a new variant of coronavirus has swept across the united kingdom and been detected in the united states, canada and elsewhere. scientists are concerned that these new strains may spread more easily.
as an evolutionary biologist, i study how mutation and selection combine to shape changes in populations over time. never before have we had so much real-time data about evolution as we do with sars-cov-2: over 380,000 genomes were sequenced last year.
sars-cov-2 has been mutating as it spreads, generating slight differences in its genome. these mutations allow scientists to trace who is related to whom across the family tree of the virus.
advertisement
the latter two examples are called “founder events”: a rapid rise in frequency can occur if a particular variant is introduced into a new group and starts a local epidemic. chance events may explain the rise in frequency of several different sars-cov-2 variants .
but b.1.1.7 is an exception. it shows a very strong signal of selection. for the past two months, b.1.1.7 has risen in frequency faster than non-b.1.1.7 in virtually every week and health region in england. this data, reported on dec. 21, 2020, helped convince u.k. prime minister boris johnson to place much of the country under lockdown and led to widespread travel bans from the u.k.
the spread of b.1.1.7 through england over november and december, with london inset at top-right. pic.twitter.com/fvfl0xijcx
— theo sanderson (@theosanderson) january 8, 2021
our ability to track the evolution of sars-cov-2 is due to the massive effort by scientists to share and analyze data in real time. but the incredibly detailed knowledge we have about b.1.1.7 is also due to just plain dumb luck. one of its mutations altered a section of the genome used to test for covid-19 in the u.k., allowing the picture of evolutionary spread to be drawn from more than 275,000 cases .
advertisement
epidemiologists have concluded that b.1.1.7 is more transmissible, but there are no signs that it is more deadly. some researchers estimate that b.1.1.7 increases the number of new cases caused by an infected individual (called the reproductive number or rt) by between 40 and 80 per cent ; another preliminary study found that rt increased by 50-74 per cent .
a 40-80 per cent advantage means that b.1.1.7 isn’t just a little more fit, it’s a lot more fit. even when selection is this strong, evolution isn’t instantaneous. our mathematical modelling, as well as that by others in canada and the u.s. , shows that it takes b.1.1.7 a couple of months to reach its meteoric rise, because only a small fraction of cases initially carries the new variant.
advertisement
the virus may have been carried by an immunocompromised individual . people with weaker immune systems fight the virus constantly, with prolonged infections, recurrent rounds of viral replication and only a partial immune response to which the virus is constantly evolving .
preliminary research reports that have yet to be verified have described two other variants of concern: one originally from south africa (b.1.351) and one from brazil (p1) . both variants show a recent history of excess mutations and rapid increases in frequency within local populations. scientists are currently gathering the data needed to confirm that selection for higher transmission, not chance, is responsible.
selection plays two roles in the evolution of these variants. first consider the role within those individuals in which the large number of mutants arose. b.1.1.7’s 23 mutations and p1’s 21 mutations aren’t randomly arrayed across the genome but clustered in the gene encoding the spike protein .
one change in the spike, called n501y, arose independently in all three variants, as well as in immunocompromised patients studied in the u.s. and u.k. other changes in the spike (e.g. e484k, del69-70) are seen in two of the three variants.
advertisement
beyond the spike, the three variants of concern share one additional mutation that deletes a small part of the drably named “non-structural protein 6” (nsp6). we don’t yet know what the deletion does, but in a related coronavirus nsp6 tricks a cellular defence system and may promote coronavirus infection . nsp6 also hijacks this system to help copy the viral genome . either way, the deletion might alter the ability of the virus to take hold and replicate within our cells.
the parallel evolution of the same mutations in different countries and in different immunocompromised patients suggests that they convey a selective advantage to evade the immune systems of the individuals in which the mutations occurred. for n501y, this has been backed up by experiments in mice .
that said, several of these variants have arisen before on their own and haven’t led to rapid spread. one study showed that n501y had only a weak transmission advantage on its own , rising rapidly only when coupled with the suite of mutations observed in b.1.1.7.
advertisement
while the evolutionary story of covid is still being written, one important message is emerging now. the 40-80 per cent transmission advantage of b.1.1.7, and potentially the other variants b.1.351 and p1, will overwhelm many countries in the next few months .