ArticleFrontiers in cellular and infection microbiology2021
The Chemokine CCL5 Inhibits the Replication of Influenza A Virus Through SAMHD1 Modulation.
Article in Frontiers in cellular and infection microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- CCL5 Levels, Disease Progression, and Mortality in Respiratory Viral Infections: A Systematic Review and Meta-Analysis.JAMA network open · 2026Pooled it
- Identification of host lncRNAs that impact Venezuelan equine encephalitis virus TC-83 replication.Journal of virology · 2026Article
- Host restriction factor SAMHD1 does not restrict seasonal influenza virus replication in human epithelial or macrophage-like cells.Virology journal · 2026Article
- Article
- Deciphering the antiviral mechanisms of Fangqin Qinggan decoction against influenza A virus: a multi-omics and machine learning approach.Chinese medicine · 2025Article
- A live attenuated NS1-deficient vaccine candidate for cattle-origin influenza A (H5N1) clade 2.3.4.4.b viruses.NPJ vaccines · 2025Article
- SAMHD1 enhances HIV-1-induced apoptosis in monocytic cells via the mitochondrial pathway.mBio · 2025Article
- Purine nucleoside phosphorylase dominates Influenza A virus replication and host hyperinflammation through purine salvage.Signal transduction and targeted therapy · 2025Article
- Decreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome.EBioMedicine · 2025Article
- Recombinant serralysin metalloproteases D enhances the intracellular replication of infectious bovine rhinotracheitis virus.Frontiers in microbiology · 2025Article
- Article
- Comprehensive snapshots of natural killer cells functions, signaling, molecular mechanisms and clinical utilization.Signal transduction and targeted therapy · 2024Review
- Immune Biomarkers at Birth Predict Lower Respiratory Tract Infection Risk in a Large Birth Cohort.Pathogens (Basel, Switzerland) · 2024Article
- Review
- Host Response Changes and Their Association with Mortality in COVID-19 Patients with Lymphopenia.American journal of respiratory and critical care medicine · 2024Article
- Antiviral and immunoregulatory effects of curcumin on coxsackievirus B3-infected hepatitis.Virus research · 2023Article
- Coronavirus Porcine Epidemic Diarrhea Virus Utilizes Chemokine Interleukin-8 to Facilitate Viral Replication by Regulating CaJournal of virology · 2023Article
- Seneca Valley virus induces proinflammatory cytokine and chemokine responseCanadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2023Article
- Low-Dose Lipopolysaccharide Protects from Lethal Paramyxovirus Infection in a Macrophage- and TLR4-Dependent Process.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) is the main etiological agent of acute respiratory tract infections. During IAV infection, interferon triggers the overexpression of restriction factors (RFs), the intracellular antiviral branch of the innate immune system. Conversely, severe influenza is associated with an unbalanced pro-inflammatory cytokine release. It is unclear whether other cytokines and chemokines released during IAV infection modulate RFs to control virus replication. Among the molecules enhanced in the infected respiratory tract, ligands of the CCR5 receptor play a key role, as they stimulate the migration of inflammatory cells to the alveoli. We investigated here whether ligands of the CCR5 receptor could enhance RFs to levels able to inhibit IAV replication. For this purpose, the human alveolar basal epithelial cell line (A549) was treated with endogenous (CCL3, CCL4 and CCL5) or exogenous (HIV-1 gp120) ligands prior to IAV infection. The three CC-chemokines tested reduced infectious titers between 30% to 45% upon 24 hours of infection. Eploying RT-PCR, a panel of RF mRNA levels from cells treated with CCR5 agonists was evaluated, which showed that the SAMHD1 expression was up-regulated four times over control upon exposure to CCL3, CCL4 and CCL5. We also found that IAV inhibition by CCL5 was dependent on PKC and that SAMHD1 protein levels were also increased after treatment with CCL5. In functional assays, we observed that the knockdown of SAMHD1 resulted in enhanced IAV replication in A549 cells and abolished both CCL5-mediated inhibition of IAV replication and CCL5-mediated cell death inhibition. Our data show that stimuli unrelated to interferon may trigger the upregulation of SAMHD1 and that this RF may directly interfere with IAV replication in alveolar epithelial cells.
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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 Socratic graph.