Cron and other researchers believe such a balance is possible. Cytokine storms are not unique to COVID-19. The same basic process happens in response to other viruses, such as dengue and Ebola, as well as influenza and other coronaviruses. It is life-threatening and difficult to treat, but not beyond the potential for mitigation.

At Johns Hopkins University, the biomedical engineer Joshua Vogelstein and his colleagues have been trying to identify patterns among people who have survived cytokine storms and people who haven’t. One correlation the team noticed was that people taking the drug tamsulosin (sold as Flomax, to treat urinary retention) seemed to fare well. Vogelstein is unsure why. Cytokine storms do trigger the release of hormones such as dopamine and adrenaline, which tamsulosin can partially block. The team is launching a clinical trial to see if the approach is of any help.

One of the more promising approaches is blocking cytokines themselves—once they’ve already been released into the blood. A popular target is one type of cytokine known as interleukin-6 (IL-6), which is known to peak at the height of respiratory failure. Benjamin Lebwohl, director of research at Columbia University’s Celiac Disease Center, says that people with immune conditions like celiac and inflammatory bowel disease may be at higher risk of severe cases of COVID-19. But he’s hopeful that medications that inhibit IL-6 or other cytokines could pare back the unhelpful responses while leaving others intact. Other researchers have seen promising preliminary results, and clinical trials are ongoing.

If interleukin inhibitors end up playing a significant role in treating very sick people, though, we would run out.