Really? I would say the evidence is incredibly strong at this point, and it's very hard to explain it spreading this successfully via any effect other than sele

Really? I would say the evidence is incredibly strong at this point, and it's very hard to explain it spreading this successfully via any effect other than selective advantage. The "founder effect" and "post facto identification" explanations are just not credible any more, given that the explosive growth of B.1.1.7 compared to the wildtype has continued for almost a month after it was raised as a concern, and the pattern having now repeated in at least three other countries with enough data to make prevalence estimates (Ireland, Denmark and Switzerland). What alternative explanation would you propose? If the new variant is 50% more transmissive, then to get R to 1 requires measures that would previously have taken R to about 0.66. Clearly that is possible to achieve. But it's also not really enough. Can they get it significantly below 1, and for how long?