Thanks to Brilliant for supporting this episode of SciShow. Go to Brilliant.org/SciShow to
learn more about their Statistics Fundamentals course.
[ ♪INTRO ]
This episode was filmed on April 22nd. If we have a more recent episode about reinfection,
we’ll include it in the description.
There are now dozens of potential vaccines in development to fight the COVID-19 pandemic,
some of which are already being tested in humans.
Vaccines are one of the most powerful tools in medicine because they offer a path to immunity
without having to get seriously sick.
And once enough people have immunity, either because they got vaccinated or survived the
disease, we can achieve herd immunity and dramatically slow the infection rate.
Except... all of this only works if it’s actually possible to build up long-term resistance
to SARS-CoV-2, the virus that causes COVID-19.
And that, unfortunately, is not a sure thing.
So, today, let’s look at how immunity works, how the coronavirus could sidestep it, and
why — thankfully — it’s too soon for us to be worried.
The immune system is basically our body’s defense against infections and, like any good
defense, it has a number of layers.
In broad terms, you can break the immune system into two chunks, the innate and the adaptive.
The innate immune system provides our generic defenses that are always in action.
These can be physical, like your skin or the tiny hairs inside your nose, both of which
help keep pathogens from entering your body at all.
But the innate system also provides special kinds of cells that circulate through the
body and attack anything that seems too out of place.
For example, macrophages surround and basically consume hostile cells while releasing chemicals
that activate other parts of the immune system.
There are also the amazingly-named natural killer cells, which quickly attack viral infections
to buy time for other, more specific helpers to arrive.
Those helpers come from the adaptive immune system, which tailors itself to the specific
attacker the body is facing.
The adoptive system uses things like B cells, which quickly reproduce and create antibodies
designed to overwhelm and destroy some specific pathogen.
It also uses T cells, which can help regulate everything or even attack viruses themseves.
When your body sees a new intruder, like SARS-CoV-2, it takes time for these specialized cells
to develop and reproduce.
And once you get better, most of them die, but a few, called memory cells, can stick around.
They hang out in places like your lymph nodes and spleen and, if they see their old enemy
again, can quickly produce the cells needed to destroy it.
When this happens, someone is said to have active immunity. And it’s what scientists
are generally talking about when they talk about lasting immunity to COVID-19.
In some cases, like for chickenpox, immunity can last a lifetime.
But for other infections, like whooping cough, that protection can last only a few years.
After that, the body decides — for some reason or another — that it doesn’t need
those memory cells anymore.
So, the big question facing researchers right now is where on that spectrum the novel coronavirus falls.
Right now, there’s at least a little evidence that it’s possible to get sick with COVID-19 a second time.
For instance, the South Korean CDC has reported at least 180 cases of apparent reinfection,
which is about two percent of everyone who’s recovered. And about half of those people
have mild symptoms again, although there’s no evidence that they go back to being contagious.
But there are a few reasons patients might test positive after having seemingly recovered.
One could be that the test South Korea is using just isn’t that accurate, but that’s
not very likely. To be declared recovered, patients have to have two consecutive, negative
tests, spaced out by at least a day.
It is possible that the test is giving misleading results, though — that it’s correctly
picking up bits of SARS-CoV-2’s genetic material, but that those bits are just the
destroyed remains of the virus.
There’s even a little evidence to suggest that.
Because of that, some experts aren’t concerned about reinfections, but others are keeping
an eye on it — because testing aside, there are two big biological explanations for why
a recovered patient might get sick again.
The first is called latency, and it’s the idea that the virus can hide out in the body
only to reemerge later.
A common example of viral latency is herpes.
Around 90% of people worldwide are infected with the type-1 herpes simplex virus, which
can cause cold sores to develop.
Most of us don’t have cold sores all the time because the adaptive immune system can
effectively remove the virus once it’s detected.
But, because of latency, herpes stays with us for our entire lives by embedding itself
inside sensory neurons within the brain.
Since our immune system knows not to just blithely destroy brain cells — which y’know,
is nice of it — herpes can hang out there long-term, as long as it stays relatively quiet.
Then, under various circumstances — like, if you’re stressed out — the virus can
reactivate, and a new round of cold sores forms.
Latency, though, isn’t typically seen in other human coronaviruses, like the ones that
cause the common cold.
So unless we find evidence that suggests otherwise, there isn’t a huge reason to believe this
is true of this novel coronavirus.
The other big possibility is that SARS-CoV-2 just might not elicit a long-term immune response.
If your immune system doesn’t create many memory cells, or if they don’t last very
long, then it would be possible to catch COVID-19, get better, and then catch it all over again
like it was new.
That seems to be the case with the coronaviruses that cause the common cold.
Like, in one study of recruits for the US Marine Corps in the early 1970s, less than
half of those who caught a certain strain of the cold produced enough antibodies to
fend off a reinfection.
Why this happens is still more or less a mystery, in part because colds are so mild that researchers
in the 20th century didn’t put much effort into studying coronaviruses. And unless there’s
a major outbreak, researchers today don’t tend to focus much on them, either.
But some scientists think that memory B-cells are created with specific lifetimes and that
viruses that cause a bigger immune response result in longer-lived memory cells.
Since coronaviruses can suppress the immune system’s response, that might lead to shorter
periods of immunity.
Fortunately, not all coronaviruses create immunity as ineffectively as the common cold.
The virus causing COVID-19 seems to share much of its structure with the one that caused
SARS back in the early 2000s. And that infection did result in longer-term immunity for most people.
In a 2007 study of 176 people who survived their SARS infection, protective levels of
antibodies lasted for an average of around two years.
And a study of three patients published in 2016 found the presence of memory T cells
eleven years after their recovery from SARS.
Of course, just because the SARS virus is similar to the one that causes COVID-19 doesn’t
mean immunity has to work the same way in both diseases.
Looking at SARS is one way we can form hypotheses about COVID-19, but in the end, there aren’t
really any shortcuts to figuring out our lasting immunity to this virus.
If the answer is ultimately what we want to hear — like, say, if infected or vaccinated
people develop immunity for a decade or more —we won’t really know that for a decade or more.
But, if the answer isn’t as encouraging — like, if immunity lasts only weeks or
months — we’ll start to find that out sooner.
No matter what the answer is, though, it will be an important one, because it will guide
where scientists focus their effort and resources.
Like, if this virus has a very short period of immunity, all hope won’t be lost. That
would just mean it could be more important to find effective treatments rather than a
vaccine. Which researchers are working on already!
And actually we just did a whole episode about some of our best bets, which you could watch
right after this.
Ultimately, because of all this, it’s too early to really worry about COVID-19 reinfections.
And no matter what future studies say, there will still be things all of us can do to keep
ourselves and each other safe.
After all, wearing masks and keeping our distance will help reduce transmission regardless of
whether someone has been sick before or not.
In the meantime, doctors and scientists are working quickly to learn key details about
the new coronavirus and, once they’ve got them, they can help the world make decisions
about what we should do next.
If you want to learn more about how people study pandemics, learning about statistics
is a good first step. And if that sounds up your alley, you might enjoy Brilliant’s
Statistics Fundamentals course.
One of its goals is to help you pull truth out of a data set, and it’s got lots of
quizzes and interactive modules to help you get there.
Brilliant also has plenty of other courses about science, engineering, comp sci, and
math, so whatever you’re into, you’ve got options.
If you want to check it out, the first 200 people to sign up at Brilliant.org/SciShow
will get 20% off the annual Premium subscription.
[ ♪OUTRO ]