ArticleScientific reports2018
Stimulation of alpha2-adrenergic receptors impairs influenza virus infection.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Chronic Stress Induces Hepatic Steatosis via Brain-Hepatic Sympathetic Axis Mediated Catecholamine Resistance.International journal of biological sciences · 2026Article
- Screening of neurotransmitter receptor modulators reveals novel inhibitors of influenza virus replication.Frontiers in cellular and infection microbiology · 2025Article
- Beyond Antivirals: Alternative Therapies for Long COVID.Viruses · 2024Review
- Receptor-Loaded Virion Endangers GPCR Signaling: Mechanistic Exploration of SARS-CoV-2 Infections and Pharmacological Implications.International journal of molecular sciences · 2021Review
- The neuropsychiatric manifestations of COVID-19: Interactions with psychiatric illness and pharmacological treatment.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Anti-Influenza Drug Discovery and Development: Targeting the Virus and Its Host by All Possible Means.Advances in experimental medicine and biology · 2021Article
- The Association of an Alpha-2 Adrenergic Receptor Agonist and Mortality in Patients With COVID-19.Frontiers in medicine · 2021Article
- SARS-CoV-2 and the sympathetic immune response: Dampening inflammation with antihypertensive drugs (Clonidine and Propranolol).Medical hypotheses · 2020Article
- Host-Directed Antiviral Therapy.Clinical microbiology reviews · 2020Review
- Article
- The G Protein-Coupled Receptor FFAR2 Promotes Internalization during Influenza A Virus Entry.Journal of virology · 2020Article
- Advancements in Host-Based Interventions for Influenza Treatment.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A viruses cause seasonal epidemics and occasional pandemics. The emergence of viruses resistant to neuraminidase (NA) inhibitors and M2 ion channel inhibitors underlines the need for alternate anti-influenza drugs with novel mechanisms of action. Here, we report the discovery of a host factor as a potential target of anti-influenza drugs. By using cell-based virus replication screening of a chemical library and several additional assays, we identified clonidine as a new anti-influenza agent in vitro. We found that clonidine, which is an agonist of the alpha2-adrenergic receptor (α2-AR), has an inhibitory effect on the replication of various influenza virus strains. α2-AR is a Gi-type G protein-coupled receptor that reduces intracellular cyclic AMP (cAMP) levels. In-depth analysis showed that stimulation of α2-ARs leads to impairment of influenza virus replication and that α2-AR agonists inhibit the virus assembly step, likely via a cAMP-mediated pathway. Although clonidine administration did not reduce lung virus titers or prevent body weight loss, it did suppress lung edema and improve survival in a murine lethal infection model. Clonidine may thus protect against lung damage caused by influenza virus infection. Our results identify α2-AR-mediated signaling as a key pathway to exploit in the development of anti-influenza agents.
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Registered trials
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