There is growing evidence the UK variant of the coronavirus - more infectious and possibly deadlier than previous strains - picked up all of its mutations inside a single immunocompromised person.
Over the past two months, B.1.1.7 has become the dominant strain in the UK. Its impact is even affecting mostly COVID-free countries like Australia and New Zealand, whose short-lived travel bubble was canned when a community case showed up in Auckland, in a woman who likely contracted it at a quarantine hotel.
B.1.1.7 has 23 mutations, a lot for SARS-CoV-2, which evolves relatively slowly by virus standards. Its origins remain unclear, but scientists suspect all the mutations may have occurred in a single person whose immune system struggled to defeat the virus.
Researchers in the UK collected blood samples from a patient who had an active COVID-19 infection for 101 days before they died. Most people infected - even those suffering long-haul symptoms - have cleared the actual live virus out of their systems within two or three weeks.
Over the first two months, virus samples collected from the patient showed no sign of mutations - the doctors crediting the use of the drug remdesivir, which inhibits viral replication. The fewer replications, the fewer chances a virus has to mutate.
But with no signs of improvement, doctors switched to convalescent plasma - aiming to boost the patient's immune system and kill the virus outright.
"Following each convalescent plasma treatment important changes in the virus genome were observed, with the emergence of a viral variant bearing two mutations in the spike protein", the COVID-19 Genomics UK (COG-UK) group said in a statement.
The spike protein is the bit of the virus which allows it to enter our cells. Without eliminating the infection outright, the treatment put evolutionary pressure on the virus - killing off weaker cells, allowing only the stronger to survive, much like how overuse of antibiotics is leading to the creation of superbugs.
"The whole time, their immune system is effectively beating [the virus] up, so the virus has a chance to learn how to live with the human immune system," virus researcher Emma Hodcroft of the University of Bern told Wired.
The patient looked at in the COG-UK research isn't believed to be the specific individual whose body birthed the B.1.1.7 variant, but similar rapid evolution has been seen in other patients suffering lingering active infections of the virus.
The more hosts a virus infects, the more chance it has to mutate into various forms - but SARS-CoV-2 is so infectious, it doesn't get much time to rack up changes before it's onto the next host.
But inside the patient COG-UK studied, by the time he died the entire viral load was being replaced by new strains in as little as a week.
"What's going on biologically within a person is probably going to explain this because there are very different selection pressures going on," Prof Ravindra Gupta, who led the research, told Wired.
There are fears half-finished vaccine rollouts - where people get first shots, but not the second, as proposed in the UK - could do something similar on a population-wide scale. While there's evidence a single shot of two-shot vaccines like those from AstraZeneca and Pfizer/BioNTech does offer some protection, some epidemiologists fear having a population of partially-vaccinated people will simply apply evolutionary pressure to the virus, much like a person with a compromised immune system.
