Medical staff members hugging each other in an isolation ward at a hospital in Zouping in China’s easter Shandong Province.
Photograph by STR/AFP via Getty Images
Mucus, though gross when outside the body, helps protect lung tissue from pathogens and make sure your breathing organ doesn’t dry out. The cilia cells beat around the mucus, clearing out debris like pollen or viruses.
Frieman explains that SARS loved to infect and kill cilia cells, which then sloughed off and filled patients’ airways with debris and fluids, and he hypothesizes that the same is happening with the novel coronavirus. That’s because
the earliest studies on COVID-19 have shown that many patients develop pneumonia in both lungs, accompanied by symptoms like shortness of breath.
That’s when phase two and the immune system kicks in. Aroused by the presence of a viral invader, our bodies step up to fight the disease by flooding the lungs with immune cells to clear away the damage and repair the lung tissue.
When working properly, this inflammatory process is tightly regulated and confined only to infected areas. But sometimes your immune system goes haywire and those cells kill anything in their way, including your healthy tissue.
“So you get more damage instead of less from the immune response,” Frieman says. Even more debris clogs up the lungs, and pneumonia worsens. (
Find out how the novel coronavirus compares to flu, Ebola, and other major outbreaks).
During the third phase, lung damage continues to build—which can result in respiratory failure. Even if death doesn’t occur, some patients survive with permanent lung damage. According to
the WHO, SARS punched holes in the lungs, giving them “a honeycomb-like appearance”—and these lesions are present in those afflicted by novel coronavirus, too.
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These holes are likely created by the immune system’s hyperactive response, which creates scars that both protect and stiffen the lungs.
When that occurs, patients often have to be put on ventilators to assist their breathing. Meanwhile, inflammation also makes the membranes between the air sacs and blood vessels more permeable, which can fill the lungs with fluid and affect their ability to oxygenate blood.
“In severe cases, you basically flood your lungs and you can’t breathe,” Frieman says. “That’s how people are dying.”
The Stomach: A shared gateway
During the SARS and MERS outbreaks,
nearly a quarter of patients had diarrhea—a much more significant feature of those zoonotic coronaviruses. But Frieman says it’s still not clear whether gastrointestinal symptoms play a major part in the latest outbreak, given cases diarrhea and abdominal pain have been rare. But why does a respiratory virus bother the gut at all?
When any virus enters your body, it looks for human cells with its favorite doorways—proteins on the outside of the cells called receptors. If the virus finds a compatible receptor on a cell, it can invade.
Some viruses are picky about which door they choose, but others are a little more promiscuous. “They can very easily penetrate into all types of cells,” says Anna Suk-Fong Lok, assistant dean for clinical research at the University of Michigan Medical School and former president of the American Association for the Study of Liver Diseases.
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SARS and MERS viruses can access the cells that line your intestines and large and small colon, and those infections appear to flourish in the gut, potentially causing the damage or the leakage of fluid that becomes diarrhea.
But Frieman says we don’t know yet if the novel coronavirus does the same. Researchers
believe COVID-19 uses the same receptor as SARS, and this doorway can be found in your lungs and small intestines.
one in the and New England Journal of Medicine one preprint in medRxiv involving 1,099 cases—have also detected the virus in stool samples, which might indicate the virus could spread via feces. But this is far from conclusive.
“Whether that kind of fecal transmission is occuring for this Wuhan virus, we don’t know at all,” Frieman says. “But it definitely looks like it’s there in the stool and it looks like people do have GI symptoms associated with this.”
Coronaviruses can also cause problems in other systems of the body, due to the hyperactive immune response we mentioned earlier.
2014 study showed that 92 percent of patients with MERS had at least one manifestation of the coronavirus outside of the lungs. In fact, signs of a full body blitz have been witnessed with all three of the zoonotic coronaviruses: elevated liver enzymes, lower white blood cell and platelet count, and low blood pressure. In rare cases, patients have suffered from acute kidney injury and cardiac arrest.
But this isn’t necessarily a sign that the virus itself is spreading throughout the body, says Angela Rasmussen, a virologist and associate research scientist at Columbia University Mailman School of Public Health. It might be a cytokine storm.
Cytokines are proteins used by the immune system as alarm beacons—they recruit immune cells to the site of infection. The immune cells then kill off the infected tissue in a bid to save the rest of the body.
Humans rely on our immune systems to keep their cool when facing a threat. But during a runaway coronavirus infection, when the immune system dumps cytokines into the lungs without any regulation, this culling becomes a free-for-all, Rasmussen says “Instead of shooting at a target with a gun, you’re using a missile launcher,” she says. That’s where the problem arises: Your body is not just targeting the infected cells. It is attacking healthy tissue too.
The implications extend outside the lungs. Cytokine storms create inflammation that weakens blood vessels in the lungs and causes fluid to seep through to the air sacs. “Basically you’re bleeding out of your blood vessels,” Rasmussen says. The storm
spills into your circulatory system and creates systemic issues across multiple organs.
From there, things can take a sharp turn for the worse. In some of the most severe COVID-19 cases, the cytokine response—combined with a diminished capacity to pump oxygen to the rest of the body—
can result in multi-organ failure. Scientists don’t know exactly why some patients experience complications outside of the lung, but it might be linked to underlying conditions like heart disease or diabetes.
“Even if the virus doesn’t get to kidneys and liver and spleen and other things, it can have clear downstream effects on all of those processes,” Frieman says. And that’s when things can get serious.
Liver: Collateral damage
When a zoonotic coronavirus spreads from the respiratory system, your liver is often one downstream organ that suffers. Doctors have seen indications of liver injury with SARS, MERS, and COVID-19—often mild, though more severe cases
have led to severe liver damage and even liver failure. So what’s happening?
“Once a virus gets into your bloodstream, they can swim to any part of your body,” Lok says. “The liver is a very vascular organ so [a coronavirus] can very easily get into your liver.”
Your liver works pretty hard to make sure your body can function properly. Its main job is to process your blood after it leaves the stomach, filtering out the toxins and creating nutrients your body can use. It also makes the bile that helps your small intestine break down fats. Your liver also contains enzymes, which
speed up chemical reactions in the body.
In a normal body, Lok explains, liver cells are constantly dying off and releasing enzymes into your bloodstream. This resourceful organ then quickly regenerates new cells and carries on with its day. Because of that regeneration process, the liver can withstand a lot of injury.
When you have abnormally high levels of enzymes in your blood, though—as has been a common characteristic of patients suffering from
SARS and MERS—it’s a warning sign. It might be a mild injury that the liver will quickly bounce back from or it could be something more severe—even liver failure.
Lok says scientists don’t completely understand how these respiratory viruses behave in the liver. The virus might be directly infecting the liver, replicating and killing off the cells itself. Or those cells might be collateral damage as your body’s immune response to the virus sets off a severe inflammatory reaction in the liver.
Either way, she notes that liver failure was never the sole cause of death for SARS patients. “By the time the liver fails,” she says, “oftentimes you’ll find that the patient not only has lung problems and liver problems but they may also have kidney problems. By then it becomes a systemic infection.”
Kidney: It’s all connected
Yes, your kidneys are caught up in this mess, too.
Six percent of SARS patients—and a full quarter of MERS patients—suffered acute renal injury. Studies have shown the novel coronavirus can do the same. It may be a relatively uncommon feature of the disease, but it is a fatal one. Ultimately 91.7 percent of SARS patients with acute renal impairment died, according to a 2005 study in . Kidney International
Like the liver, your kidneys act as a filter your blood. Each kidney is filled with about 800,000 of microscopic distilling units called nephrons. These nephrons have two main components: a filter to clean the blood and a little tubes that return the good stuff back to your body or send the waste down to your bladder as urine.
It’s the kidney tubules that seem to be most affected by these zoonotic coronaviruses. After the SARS outbreak,
the WHO reported that the virus was found in kidney tubules, which can become inflamed.
It’s not uncommon to detect a virus in the tubules if it’s in your bloodstream, says Kar Neng Lai, a professor emeritus at the University of Hong Kong and consultant nephrologist at Hong Kong Sanatorium and Hospital. As your kidneys are continuously filtering blood, sometimes the tubular cells can trap the virus and cause a transient, or milder, injury.
That injury could become lethal if the virus penetrates the cells and begins to replicate. But Lai—who was also a member of the first group of researchers reporting on SARS and contributed to the
Kidney International study—says there was no evidence that the SARS virus was replicating in the kidney.
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That finding, Lai says, suggests acute kidney injury in SARS patients might be due to a diverse set of causes, including low blood pressure, sepsis, drugs, or a metabolic disturbance. Meanwhile, the more severe cases that led to acute renal failure showed signs of—you guessed it—a cytokine storm.
Acute renal failure can also sometimes be brought on by antibiotics, multi-organ failure, or being connected to a ventilator for too long. Everything is connected.
Pregnancy and coronavirus?
It’s the great irony of the Twitter age that we know too little about the novel coronavirus as we drown in information updates about it. Medical journals have published several studies about this outbreak—some more vetted than others as researchers rush to feed the maw. Meanwhile, news outlets are reporting every development. All this information whirls around the internet where discerning fact from fiction is a notorious challenge.
“This is really unprecedented in terms of the up-to-the-minute reporting on what’s going on in these studies,” Rasmussen says. “It’s really tricky trying to sort through all of the information and figure out what’s really supported, what’s speculative, and what’s plain wrong.”
For example last week, doctors at a hospital in Wuhan reported that
two infants tested positive for the novel coronavirus, one just 30 hours after birth. Naturally, this troubling headline spread across news organizations, given it raised questions of whether pregnant women can infect their unborn children in utero or whether the disease can be transmitted during birth or through breast milk.
But let’s pump the brakes. Mother-to-infant transmission wasn’t observed
with SARS nor MERS despite numerous cases involving pregnant women. Plus, there are other ways a newborn could catch the coronavirus, Rasmussen says, such as by being born at hospital overrun with infected patients during a hectic emergency.
a new study published Thursday in offers preliminary evidence that the coronavirus cannot be passed from mother to child. The Lancet
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In the report, researchers observed nine women in Wuhan who had COVID-19 pneumonia. Some of the women had pregnancy complications, but all cases resulted in live births without evidence of transmitting the infection. While this study doesn’t completely rule out the possibility of transmission during pregnancy, it underscores the need to exercise caution in speculating about this disease.
“There needs to be a high standard of evidence before you can say that’s happening definitively—and certainly before you start making changes to how cases are managed clinically or in terms of public policy,” Rasmussen says.
“Right after the SARS outbreak, there was a big bunch of money and then it went away,” Frieman says. “Why don’t we have these answers? Nobody funded these things.”
This article has been updated to reflect the death toll and case count as of February 18. It was originally published on February 14. Also, the article originally misstated Anna Suk-Fong Lok’s title. She is the assistant dean for clinical research at the University of Michigan Medical School and former president of the American Association for the Study of Liver Diseases.
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