Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 409 - 433
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 255 - 299
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 319 - 335
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 21 - 47
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Journal of environmental chemical engineering, Год журнала: 2024, Номер unknown, С. 115133 - 115133
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
4Antiviral Research, Год журнала: 2025, Номер 235, С. 106101 - 106101
Опубликована: Фев. 7, 2025
The global response to the COVID-19 pandemic, caused by novel SARS-CoV-2 virus, has seen an unprecedented increase in development of antiviral therapies. Traditional strategies have primarily focused on direct-acting antivirals (DAAs), which specifically target viral components. In recent years, increasing attention was given alternative approach aiming exploit host cellular pathways or immune responses inhibit replication, led so-called host-targeted (HTAs). emergence and promoted a boost this field. Numerous HTAs been tested demonstrated their potential against through vitro vivo studies. However, striking contrast, only limited number successfully progressed advanced clinical trial phases (2-4), even less entered practice. This review aims explore current landscape targeting that reached phase 2-4 trials. Additionally, it will challenges faced gaining regulatory approval market availability.
Язык: Английский
Процитировано
0Viruses, Год журнала: 2025, Номер 17(3), С. 390 - 390
Опубликована: Март 10, 2025
Chronic viral infections like HIV, HBV, and HCV establish persistent interactions with the host immune system, resulting in evasion long-term dysfunction. These viruses use a range of strategies to limit defenses, such as downregulating MHC class I, disrupting interferon signaling, altering apoptosis pathways, suppressing cytotoxic T-cell activity. Key proteins, including HIV Nef, HBV X protein, NS5A, interfere antigen presentation JAK/STAT thereby reducing antiviral responses. induce exhaustion due exposure, which leads expression inhibitory receptors PD-1 CTLA-4 on T cells. Viral epigenetic changes, N6-methyladenosine modifications histone deacetylation, enhance by modulating gene infected Viruses further manipulate cytokine networks promoting an immunosuppressive environment through IL-10 TGF-β secretion, suppress inflammatory responses inhibit activation. This review examines molecular/cellular mechanisms that enable chronic escape immunity, focusing antigenic variation, disruption, control apoptotic pathways. It also addresses how genetic factors, HLA polymorphisms, influence disease progression. Lastly, we discuss host-targeted therapies, checkpoint inhibitors, treatments, CRISPR.
Язык: Английский
Процитировано
0Опубликована: Апрель 17, 2025
Язык: Английский
Процитировано
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