When the pandemic virus emerged a year ago, one refrain from scientists provided reassurance: It’s not mutating so quickly—the pathogen looks pretty stable. But recent news from the UK suggests that SARS-CoV-2 might be more of a moving target than we thought. Sequencing data from that nation described in a research manuscript posted online but not yet formally published in a scientific journal suggests that a widespread variant of the virus accumulated 17 new mutations in a short time span. Now virologists are scrambling to figure out whether these mutations render the virus more transmissible, a possibility that has already led 40 nations to implement travel restrictions against the UK.

The emergence of this worrying variant comes at a pivotal moment in the course of the pandemic: Public health officials are just now trying to decide who should be prioritized to receive the first Covid-19 vaccines approved for distribution in the US. Reports that so many mutations have arisen all at once in the new coronavirus—and that these mutations could have epidemiological consequences—add an important, but so far unappreciated, wrinkle to these deliberations. The pathogen likely has more opportunity to develop mutations in immunocompromised individuals than in other carriers. As a result, to guard against the emergence of new and more dangerous variants of SARS-CoV-2, we should consider moving immunocompromised people—who are themselves at higher risk of dying from Covid-19—closer to the front of the vaccination line.

Scientists are still puzzling over how the streak of new mutations arose in the UK variant. It could just be a fluke of how the virus has been tracked, where they somehow missed a gradual accumulation of changes as it passed from person to person through the population. But the abruptness with which the suite of new mutations cropped up has left researchers worried that all or most of the changes developed in a single person. When an active infection lingers in someone’s body, an arms race may develop between the virus and the immune system. Over time, mutations that allow the virus to evade successive waves of defenses such as antibodies could stack up; and the longer an infection lasts in a person, the more opportunities the virus has to add such variants.

Since early in the pandemic, doctors have suspected that people who are immunocompromised are particularly prone to just that kind of extended illness. Most people with Covid-19 are thought to stop shedding infectious virus after around 10 days from the time they were infected, but numerous outlier cases have been identified. These tend to involve people with weakened immune systems. A 71-year-old woman who became infected with the virus at a Washington nursing home in February, and who had a kind of cancer that limited her antibody production, ended up harboring the coronavirus for at least 105 days and being infectious for at least 70.

Could the virus mutate rapidly under such conditions? It’s certainly pretty stable over the course of a normal, shorter bout of Covid. A study posted online, which has not yet been formally reviewed and published in a journal, found very little viral mutation occurring in a general sampling of more than 1,000 people with the disease. At the same time, studies that have closely followed immunocompromised individuals have been less reassuring. Michigan researchers followed a 60-year-old man with cancer who was on medication to suppress his immune system’s B cells, which normally produce antibodies. Over the four months that they tracked him, the researchers found that SARS-CoV-2’s spike protein, which is the principal target of Covid vaccines, remained unchanged. However they did observe other mutations that popped up elsewhere in the virus, unrelated to the spike protein.

Meanwhile, scientists who studied the immunocompromised woman from the Washington nursing home “observed marked within-host genomic evolution of SARS-CoV-2 with continuous turnover of dominant viral variants.” In other words, the virus was definitely evolving variants—including those with changes to the spike protein sequence—during the course of her infection.