginally affected. Contrastingly, levels of the 50 kDa form of the sodium/hydrogen exchanger 6 (NHE6) were greatly reduced.
View Article and Find Full Text PDFHIV-1 assembly is initiated by the binding of Gag polyproteins to the inner leaflet of the plasma membrane, mediated by the myristylated matrix (MA) domain of Gag. Subsequent to membrane binding, Gag oligomerizes and buds as an immature, non-infectious virus particle, which, upon cleavage of the Gag precursor by the viral protease, transforms into a mature, infectious virion. During maturation, the MA lattice underlying the viral membrane undergoes a structural rearrangement and the newly released capsid (CA) protein forms a mature capsid that encloses the viral genome.
View Article and Find Full Text PDFThe persistence of HIV-1 proviruses in latently infected cells allows viremia to resume upon treatment cessation. To characterize the resulting immune response, we compare plasma proteomics and single-cell transcriptomics of peripheral blood mononuclear cells (PBMCs) before, during, and after detectable plasma viremia. We observe unique transcriptional signatures prior to viral rebound including a significant increase in CD16 monocytes with increased anti-viral gene expression.
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