One way the novel coronavirus can make humans very sick happens deep inside our lungs — a deadly dance between the virus and our immune systems run amok. KQED's Deep Look video team put together a primer to help explain how that happens.
Viruses hijack human cells
Viruses are simply genetic material wrapped in a layer of protein and fat. They exist in a gray zone between life and death — active inside a living host, powerless out in the open, then able to rise again in another host.
"The purpose of a virus is to persist," Ott says. Viruses do so by infecting and commandeering human cells — basically making each host cell into a "mini virus-producing machine," she says. From there, new virus particles spread.
Ott says the coronavirus has found a particularly good home in humans; it's able to cause less severe symptoms in many people, sometimes even being spread by those who are unaware they are carrying it.
"It's actually one step ahead of us in the way that it spreads relatively undetected in some people," she says. That allows this virus to "multiply and persist much longer than other deadly viruses."
An individual virus particle, called a virion, is invisible to the naked eye. It would take roughly 1,000 coronavirus particles to span the width of a human hair.
The virus spreads on moisture droplets through the air or on surfaces, eventually finding its way inside our bodies — typically through the eyes, nose or mouth.
A vicious double punch
Inside the body, the coronavirus attacks the cells in the back of the infected person's nose, replicating and spreading downward, and infecting healthy cells along the way.
Some viruses, like those that cause the common cold, infect upper airways, including the nose and throat. Others can cause viral pneumonia that usually infects smaller areas of just one lung.
The coronavirus packs a vicious double punch: It can infect the entire respiratory system, all the way down to millions of tiny air sacs in the lungs called alveoli.
"There aren't a lot of respiratory viruses that go both upper and lower, and this is one of them," says Dr. Michael Schivo, a pulmonologist at UC Davis Health. "No. 1, [the novel coronavirus] can make us sicker. And No. 2, it can cause low oxygen."
Alveoli make up 99% of the surface area of the lung, and they keep people alive by delivering oxygen from the lungs to the bloodstream and moving carbon dioxide from the blood to the lungs, so that gas can be exhaled.
When particles of the coronavirus enter the alveoli, they continue to replicate, injuring the lungs.
How our immune cells help us, but sometimes amplify damage
Inside the alveoli are immune cells called macrophages, which act as sentinels for the lungs. They're "waiting to fight off the cigarette smoke or pollution or anything else," says Dr. Michael Matthay, a professor of medicine at the University of California, San Francisco.
These macrophages act as first responders, Schivo says. "They recognize danger, and they try to get rid of it." If the body needs more help, it recruits more immune cells — white blood cells called neutrophils.
Sometimes, however, the immune system goes haywire during the battle, throwing relentless resources at the virus and wreaking more havoc than repair. This immune system overreaction is called a cytokine storm.
This two-pronged attack — from the virus and from our immune system's explosive response — makes some cases of the coronavirus deadly.
In the worst-case scenario, the walls of the alveoli begin to break down.
Fluid rushes from the blood vessels into the alveoli in these severe cases, filling up the tiny air sacs and blocking the exchange of gases. When this happens, the body can't excrete enough carbon dioxide or absorb enough oxygen. It becomes much more difficult to breathe.
These lung injuries can lead to acute respiratory distress syndrome, a condition that develops when fluid fills many alveoli on both sides of the lungs. ARDS is what kills most people who die from COVID-19.
To prevent those deaths and severe illness, scientists around the world are working simultaneously on treatments and — the ultimate hope — a protective vaccine.
"There's no reason to think we can't generate a vaccine," says Luis P. Villarreal, professor emeritus at the School of Biological Sciences at the University of California, Irvine. "Then it will be controlled just like measles was, and it can be eradicated if you choose to really implement it on a large scale. It would be difficult, but it could be eradicated."
This story and video were produced by our friends at Deep Look, a science video series from KQED and PBS Digital Studios that explores "the unseen at the very edge of our visible world." KQED's Jenny Oh is digital media producer for the series; health reporter Laura Klivans is the series' host. Additional reporting by Gabriela Quirós and Annie Roth.