Some existing drugs might fight COVID-19. One may make it worse
In monkey cells, a common cough medicine ingredient stimulated virus growth
Scientists are investigating a variety of drugs, including ones for anxiety and allergies, that might prevent the coronavirus from hijacking different cell systems to replicate itself. But one medicine that patients with COVID-19 may be using to treat a symptom of the disease could make things worse, lab experiments hint.
A common ingredient in cough medicines, dextromethorphan, stimulated the growth of SARS-CoV-2 in monkey cells in lab dishes, researchers report April 30 in Nature. Dextromethorphan seems to activate a cellular stress-coping process that is also exploited by the virus for its replication.
“We’re not necessarily recommending that everyone stop taking dextromethorphan,” said Brian Shoichet of the University of California, San Francisco School of Pharmacy.
This work is only in lab experiments, he noted during a news briefing on April 30. In people, cough suppressants have not been shown to make infections worse. But because the lab results demonstrate “a pro-viral effect, it would be wrong not to highlight it, because it could be detrimental,” Shoichet said, noting that more work needs to be done. It’s “something to look out for.”
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Shoichet was part of an international team that mapped interactions between the coronavirus’s proteins and proteins found in human and monkey cells. Lung cells produce more of the proteins involved in these viral interactions, the researchers discovered, which may help explain why the virus causes severe disease in the lungs (SN: 4/27/20).
Scientists tested a battery of drugs to see if any could interrupt those interactions and limit the virus’s growth. Drugs that have shown some promise in lab experiments involving monkey cells include antipsychotics haloperidol and cloperazine; an anxiety and depression drug called siramesine; antihistamines clemastine and cloperastine; and an experimental drug called zotatifin, now in clinical trials testing its efficacy against cancer.
None has been tried against COVID-19 in people.
The team also found an experimental compound, PB28, that performed better than hydroxychloroquine at inhibiting the virus’s growth by interfering with certain protein interactions. Unlike hydroxychloroquine, PB28 doesn’t mess with heart rhythm proteins, so may have fewer side effects (SN: 4/21/20). PB28 also hasn’t been tested in people.
The hormone progesterone also interfered with the virus’s replication, perhaps partially explaining why women are less prone to die from COVID-19 than men (SN: 4/23/20).