This is a must-read article by @mlipsitch and @kesvelt and I strongly agree with the central points: we urgently need to step up genomic surveillance & get transmission down now in the US while these are rare.

But a couple things to expand on from a virology point of view.

The piece talks about the B117 variant as if it’s not SARS-CoV-2, but it is. B117 is distinguished by 23 changes across the genome, but it’s still fundamentally the same virus. It’s a different variant (some are calling it a strain depending on how that’s defined).

But 23 nucleotide changes aren’t sufficient to make this a completely different virus. So we are still fighting SARS-CoV-2. Just a new and improved version. Improved how? Well it’s more transmissible but the mechanism isn’t yet known.

When viruses become more transmissible it can happen in a few different ways:
-virus can be more fit (replicate to higher titers, hence more shedding)
-virus can replicate more efficiently in specific tissues (like the nose)
-spike can bind the receptor more efficiently and...

...thus infect host cells more efficiently
-virus can get better at evading/antagonizing innate host antiviral defenses
-increased environmental stability
-people can shed virus for longer periods of time