Why Is This Virus So Contagious?

 Why Is This Virus So Contagious?

SARS-CoV-2 is super contagious, and researchers don’t yet know all the reasons why. But by comparing this new virus to the similar one that causes SARS, we’ve found a lot of promising leads that could help us figure out how to beat this thing.

 Scientists have learned a lot about the virusthat causes COVID-19 since its discovery a few months ago, butone of the big lessons is that people with it are super contagious. For instance, on April 7th, the US Centersfor Disease Control published an analysis which estimated that,on average, each person who caught the virus in Wuhanmay have infected five to six other people. That’s about twice the estimate for SARSback 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 aboutsix people, who each infect five or six people, et cetera—afterthose five rounds, more than 6000 people have caught it. 

We don’t know all the reasons this diseaseis so contagious. Researchers around the globe are still piecingtogether clues. But by comparing this new virus to the relatedvirus that causes SARS, they’ve found some promising leads—andthose leads might help us figure out how to actually beat this thing. How contagious a disease is depends on a lotof things, and many of them overlap or interact. Like, we know that one big thing that makesthe new coronavirus stand out is that people canpass along the infection before they start showing symptoms. This is what you might have seen referredto as presymptomatic transmission. And with this virus, there also appears tobe at least some asymptomatic transmission: people passingit along who never become sick themselves. 

For many diseases—including SARS—thosekinds of transmission just don’t happen. The tricky part is explaining why. The short answer is that those older diseasesneed relatively large droplets of fluid from theairways to successfully leap into someone else—thekind only expelled by coughs or sneezes. Meanwhile, this new virus may be making thejump on smaller droplets, like the ones made by talking or breathing. And if that’s true, we’re not entirelysure how it pulls that off. One possibility is that people who are infectioushave a ton of virus particles in them, or a high viralload. It’s basically a numbers game. If their throat and nose contain a lot ofviruses, then even the smaller droplets they breatheout could contain enough viruses to infect someone— or what epidemiologists call the infectiousdose. 

Now, you might think you’d know if yourbody 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 theoriginal SARS, the symptoms actually come from your immunesystem’s reaction rather than the virus itself. And researchers are finding that people withCOVID-19 can have really high viral loads even though they aren’tsuper sick. In fact, the timing of peak viral load, especiallyin the nose and throat, seems to be really early on, likearound or even before the onset of symptoms. That’s totally different than with SARS. With that virus, peak viral load occurredabout ten days after people first showed symptoms. That suggests the COVID-19 virus can infectcells and replicate more quickly—or, in virology terms, it isa fitter virus. 

So, essentially, this virus is more efficientat virusing than the original SARS. Which might seem strange since the two virusesare so alike. I mean, they even get into cells the exactsame way. Both hitch a ride in on protein on our cellmembranes called angiotensin converting enzyme 2 orACE2. Normally, these enzymes play a big role inmaintaining blood pressure, so they’re found on a lot of cells, especiallyones in your respiratory system. And both viruses use a specific protein tograb onto ACE2. It’s called the spike protein because, well,it looks like a spike sticking out of the surface of thevirus. 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 coronavirusbinds ten times more tightly to human ACE2s. And that’s probably because it has a numberof changes to the part of the spike that actually bindswith the enzyme. In fact, about half of the amino acids inthis particular region differ between the two viruses. This matters because the better a virus isat binding to its receptor, the fewer viruses you need to infect a cell. And ultimately, that may mean the infectiousdose is actually lower for this virus than SARS or other respiratory viruses. If so, that could also help explain why peoplecan spread this virus before they’re really ill, and why it cantravel in smaller droplets. It’s back to that numbers game—if it takesfewer viruses to infect someone, then even small exposuresto the virus are more likely to get someone sick. But there may also be other things helpingto lower the infectious dose, too. Like, there’s a small chunk added to thespike protein that experts think might make it more infection-readyfrom the get-go. In other viruses, similar additions seem tomake them more dangerous. So this is one of the leads scientists areeagerly following up on to figure out how this virus spreads so easily. Even still, the infectious dose is just partof the story.

 To fully understand why this virus can replicateso well, scientists also need to understand everythingthat happens after it’s pulled into the cell. So far, what’s clear is that, like othercoronaviruses, 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 itcan digest for parts. SARS-CoV-2 can hitch a ride in these bubblesand use them as a one-way ticket to the cell’s proteinfactories. Then, instead of being digested, it breaksout—putting its genome right where it will be translated and copiedto make new viruses. It’s possible the new coronavirus can doall this more efficiently than other viruses—at least, it seems toin some cultured cells. That could help explain how it’s able tocopy itself so quickly. But again, this is more of a lead than a conclusionat this point. Finally, if all that’s not enough, the newvirus might replicate faster and spread from people who aren’tsick because it’s also better at evading the immune system. 

For example, its spike protein has extra bindingsites for sugars which could help “hide” important partsthat the immune system would normally recognize. 

But also, the virus’s genome contains theblueprints for about two dozen proteins that aren’t directlyinvolved in building new viruses. Many of these probably help it dodge the cell’svirus detectors —but we don’t know a whole lot about themyet. What we do know is that there are nearly 400specific 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 thisvirus is so contagious. But we do know enough to follow up on somepromising leads. And doing that won’t just help answer thequestion in the title of this post. It’ll also help doctors hunt down the mosteffective treatments and point researchers towards the best vaccinetargets.

 So, really, understanding what makes thisvirus so infectious will help us figure out how best to defeatit.