Since the SARS-CoV-2 strain of coronavirus that causes COVID-19 first began to circulate at the end of 2019, there has been much debate as to how its symptoms and efficacy at spreading compared to previous outbreaks such as flu, the common cold, and historic coronaviruses such as SARS and MERS. For a short while many were falsely claiming that the death rate and symptoms likened the COVID-19 disease to flu a dangerous assumption that led to misplaced complacency and was not supported by the mounting evidence for SARS-CoV-2’s incredible ability to spread. It’s since been more accurately compared to the historic coronaviruses, SARS and MERS.
SARS (severe acute respiratory syndrome) first emerged in the early 2000s. Similarly to COVID-19, it’s a coronavirus of zoonotic origin meaning it spread from animals. It’s believed to have passed from horseshoe bats to civets before being transmitted by humans. We now know, after close inspection of the novel SARS-CoV-2 pathogen, that it shares many physical properties with SARS, hence its name. Being members of the coronavirus family, both pathogens possess spike proteins which is how the invasive coronavirus cells are able to attack human cells. SARS-CoV-2 is also thought to have come from bats, with one of the most highly suspected intermediaries currently being pangolins the most trafficked animal in the world.
Despite the two pathogens’ similarities, they are not behaving in the same way as we compare the current outbreak of COVID-19 to that of the SARS outbreak in 2002-2003. A recent and very detailed Twitter thread from Peter Kolchinksy, virologist and author of The Great American Drug Deal, gives an in-depth account as to why the SARS-CoV-2 pathogen is a “nastier” virus than that which caused SARS. The answers reveals why adhering to physical (social) distancing guidelines is so essential in halting the spread of this deadly pathogen.
For clarification, in the tweets, Kolchinsky refers to the original SARS coronavirus as SARS-1 and the COVID-19 coronavirus as SARS-2.
…attach via their external spike protein to a protein on our cells called ACE2. Think of it as a particular doorknob that the virus knows how to turn. Every virus has a particular type of doorknob that it attaches to and turns so it can enter (infect) a cell.
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
For example, HIV has to turn two doorknobs: CD4 and typically CCR5. MERS attached to one called DPP4. All our cells are covered in all kinds of proteins that make them distinctive from one another. Those proteins aren’t there to let in viruses. They have all kinds of functions…
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
…& hence, are not quite alive). So what viruses see are a bunch of houses w/ varying doorknobs & they try to spread through the neighborhood (our bodies) looking for houses (cells) covered in the doorknobs that they know how to turn. HIV enters T cells b/c T cells are…
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
…via a droplet in the air (from cough) & quickly start infecting lung cells, causing severe damage person could really feel (i.e. become symptomatic). In other words, SARS-1 quickly made its presence known. In some patients, SARS-1 would go into the upper airways to replicate…
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
…from where it could spread to others with a cough (or just breathing). But b/c SARS-1 patients got very sick from all the virus replicating in their lungs, they were quarantined before others got close enough to get sneezed or coughed on.
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
SARS-2, on the other hand, takes up residence in the throat cells first, which doesn’t cause significant symptoms. The person can remain asymptomatic or might not think they have anything worse than a cold. And from that person’s throat…
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
For those skim reading, this is the crux of the differences in the two pathogens: how they manifest and spread, and why the SARS-1 virus was eventually halted.
So SARS-1 was a comparatively dumb virus. It went straight for the lungs, announced itself before it could spread to others, and so got social distanced into extinction. But SAR-2, the one plaguing us now, is stealthier, spreading first before revealing itself (and causing harm).
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
What’s the take-away for all of us? It’s that beating this virus means social distancing & wearing masks even if we think we aren’t infected. Because we might be. The virus might be replicating in our throats without us knowing (that’s its evil plan!), so put up a roadblock.
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
He also offered up some reassurances from what we’ve found out about the new coronavirus so far.
Another reassuring insight is that, as these patients’ immune systems revved up and produced antibodies, they stopped producing viable viruses. The researchers could still detect bits of the virus, but they couldn’t find evidence that, among those bits, there was any virus…
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
…prompt our immune system to produce high levels of such “neutralizing” antibodies that can inactive SARS-2, we’ll have a head start on the virus. Should any virus enter our bodies, those antibodies will help shut it down before it causes harm & keep it from spreading to others.
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
Some have asked, why would SARS1 and 2 infect throat & lung cells differently if they both use ACE2. Great question. There’s a lot more to viruses than which doorknobs they turn.
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
Also, some have questions about whether virus mutates too fast for a vaccine. Short answer, no. We’ll have a vaccine. Here’s detailed explanation. https://t.co/ZQ6RF7NpHt https://t.co/QmGHYt9OUY
— Peter Kolchinsky (@PeterKolchinsky) April 6, 2020
The silent incubation period of COVID-19 means that healthy people can be strolling about getting on with their daily lives having absolutely no idea that they are spreading the pathogen as they go. While you might only suffer mild symptoms or experience no symptoms at all, the further you travel, the more people you speak to, and inanimate objects you touch the higher the chance you have of passing it on to someone who will suffer severe disease.
Perhaps if you have friends who aren’t quite grasping the consequences, the above explanation involving doors and doorknobs might help them to understand.
This gif explains the importance of staying home in 10 seconds. Stay home, save lives. pic.twitter.com/vY1vztnWOU
— IFLScience (@IFLScience) March 23, 2020
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