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Does Losartan block the receptor used by the Coronavirus?

Medically reviewed by Carmen Pope, BPharm. Last updated on March 20, 2024.

Official answer

  • Losartan is not a receptor, but it does block a chemical (angiotensin II), from binding to a receptor, type 1 angiotensin 2 (AT1), which lowers blood pressure.
  • Losartan does not block the virus causing COVID-19, called SARS-CoV-2, but it may reduce the activity of the renin-angiotensin system, which is overactive in people with high blood pressure, which may increase their risk of developing lung complications from COVID-19.
  • Some animal studies found losartan beneficial at reducing severe simulated lung injury in mice exposed to other viruses, such as SARS. Few human studies have been conducted.
  • For now, any beneficial effects of losartan are just a hypothesis (suggestion). It is not a good idea to institute any medical therapy based on an untested hypothesis since unexpected harms may outweigh any benefits.
  • For people already taking losartan or any other ARB, the advice from the medical community is to keep taking it unless your doctor tells you otherwise.

Losartan (Cozaar) belongs to a class of medicines called Angiotensin Receptor Blockers (ARBs), also known as Angiotensin II receptor antagonists.

Losartan work by blocking the action of a natural chemical called angiotensin II. ARBs prevent angiotensin II from binding to type 1 angiotensin 2 receptors (AT1) located in the heart, blood vessels, kidney, adrenal cortex, lung, and brain. Losartan, therefore, works on the renin-angiotensin system (RAS) which is a hormonal system that regulates blood pressure.

Losartan is not a receptor, but it does block a chemical (angiotensin II) from binding to a receptor (AT1), which lowers blood pressure.

Losartan has attracted interest from the medical community because losartan was used in some preclinical studies to determine its effectiveness against the SARS virus that first appeared in 2002. SARS was also a coronavirus and is like SARS-CoV-2, the virus that causes COVID-19.

The research was based on the theory that inhibition of an overactive RAS might increase the risk of pulmonary complications from viral infections. Studies that were conducted include:

  • Mice treated with losartan after an acid-induced lung injury and exposed to the SARS virus had less lung injury and fluid around their lungs than mice treated with placebo
  • Losartan, in addition to infusions of angiotensin-2, prevented severe lung injury and edema in mice that had had all their ACE-2 removed
  • Recombinant ACE2 infusions have improved lung injury in people with SARS
  • Acute respiratory distress syndrome secondary to reduced ACE2 activity has been observed in other viral pneumonias, such as H5N1 and H7N9 influenza
  • Mice given losartan after infection with H5N1 influenza had reduced lung edema and an increased rate of survival

We do not know whether the supposed benefits of ARBs during an episode of infection with SARS-CoV-2 outweigh the potential harms.

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