As the number of people who are infected with, hospitalized for, and die from SARS-CoV-2 escalates each day, the world is increasingly desperate for an effective treatment. More than a hundred and fifty hospital workers in Boston, where I live and work, have contracted the virus, and I have relatives in New York and New Jersey who are hospitalized and fighting for their lives. A potential immediate solution, based on supposedly positive results from clinical studies in Marseille, France, which President Trump touted as a possible “game changer,” is a cocktail of an antimalarial and an antibiotic, hydroxychloroquine and azithromycin. On Saturday, the F.D.A. approved hydroxychloroquine and a related medication, chloroquine, for emergency use. Advocates for the cocktail argue that desperate diseases require desperate measures. But a study published on Tuesday, led by Jean-Michel Molina, an infectious-diseases expert at Hôpital Saint-Louis, in Paris, reports that, when prescribed in the same regimen as was followed in Marseille, the cocktail shows no benefit. This should give us serious pause before we rush into widespread use of prescription medications for SARS-CoV-2 and COVID-19. These drugs can have serious side effects, particularly in people most vulnerable to the virus: the elderly and those with heart problems.

As a physician who has worked on H.I.V./AIDS in the laboratory and at the bedside since the nineteen-eighties, I have become attuned to the value both of taking risks in the face of a devastating disease and of holding fast to solid science. (Molina worked with me on this research three decades ago.) I’ve learned that false hope is a powerful lure, which in the moment gives a welcome sense of respite and comfort but ultimately can do real harm. In the late eighties, studies in the test tube showed that what was called Compound Q, extracted from a Chinese cucumber plant, killed H.I.V. Some patients in California rushed to take it; the lucky ones suffered no side effects, while others experienced severe toxicity, and several died. In the end, the treatment was deemed ineffective and abandoned; it stands as an example of how what happens in the lab is often distant and distinct from what happens in our bodies.

In the test tube, hydroxychloroquine, administered in relatively high doses, can block SARS-CoV-2. Hydroxychloroquine, in the test tube, also blocks other potentially lethal viruses, such as H.I.V., garden-variety influenza, dengue, and chikungunya, the latter two of which are spread by mosquitoes. But subsequent rigorous scientific trials with control groups showed no evidence of benefit for actual patients with dengue or H.I.V., and no evidence of benefit preventing influenza. More worrisome, there is evidence that hydroxychloroquine worsened the condition of patients with chikungunya. We should take these disappointing results as cautionary tales about jumping from test-tube findings to clinical conclusions. On Tuesday, a report from China, on a trial using hydroxychloroquine alone to treat COVID-19 patients, was posted online. Although the researchers believe that the drug appears beneficial, a careful statistical analysis shows that there were insufficient numbers of patients to draw that conclusion and flaws in the design of the trial.

Other previously approved and readily available drugs have been considered as agents to combat SARS-CoV-2, specifically the antiviral drugs ritonavir and lopinavir, which have been used successfully against H.I.V. But a recent study published in The New England Journal of Medicine shows that, over all—despite test-tube data suggesting positive effects, and anecdotal reports from doctors who believe that the drugs may have helped their patients—the drugs have scant if any clinical benefit against the virus. They also have potentially serious side effects.

An editorial in the Wall Street Journal on Monday, applauding the F.D.A.’s decision to approve emergency use of hydroxychloroquine, linked to the most recent study from Marseille. The study claims that, of eighty patients taking the cocktail of hydroxychloroquine and azithromycin, seventy-eight showed “clinical improvement.” But a careful reading of the study reveals a striking finding: eighty-five per cent of the treated patients had no fever. Ninety-two per cent were in the lowest category for clinical deterioration. We know that many people with the virus have no symptoms at all, while others have mild to moderate ones, and that, in such people, their own immune systems can purge the microbe in a matter of days or weeks.

So a reasonable alternative reading of the results might be that the “clinical improvement” had nothing to do with the treatment; rather, the vast majority of the people in the study who were known to be at very low risk of becoming severely ill may have eradicated the virus on their own, and what the researchers observed was the natural history of the infection in those who were not destined to deteriorate. Without an untreated comparison group of eighty infected people, in which eighty-five per cent of them had no fever and ninety-two per cent were categorized as being at very low risk of becoming seriously ill, we’re left to conclude that there is no compelling evidence that the cocktail has a clinical benefit. The idea that it would be unethical to withhold potential treatment from patients in a control group does not really apply in this case, because, based on the researchers’ own reporting, the patients are not destined to deteriorate.

The Paris study that Molina oversaw was a pilot to try to discern any effect in reducing the virus in the time frame reported in Marseille. But it was composed of the kinds of patients who desperately need treatment: those with underlying conditions, a fever, and significant respiratory and other symptoms. (Here it would have been unethical to withhold a potentially useful therapy.) Eleven patients who were quite ill at the time of their admission to Hôpital Saint-Louis were given the antibiotic cocktail in the precise doses and on the schedule that was purportedly beneficial. Not only were the drugs ineffective in reducing the virus within the time frame; there was no evidence that they resulted in any clinical improvement. It’s important to emphasize that, in patients with H.I.V./AIDS and certain other viral illnesses, even those with severe symptoms, authentic antiviral agents will show some positive effects. That was the stunning benefit of the H.I.V. protease inhibitors that turned the tide of the AIDS epidemic.

So we are left with conflicting results from two studies. Neither is perfect, and Molina rightly calls for continued careful and rigorous assessment of the drug cocktail. Whether the President embraces (or dismisses) a potential treatment should not color any analysis of the design and execution of clinical trials of that treatment. We are in desperate need of hope, true hope, and that means being clear-eyed about all the difficulties and obstacles we face—not only about the gaps in the findings of others but also about our own assumptions and conclusions.

The Paris study is a wake-up call, one heard loudly by those, such as myself, who witnessed what truly powerful antiviral drugs did to dramatically reverse the ravages of AIDS, even in people with impaired immune systems. We must be alert to avoid detours of false hope that risk making us complacent and consume precious time and resources. We must keep our focus on pushing forward by developing and ultimately approving drugs that show real impact on the virus, beyond the test tube, to those in need.

A Guide to the Coronavirus