Vaccines take months. That was the starting point for David Gurwitz, who wrote a short commentary in February 2020 on how to blunt the coronavirus while the world waited. His answer was not a new compound. It was a pill already sitting in millions of medicine cabinets.
Gurwitz works in the Department of Human Molecular Genetics and Biochemistry at the Sackler Faculty of Medicine, Tel Aviv University. He argued that angiotensin receptor 1 blockers, losartan being the example he named, deserved a look as a way to reduce the aggressiveness and mortality of SARS-CoV-2 infections. He was candid about the status of the idea. His own word for it was “tentative.”
The reasoning
The logic runs through a single protein. ACE2, he noted, is very probably where SARS-CoV-2 latches on, just as the earlier strain did for the SARS virus behind the 2002 to 2003 epidemic. If the receptor is the way in, then drugs that act on that pathway might change how badly the infection plays out.
There was a second argument, and it was practical. Vaccines built on viral-encoded peptides could be undone by mutations, and Gurwitz pointed out that new influenza strains force fresh immunizations every year. A treatment built on an existing drug, he suggested, would probably hold up against future mutations of the virus. Losartan is already prescribed, so no one would be starting from nothing.
What he did not offer was evidence of benefit. The commentary proposed a research direction: datamining clinical patient records to see whether people already taking such blockers fared differently. That is a way of asking the question, not an answer.
A second letter, same pathway
A separate letter in Infection Control & Hospital Epidemiology, put online on 17 March 2020, reached a similar place by another road. Its authors argued that death from COVID-19 most often follows respiratory failure from extensive, accelerating lung fibrogenesis. They described losartan as a selective, competitive AT1 antagonist that dampens the damaging ACE-AngII-AT1 axis, and said it may be suggested as protection from lung damage caused by the disease.
They too stopped well short of a claim. The hypothesis, they wrote, still has to be confirmed in laboratory and animal investigations. Neither paper tested a single patient. For all the noise a cheap, familiar drug can attract, both said the same thing: the idea was worth checking, and nobody should treat it as a treatment yet.
Sources
- Angiotensin receptor blockers as tentative SARS-CoV-2 therapeutics (Gurwitz, Drug Development Research; PubMed abstract)
- A potential protective role of losartan against coronavirus-induced lung damage (Infection Control & Hospital Epidemiology, Cambridge University Press)
