There is an interesting line in the Chinese study on remdesivir that has gone almost entirely overlooked, one that introduces an interesting, and potentially serious, conundrum. The authors of the study wrote that “Remdesivir did not result in significant reductions in SARS-CoV-2 RNA loads or detectability in upper respiratory tract or sputum specimens in this study….”
In short, what the authors are saying here is that remdesivir—an antiviral drug that is supposed to work by stopping the virus from replicating—did nothing to actually stop the virus from replicating. Patients who received remdesivir had the same viral load as those who didn’t.
Remdesivir is purported to work by inhibiting virus growth by blocking an enzyme—RNA-dependent RNA polymerase—that the virus needs to reproduce itself. If the drug worked the way it’s supposed to, the amount of measurable virus in patients administered remdesivir should be many times lower than that in the untreated control patients. That was not observed in the controlled trial done in Hubei province and published in the journal the Lancet. That means that any benefit remdesivir has as a treatment is not related to its antiviral effect, because no such effect was observed.
Many have critiqued the size of the China trial, saying it had too few enrollees to confidently assume the drug had no effect. But that argument does not apply in this case. The results from very few patients is all that is required to know whether a drug inhibits virus growth or not. Recall that AZT, the first effective treatment for HIV/AIDS, showed a very dramatic drop in virus load in a 36 patient study: 18 given the drug, 18 controls. An antiviral drug candidate that does not affect the virus load is not a promising therapy.
Remdesivir is not the equivalent of what AZT was for HIV/AIDS, as some pundits have claimed—not by a long shot. If Remdesivir is working to improve outcomes, data we are still waiting to see, it is not because it controls the virus. Most likely the Hubei study reached the appropriate conclusion—as the authors wrote, “Remdesivir is not associated with statistically significant clinical benefits.”