The Atlantic’s Ed Yong explains why this coronavirus is so contagious and deadly on this episode of Reset.
The virus responsible for the pandemic that has engulfed the globe — sickening almost half a million and killing more than 20,000 worldwide — is one of hundreds in the family of coronaviruses. Yet before the current outbreak, coronaviruses were poorly studied. They mostly circulate among animals, and in the few cases where they have infected humans, they’ve mostly caused symptoms of the common cold. And previous outbreaks of coronaviruses have been comparatively small. SARS and MERS together killed fewer people overall than this virus did in less than two months.
But now, understanding coronaviruses has become crucial as this one, SARS-CoV-2, continues to spread. And a big part of that understanding will come from looking at the virus itself. So, what do we know about this coronavirus so far, on a microscopic level? How does the virus work? And how does that impact what it does to the human respiratory system? How does it kill people?
The transcript of their conversation that appears below has been edited for length and clarity.
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What is up with this specific coronavirus? Why is it so good at spreading and infecting humans? Do we actually know that?
I would say that we don’t. But I think based on what we know, we can at least try to put together a plausible hypothesis. The thing that especially makes this virus hard is that it seems to have a long incubation time between first infecting a new person and then causing symptoms during which it seems to be able to transmit to a new host. And, specifically, the reason why its capacity to spread before symptoms is bad is that it allows it to really move around the world and within a country before people understand where it is.
But is there a specific reason why it is so good at infecting humans specifically because this thing originated in animals, right?
You’re right. Based on the structure of the virus, it seems that there are a few possible qualities that allow it to spread so easily. It seems to stick to our cells more strongly and more readily. And it seems to be able to infect cells throughout a wider part of the airways.
So the virus is basically a … ball with these proteins called spike proteins on the surface. Those spikes recognize and latch on to a protein called ACE2, which is found on the surface of our cells, and like a key fitting into a lock that is the first step to launching an infection. This is also what the original SARS virus did. It had spikes, which latched on to ACE2. But the specific shape of the spikes on this new virus, SARS-CoV-2, those spikes are much better at latching onto ACE2 they are a closer fit to the ACE2 protein.
What that means is that maybe it is easier for the virus to attach itself to our cells and maybe that might mean that it takes a lower dose of virus to begin an infection. Again, this is all pretty speculative, but it makes sense given the tight fit between those two molecules.
Okay, so the first thing is that this virus is better than previous coronaviruses at sticking to our cells. What’s the second thing?
Once that first attachment is made, the spike protein must be split into two separate halves in order for the infection to continue. With the original SARS virus, that split did not happen very easily. But with this new virus, it can be done by an enzyme called Furin, which cuts the two halves apart, and Furin notably is widespread. It’s made by the human body and it’s found in a lot of different types of tissues. And again, that might be important for explaining some of the weird characteristics of this virus.
Most respiratory viruses tend to infect either the upper or the lower airways. If they infect the upper airways, they spread very easily, but they tend to cause mild illnesses like a runny nose or what have you. If they infect the lower airways, they tend to cause more severe illness like pneumonia, but they are also harder to spread. SARS-CoV-2 seems to infect both sites, and maybe that’s because it relies on that widespread Furin enzyme and maybe that might explain some of its sneakiness. Maybe it spreads easily when it infects the upper airways before then moving to the lower ones to cause more severe illness.
It kind of sounds like it’s just very good at what it does. So what are the odds of having a coronavirus that has this particular combination of traits?
Whenever a new threat like this happens, there are always conspiracy theories about whether the new pathogen was designed or engineered to infect humans. And certainly it does nothing to quell those theories when you hear that it’s so well adapted to infecting human cells. It sounds improbable that a virus that was lurking in some wild animal should have exactly those right traits and then somehow managed to find its way into a human body. But there are a lot of coronaviruses out there that we don’t know about. And I think that’s the reality of the world that a lot of us don’t understand, that wild animals harbor millions, maybe billions of different kinds of coronaviruses.
Even though the odds that any one of them might infect us very well and cause a pandemic of the kind we’re seeing are very low, it actually becomes a reasonably likely scenario given how many possible viruses there are out there. This seems to be the one that, by pretty bad luck, had the right combination of traits to effectively and stealthily spread among human hosts.
Part of what makes this coronavirus pandemic so scary is that it’s killed a lot of people. What exactly does this virus do in the human body?
So, again, we’re left to speculate a little bit based on a combination of medical experience from people around the world, the results of, I think, only one autopsy to date, and then our understanding of what similar viruses like SARS have done in the past.
So this is a likely scenario. It may not be a 100 percent accurate one, but it’s sort of the best of what we’ve got right now. The virus seems to infect cells in the airways. It gets into those cells, reproduces, and then makes more copies of itself, causing the cells to die. Dying cells sluff off from the airways and carry the virus down into the lungs where the infections proceed even further. So now you’ve got a bunch of dead cells; you’ve got a fluid building up in the lungs. All of these can cause problems for people who are infected making it more difficult to breathe.
Is that the reason why having ventilators has suddenly become so important?
This is absolutely why ventilators are really important. The virus causes havoc in the respiratory system and makes it more difficult for people to breathe. … But the really serious problems seem to occur not just as a consequence of the infection itself but because of the body’s attempt to fight that infection. So the immune system will typically mount some kind of defense against the virus. But in some cases, that defense goes berserk. So the immune system radically overreacts and launches what is known as a cytokine storm.
And those kinds of reactions, that cytokine storm, are pretty common for a lot of new and severe infections. We saw them with the 1918 flu pandemic. We saw them with, I think, the 2009 flu pandemic. A lot of these new emerging infections cause the immune system to overreact because nothing like them has ever been encountered by an immunologically naive population before. And that overreaction drives a lot of the more severe symptoms that we see among the most severe cases of Covid-19.
I’m glad you brought up the more severe cases, because, as we all know, some people experience mild fever and chills and they eventually get over it while others are being hospitalized right now. Do we know the reason why some people are affected so strongly while others are not?
I would say that unfortunately, we don’t. Certainly, age seems to be a factor in that. Older people are at greater risk of more severe illness, and sadly, of dying from the disease. We don’t really know why that is. It might just be that older people are less able to mount an efficient initial immune response against the virus.
But there are almost certainly other factors at work here. We know that even within an age group, some people are more likely to get severe disease than others. Maybe that has something to do with their genetics. I think that’s very likely. It might have to do with, for example, the initial amounts of virus that they are exposed to.
A lot of younger people who seem to be doing really badly are health care workers who might be exposed to much higher levels of virus because they’re treating people who are very sick.
Other aspects of the immune system, like people’s pre-existing degree of immunity — not to this virus, but just in terms of how well their immune system is working — that might have an impact. There are lots of possible variables, and we don’t know which one of those is important right now, which means that we only have a very crude understanding of who is at risk and who is not.
Author: Daniel Markus