Sometime in 2019, probably in China, SARS CoV-2 figured out a way to interact with a specific “spike” on the surface of human cells, called ACE2. This interaction wasn’t perfect. The spike and the ACE2 didn’t fit together perfectly.
But the binding was good enough to trick the ACE2 receptor. And ACE2 — mistakenly — told its cell, “Hey cell, this guy is friendly. You can let him in.”
Everytime the virus copies itself inside a cell, it has the chance of mutating, or changing its genes slightly. Most of the mutations are actually harmful to the virus. They disable it. So these mutations disappear. And the regular coronavirus continues on its mission to find new cells to infect.
But every so often, the virus happens upon a set of mutations that actually help the virus.
In the case of the new variants, the mutations change the shape of the virus’s spike in a particular way — so that it fits better to the ACE2 receptor. So the spike can bind more tightly to the cell or more quickly.
As scientists say, these mutations help the virus “evade the immune system.” So a person who was infected with the older version of the virus last year may not be protected as well against these new variants. And that person may be more likely to be reinfected.