ReviewViruses2025
Deciphering Host-Virus Interactions and Advancing Therapeutics for Chronic Viral Infection.
Review in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Label-free quantification of early virus-induced cellular responses by digital holographic tomography.mSphere · 2026Article
- Integrative multi-omics analysis identifies SELL and PRF1 as key immune biomarkers and therapeutic targets in tuberculosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Past viral infections can shape inter-individual variability in anti-viral TLR responses.bioRxiv : the preprint server for biology · 2026Article
- Phage-Microbiota Interactions in the Gut: Implications for Health and Therapeutic Strategies.Probiotics and antimicrobial proteins · 2026Review
- Immune escape mechanisms and therapeutic advances in virus-associated hematological malignancies.Blood cancer journal · 2026Review
- Host Cell Virus Interactions: Molecular Mechanisms, Immune Modulation, Viral Pathogenesis, and Emerging Therapeutic Targets.Viruses · 2026Review
- Network Pharmacology and Transcriptomic Analysis Reveal the Therapeutic Mechanisms of Xiebai Bining Decoction in Hyperuricemic Nephropathy.Combinatorial chemistry & high throughput screening · 2026Article
- Modelling severe COVID-19 in TLR3-mutated hiPSCs-derived lung organoids.Cell death discovery · 2025Article
- The presence of persistent synovial inflammation after "Eradication" unmasks the "Unseen" dormant state of infection allowing the prediction of infection free survival in total joint replacements.Journal of translational medicine · 2025Article
- Sumac Polyphenols as Pan-Herpesvirus Inhibitors.International journal of molecular sciences · 2025Article
- Guanylate binding proteins (GBPs) as novel therapeutic targets against single-stranded RNA viruses.Molecular biology reports · 2025Review
- Efficacy of foot reflexology in reducing migraine pain: a randomized controlled trial.Annals of medicine and surgery (2012) · 2025Article
- Next-Generation Vaccine Platforms: Integrating Synthetic Biology, Nanotechnology, and Systems Immunology for Improved Immunogenicity.Vaccines · 2025Review
- The gut and circulating virome: emerging players in aging and longevity.Frontiers in aging · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic viral infections like HIV, HBV, and HCV establish persistent interactions with the host immune system, resulting in immune evasion and long-term immune dysfunction. These viruses use a range of strategies to limit host defenses, such as downregulating MHC class I, disrupting interferon signaling, altering apoptosis pathways, and suppressing cytotoxic T-cell activity. Key viral proteins, including HIV Nef, HBV X protein, and HCV NS5A, interfere with antigen presentation and JAK/STAT signaling, thereby reducing antiviral immune responses. Chronic infections induce immune exhaustion due to persistent antigen exposure, which leads to the expression of inhibitory receptors like PD-1 and CTLA-4 on T cells. Viral epigenetic changes, such as N6-methyladenosine modifications and histone deacetylation, enhance immune evasion by modulating gene expression in infected cells. Viruses further manipulate host cytokine networks by promoting an immunosuppressive environment through IL-10 and TGF-β secretion, which suppress inflammatory responses and inhibit T-cell activation. This review examines the molecular/cellular mechanisms that enable chronic viruses to escape host immunity, focusing on antigenic variation, cytokine disruption, and control of apoptotic pathways. It also addresses how host genetic factors, such as HLA polymorphisms, influence disease progression. Lastly, we discuss host-targeted therapies, including immune checkpoint inhibitors, cytokine treatments, and CRISPR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.