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Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses
Published on: January 20, 2017
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Methadone enhances human influenza A virus replication.
Yun-Hsiang Chen1,2, Kuang-Lun Wu1, Ming-Ta Tsai1
1Center for Neuropsychiatric Research, National Health Research Institutes, Taiwan.
Addiction Biology
|September 10, 2015
Summary
Methadone, but not morphine or buprenorphine, enhanced human influenza A virus (H1N1) replication in lung cells and mice. This suggests methadone may increase the risk of severe flu in patients undergoing treatment.
Area of Science:
- Virology
- Immunology
- Pharmacology
Background:
- Opioids are known to enhance human immunodeficiency virus and hepatitis C virus replication.
- The effect of opioids on other viral pathogens, like influenza A, remains largely uncharacterized.
Purpose of the Study:
- To investigate the interaction between opioid agonists and human influenza A virus (H1N1) in lung epithelial cells and a mouse model.
- To determine if methadone, morphine, or buprenorphine affects H1N1 replication.
Main Methods:
- Human lung epithelial A549 cells were exposed to morphine, methadone, or buprenorphine, followed by H1N1 infection.
- Viral propagation, adsorption, susceptibility, and protein synthesis were assessed.
- Adult mice were treated with methadone and infected with H1N1 to evaluate in vivo replication.
Main Results:
- Methadone significantly enhanced H1N1 viral propagation, increasing virus adsorption, susceptibility, and protein synthesis.
- Morphine and buprenorphine did not affect H1N1 replication.
- Methadone treatment led to increased H1N1 viral replication in mouse lungs.
Conclusions:
- Methadone facilitates influenza A virus infection in human lung cells and mouse lungs, potentially independent of opioid receptors.
- Findings raise concerns about an increased risk of severe influenza A virus infection in individuals receiving methadone maintenance treatment.
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