Pfizer’s antiviral pill Paxlovid is among the most valuable tools to pound COVID-19; it can reduce the relative risk of hospitalization and death by 89 percent in unvaccinated patients at high risk of serious disease. But as use of the convenient drug has increased in the US, there have also been worrying reports of rebound cases – people who took the pill early in their infection, felt better and even tested negative, but then had symptoms again and tested positive again were tested days later.
It is still unclear how common the phenomenon is, but it certainly occurs in a proportion of patients treated with Paxlovid. In May, the Centers for Disease Control and Prevention even issued a health alertt about the rebound reports.
But amidst the growing awareness, it has also become clear that patients who have not been treated with Paxlovid can recover. In fact, in Pfizer’s Paxlovid clinical trials, researchers found that about 1 to 2 percent of both the treatment and placebo groups had rebounds.
Taken together, this has raised a number of questions: are the rebounds reinfections? Are humans still contagious? Do they have to resume isolation? Are they at risk of serious illness again? Has your immune system not shown an effective response? Does the virus mutate to become resistant to Paxlovid? Does omicron cause more rebounds than previous variants?
So far there is only limited data and mostly only anecdotal reports. but a new, small, pre-print study led by researchers at the National Institutes of Health offers some encouraging news about COVID rebounds. The study, which included data from seven rebound patients — six of whom were treated with Paxlovid and one was not — found no evidence of Paxlovid-resistant mutations, viral replication run rampant, or stalled immune responses.
Intact immune responses
Instead, a detailed study of their immune responses revealed that rebounds were associated with increases in antibody and cellular immune responses specific to SARS-CoV-2. At the same time, rebounds were accompanied by downward trends in markers of innate (non-specific) immune responses and SARS-CoV-2 nucleocapsid fragments in the blood.
Taken together, the results suggest the rebounds could be partly due to a reignited immune response as the body works to clear cellular debris and viral debris from a rapidly smothered infection. Or, as the authors put it, “Rebound symptoms may actually be caused in part by the emerging immune response against residual viral antigens that may be shed from dying infected cells throughout the respiratory tract due to cytotoxicity and tissue repair.”
To further support this, the authors, led jointly by infectious disease experts Brian Epling and Joe Rocco, note that while three out of four control subjects had curable, live virus during their acute infection, only one out of seven patients did were recovering had a living virus at the time of their rebound. And this one patient also had underlying immunosuppression, which could explain the finding. In addition, none of the rebound patients developed serious illness.
Again, the study is very small and may not generalize to all rebound cases. The authors call for rebound studies with larger cohorts. However, some elements of the results are already secured. For example, other studies have also Paxlovid-resistant mutations could not be identified. And on Tuesday the CDC published a study of more than 5,000 patients treated with Paxlovidnoting that less than 1 percent of patients in the recovery phase had 5 to 15 post-treatment emergency visits or hospitalizations.
For now, the NIH researchers find their new findings “encouraging.” As Epling wrote in a tweet on Tuesday“The results suggest that “an adequate immune response develops such that a rebound is not caused by people not developing an immune response to COVID while taking Paxlovid.”
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