Anti-depression drug suppresses replication of Sars-Cov-2
A study conducted by researchers at the Julius Maximilians University in Würzburg has shown that an anti-depression drug can be effective against high-risk acute respiratory syndrome caused by coronavirus in high-risk groups. Doctors have been using the antidepressant fluoxetine to treat mental health problems in patients for more than four decades. Now its active ingredient could also help fight Covid-19.
Can a medication for depression inhibit symptoms?
A study carried out by virologists and chemists from the University of Würzburg has shown that fluoxetine significantly inhibits the virus replication of SARS-CoV-2. The scientists believe that this is suitable for the early treatment of infected patients who are at higher risk of serious diseases. Jochen Bodem and colleagues found that the selective serotonin reuptake inhibitor (SSRI) fluoxetine inhibited the multiplication of the virus. In addition, the anti-depression drug specifically reduces the expression of viral proteins.
However, the team points out that the patent expired a long time ago. Clinicians started using fluoxetine back in the 1970s. It is also said that therapy with this well-studied depression medication is widespread and relatively inexpensive. Since December 2019, the corona virus has spread around the world. More than seven million infections have been registered worldwide and more than 400,000 people have died from the disease. Remdesivir remains the only medication option for treating seriously ill patients. The active ingredient has been shown to have a positive effect on the course of the disease. Other substances that are ideally more effective are therefore urgently sought. Scientists around the world are working hard to localize them.
The science team reports that the 0.8 µg / ml dose of fluoxetine effectively inhibits SARS-CoV-2 replication. However, the researchers claim that this suppressive effect is unlikely to include inhibition of the serotonin reuptake transporter, since neither paroxetine nor escitalopram inhibited virus replication. In addition, fluoxetine contains two optical isomers, and the S configuration is the dominant serotonin reuptake inhibitor. When they investigated which isomer inhibited SARS-CoV-2 replication, both had a similar effect. This underlines that the antiviral effect is not related to the serotonin reuptake receptor.
Using immunofluorescence imaging to further investigate the mechanism, the team found that treatment with fluoxetine reduced expression of viral proteins, indicating that the drug is acting before gene expression. Finally, the team tested the specificity of fluoxetine by determining its effects on other viruses. Fluoxetine did not inhibit the replication of the rabies virus or the human respiratory syncytial virus or the gene expression of the human herpes virus 8 or the herpes simplex virus. This shows that the anti-depression drug is also virus-specific, as the team describes it. The researchers believe that fluoxetine could play an important role in the early treatment of SARS-CoV-2 infected patients in high-risk groups.
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