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  • 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

  • whythankfullyit'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 decidesfor some reason or anotherthat 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, thoughthat 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 itbecause 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 cellswhich y'know,

  • is nice of itherpes can hang out there long-term, as long as it stays relatively quiet.

  • Then, under various circumstanceslike, if you're stressed outthe 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 hearlike, say, if infected or vaccinated

  • people develop immunity for a decade or morewe won't really know that for a decade or more.

  • But, if the answer isn't as encouraginglike, if immunity lasts only weeks or

  • monthswe'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 ]

Thanks to Brilliant for supporting this episode of SciShow. Go to Brilliant.org/SciShow to

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感染COVID-19會讓你免疫嗎?| 科學秀新聞 (Does Getting COVID-19 Make You Immune to It? | SciShow News)

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