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This episode was filmed on April 28th, 2020.
If we have more recent episodes on COVID-19, we will include them
in the description.
Scientists have learned a lot about the virus that causes COVID-19
since its discovery a few months ago, but one of the big lessons
is that people with it are super contagious.
For instance, on April 7th, the US Centers for Disease Control
published an analysis which estimated that, on average,
each person who caught the virus in Wuhan may have infected
five to six other people.
That’s about twice the estimate for SARS back in the early 2000s.
And, keep in mind that outbreaks grow exponentially, not linearly.
So if one person with SARS infects three others, and each of them
infect three, and so on, after five rounds, the disease has spread
to about 250 people.
But if a person with COVID-19 infects about six people,
who each infect five or six people, et cetera—after those five rounds,
more than 6000 people have caught it.
We don’t know all the reasons this disease is so contagious.
Researchers around the globe are still piecing together clues.
But by comparing this new virus to the related virus that causes SARS,
they’ve found some promising leads—and those leads might help us
figure out how to actually beat this thing.
How contagious a disease is depends on a lot of things,
and many of them overlap or interact.
Like, we know that one big thing that makes the
new coronavirus stand out is that people can pass along the infection
before they start showing symptoms.
This is what you might have seen referred to
as presymptomatic transmission.
And with this virus, there also appears to be at least some
asymptomatic transmission: people passing it along
who never become sick themselves.
For many diseases—including SARS—those kinds of transmission
just don’t happen.
The tricky part is explaining why.
The short answer is that those older diseases need
relatively large droplets of fluid from the airways
to successfully leap into someone else—the kind only expelled
by coughs or sneezes.
Meanwhile, this new virus may be making the jump on smaller droplets,
like the ones made by talking or breathing.
And if that’s true, we’re not entirely sure how it pulls that off.
One possibility is that people who are infectious have a ton
of virus particles in them, or a high viral load.
It’s basically a numbers game.
If their throat and nose contain a lot of viruses,
then even the smaller droplets they breathe out
could contain enough viruses to infect someone—
or what epidemiologists call the infectious dose.
Now, you might think you’d know if your body is chock full
of viruses—you’d assume you’d have, like, symptoms.
But that’s not necessarily the case here.
With many respiratory viruses, including the original SARS,
the symptoms actually come from your immune system’s reaction
rather than the virus itself.
And researchers are finding that people with COVID-19 can have
really high viral loads even though they aren’t super sick.
In fact, the timing of peak viral load, especially in the nose
and throat, seems to be really early on, like around
or even before the onset of symptoms.
That’s totally different than with SARS.
With that virus, peak viral load occurred about ten days
after people first showed symptoms.
That suggests the COVID-19 virus can infect cells and replicate
more quickly—or, in virology terms, it is a fitter virus.
So, essentially, this virus is more efficient at virusing
than the original SARS.
Which might seem strange since the two viruses are so alike.
I mean, they even get into cells the exact same way.
Both hitch a ride in on protein on our cell membranes
called angiotensin converting enzyme 2 or ACE2.
Normally, these enzymes play a big role in maintaining blood pressure,
so they’re found on a lot of cells, especially ones
in your respiratory system.
And both viruses use a specific protein to grab onto ACE2.
It’s called the spike protein because, well, it looks like
a spike sticking out of the surface of the virus.
But what differs between the SARS virus, SARS-CoV-1, and this virus
is how well they stick to ACE2.
Researchers estimate that this newer coronavirus binds
ten times more tightly to human ACE2s.
And that’s probably because it has a number of changes
to the part of the spike that actually binds with the enzyme.
In fact, about half of the amino acids in this particular region
differ between the two viruses.
This matters because the better a virus is at binding to its receptor,
the fewer viruses you need to infect a cell.
And ultimately, that may mean the infectious dose
is actually lower for this virus than SARS
or other respiratory viruses.
If so, that could also help explain why people can spread this virus
before they’re really ill, and why it can travel in smaller droplets.
It’s back to that numbers game—if it takes fewer viruses
to infect someone, then even small exposures to the virus
are more likely to get someone sick.
But there may also be other things helping to lower
the infectious dose, too.
Like, there’s a small chunk added to the spike protein
that experts think might make it more infection-ready from the get-go.
In other viruses, similar additions seem to make them more dangerous.
So this is one of the leads scientists are eagerly following up on
to figure out how this virus spreads so easily.
Even still, the infectious dose is just part of the story.
To fully understand why this virus can replicate so well,
scientists also need to understand everything that happens
after it’s pulled into the cell.
So far, what’s clear is that, like other coronaviruses,
this virus hijacks a process called endocytosis.
This is when a cell’s membrane folds inward, creating a little bubble
that carries in proteins and other stuff it can digest for parts.
SARS-CoV-2 can hitch a ride in these bubbles and use them
as a one-way ticket to the cell’s protein factories.
Then, instead of being digested, it breaks out—putting its genome
right where it will be translated and copied to make new viruses.
It’s possible the new coronavirus can do all this more efficiently
than other viruses—at least, it seems to in some cultured cells.
That could help explain how it’s able to copy itself so quickly.
But again, this is more of a lead than a conclusion at this point.
Finally, if all that’s not enough, the new virus might replicate
faster and spread from people who aren’t sick because it’s also
better at evading the immune system.
For example, its spike protein has extra binding sites for sugars
which could help “hide” important parts that the immune system
would normally recognize.
But also, the virus’s genome contains the blueprints for about
two dozen proteins that aren’t directly involved
in building new viruses.
Many of these probably help it dodge the cell’s virus detectors
—but we don’t know a whole lot about them yet.
What we do know is that there are nearly 400 specific differences
between the proteins of SARS-CoV-1 and SARS-CoV-2,
most of which are in these other proteins.
So there’s a lot more to look at.
So, we don’t know all of the reasons this virus is so contagious.
But we do know enough to follow up on some promising leads.
And doing that won’t just help answer the question in the title
of this video.
It’ll also help doctors hunt down the most effective treatments
and point researchers towards the best vaccine targets.
So, really, understanding what makes this virus so infectious
will help us figure out how best to defeat it.
One way to sharpen the reasoning skills that get us to answers
is to study logic.
Because that’s not just something for Mr. Spock to go on about --
it’s a whole discipline that forms the basis
for mathematical reasoning.
Brilliant offers an introductory course on logic, and if you like it,
you can also take Logic part II.
Brilliant’s courses in math, computer science, engineering, and more
all aim to help you hone your scientific thinking skills.
So if you’re interested in sharpening your mind, the first 200 people
to sign up at Brilliant.org/SciShow will get 20% off
the annual Premium subscription.
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