Coronavirus might be a new word for most people, but for a small cohort of scientists, that term has dominated their careers for decades. “I was writing reports about coronaviruses before it was cool,” jokes Frank Esper, a pediatric infectious disease specialist at the Cleveland Clinic.
That’s because the virus causing the COVID-19 pandemic isn’t the coronavirus — it’s a coronavirus, meaning it belongs to a larger group of pathogens that share the name because they look similar to one another. A couple of other viruses in this category have made headlines in recent years after international outbreaks, namely SARS in 2003 and the Middle East respiratory syndrome (MERS) outbreak that started in 2012.
Of the seven coronaviruses that have been circulating among humans, however, four of them just give someone a cold. Most people pick up at least one of these congestion-inducing viruses in their lifetime, and they’ve been bouncing between humans for a long time.
So how come some of these viruses grind society to a halt while others are part of our daily lives? After all, “none of those coronaviruses have rallied the world,” Esper says. “There’s no company working on a vaccine, let alone 100, against those other old coronaviruses.”
The answer depends on what the virus does to our bodies, as well as whether symptoms are obvious.
One way to distinguish this coronavirus, officially called SARS-CoV-2, from some of its other known human-infecting relatives is by the way it gets into cells. The viral proliferation process is straightforward, Esper says. “Find the back door into the cell, make a million copies, and get out.”
The “back door” refers to proteins covering cell surfaces called receptors. Since not all cells carry the same receptors, a virus that takes advantage of only one kind of receptor can only infect tissues that carry its necessary entry point. The new coronavirus takes advantage of a receptor common in the lung, heart, blood vessels and kidneys. Its virus relative that started the MERS outbreak hijacks another receptor featured in the lungs and digestive tract — which might explain why those who got MERS dealt with more gastrointestinal symptoms.
Which cells a coronavirus can enter doesn’t determine the severity of the disease alone, however. Part of what confuses physicians about this new coronavirus is that some of its viral relatives use the same cell receptors but cause very different illnesses. For example, the virus behind the 2003 severe acute respiratory syndrome outbreak — which, by the World Health Organization’s count, killed over 10 percent of the people it infected — used the same cell port of entry as the virus that causes COVID-19. But so does one of the coronavirus varieties that causes a cold. Death or severe illness from cold-causing coronaviruses is extremely rare, Esper says, and most common in the elderly or those with other preexisting conditions.
Also, even though the new coronavirus can enter tissue outside the lungs, Esper says he has yet to see a good study that shows the virus itself weasels into heart cells. That’s surprising, because some patients sick with this virus develop heart problems. Without the pathogen present in those tissues, some physicians like Esper think overactive immune systems are carrying out these mysterious organ damages.
To Be Successful, Be Forgetful
Besides confusing researchers with how it causes illness, the new coronavirus can also confound doctors by remaining effectively hidden in — and surreptitiously carried around by — untold numbers of symptomless patients.
Generally, the less obvious the symptoms, the more a virus can spread, Esper says. “The most successful viruses are the ones that happily trudge along and allow you to continue to go to work and go to school and shake hands.” That way, the coughs and sneezes carrying the pathogens are more likely to spread to new people. This approach explains why the common-cold coronaviruses have lingered unabated among us for so long.
The SARS and MERS outbreaks, on the other hand, were on the opposite end of the spectrum. Severe symptoms demand more medical attention, as well as warn those around sick patients not to get too close. “People were so identifiable and so bed-bound by their sickness, you couldn’t spread it very well,” Esper says.
The new coronavirus seems to have hit a disastrous sweet spot. People are infectious before they show any symptoms, and while some people hardly get a sniffle, others die in a matter of weeks. Though it doesn’t appear to be as lethal as SARS or MERS, COVID-19 can spread so far undetected that even the relatively low percentage of patients who end up incredibly ill is enough to overwhelm health care systems, Esper says.
Learning From Mistakes
Over time, the virus could go the way of the common cold. After all, if a virus is driven by evolution to survive and reproduce, sickening patients exclusively with surmountable symptoms would be a good way for the new coronavirus to linger in our communities for a long time. That process would take decades to pan out, Esper says, and is something he and his colleagues will be looking for as they collect more samples of the virus in their lab.
Even for someone who has studied other coronaviruses for a long time, there’s still a lot to learn about this new variety. “A lot of other coronaviruses have not been as attacked, from a scientific standpoint, as this one,” Esper says. And though SARS-CoV-2 is much scarier than its cold-causing relatives, those alarming features are also its greatest weakness, because they drive doctors and researchers to design interventions to stamp out COVID-19. “This one has gotten our attention,” Esper says. “And that’s exactly what they don’t want.”