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  • Thanks to Brilliant for supporting this episode of SciShow.

  • Go to Brilliant.org/SciShow to learn more about their course on Logic.

  • [♪ INTRO]

  • 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 ceteraafter 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 leadsand 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 diseasesincluding SARSthose 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 elsethe 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 virusesyou'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 quicklyor, 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 gameif 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 outputting 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 virusesat 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 helphideimportant 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.

  • [♪ OUTRO]

Thanks to Brilliant for supporting this episode of SciShow.

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