First we worried about the coronavirus.
Now we're worrying about coronavirus variants.
And there are a lot of them spreading around the world.
Some are more contagious and possibly more deadly.
What in the heck is going on with all these variants?
To answer this question, let's go back in time to January 2020, when we were all blissfully
going about our lives.
Back then, the coronavirus looked a bit like this.
Well, not really, but if it was made of puzzle pieces, it would look like this.
The virus is basically a ball with little "spikes" on the surface poking out.
Now, our cells aren't stupid.
They don't just let any virus inside willy-nilly.
The cell goes to great lengths to keep intruders out.
For anything to enter, the intruder must figure out a way for its spike to bind to another
spike on the cell's surface.
You can think of this binding as a secret handshake.
The handshake tells the cell, "Oh, it's OK.
We can let this guy inside."
That's exactly what SARS CoV-2 has done.
Sometime in 2019, probably in China, it figured out a way to interact with a specific "spike"
on the surface of human cells.
This interaction wasn't perfect.
But the binding was good enough to trick the cell s receptor.
And the receptor mistakenly told its cell, "Hey cell, this guy is friendly.
You can let him in."Ooooh.
Big mistake.
Once the virus was inside, it made a bunch of copies of itself, busted the cell wide
open and released new virus particles inside the blood, which went out and found another
cell to infect.
During this time, the body isn't standing by idly letting this attack occur.
Oh, no.
The immune system is already preparing a counterattack.
It's manufacturing antibodies.
Some of those antibodies act like little caps that stick to the ends of the virus's spike,
like this.
Once "capped," the spikes can no longer stick to the cell s receptor.
The infection can't move forward, and the body wins!
That was pretty much how coronavirus infections played out for nine months or so, until September
2020.
Then ... the virus got crafty.
And the pandemic began a new phase.
Every time 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.
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.
The result?
A person's cells get infected more easily or more of their cells let the virus inside.
We don't really know why, but that person may make more virus particles inside their
nose and upper respiratory system.
So when they sneeze, cough or just talk, they expel more virus.
And that's likely why the new variant is more contagious.
But wait, what about the antibodies?
What about the little caps on the spike?
Aren't they coming to save us again?
Well, yes ... and no.
Turns out, some of the mutations change the shape of the virus's spike in a way that's
double trouble for the cell.
Some antibodies no longer fit well to the end of the spike, so they can't form the little
caps that block viral infection.
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 may not be protected
as well against these new variants.
And that person may be more likely to be reinfected.
Now, antibodies are a diverse crew.
They come in a lot of different shapes that can bind to a lot of different parts of the
virus.
All of these other antibodies can help take down the virus and reduce infections.
So even though some antibodies become less useful, hopefully, others will take up the
slack and still get the job done or at least, stall the infection long enough so the body
can make new antibodies that fit perfectly on the mutated spike.