New York: How the Coronavirus Could Take Over Your Body (Before You Ever Feel It)

You call a friend and arrange to meet for lunch. It’s unseasonably springlike, so you choose a place with outdoor seating, which seems like it should be safer. As usual, you take all reasonable precautions: You use hand sanitizer, sit a good distance from other customers, and try to avoid touching your face, though that last part is hard. A part of you suspects that this whole thing might be overblown.

What you don’t know is that ten days ago, your friend’s father was a guest of his business partner at the University Club, where he caught the novel coronavirus from the wife of a cryptocurrency speculator. Three days after that, he coughed into his hand before opening the door of his apartment to welcome his son home. The saliva of COVID-19 patients can harbor half a trillion virus particles per teaspoon, and a cough aerosolizes it into a diffuse mist. As your friend walked through the door he took a breath and 32,456 virus particles settled onto the lining of his mouth and throat.

Viruses have been multiplying inside his body ever since. And as he talks, the passage of his breath over the moist lining of his upper throat creates tiny droplets of virus-laden mucus that waft invisibly into the air over your table. Some settle on the as-yet-uneaten food on your plate, some drift onto your fingers, others are drawn into your nasal sinus or settle into your throat. By the time you extend your hand to shake good-bye, your body is carrying 43,654 virus particles. By the time you’re done shaking hands, that number is up to 312,405

One of the droplets gets drawn into the branching passages of your lungs and settles on the warm, wet surface, depositing virus particles into the mucus coating the tissue. Each particle is round and very small; if you magnified a human hair so that it was as wide as a football field, the virus particle would be four inches across. The outer membrane of the virus consists of an oily layer embedded with jagged protein molecules called spike proteins. These stick out like the protrusions on a knobby ball chew toy. In the middle of the virus particle is a coiled strand of RNA, the virus’s genetic material. The payload.

As the virus drifts through the lung’s mucus, it bumps into one of the cells that line the surface. The cell is considerably larger than the virus; on the football-field scale, it’s 26 feet across. A billion years of evolution have equipped it to resist attackers. But it also has a vulnerability — a backdoor. Protruding from its surface is a chunk of protein called angiotensin converting enzyme 2, or ACE2 receptor. Normally, this molecule plays a role in modulating hormone activity within the body. Today, it’s going to serve as an anchor for the coronavirus.

As the spike protein bumps up against the surface of the lung cell, its shape matches that of the ACE2 so closely that it sticks to it like adhesive. The membrane of the virus then fuses with the membrane of the cell, spilling the RNA contents into the interior of the lung cell. The virus is in.

The viral RNA gets busy. The cell has its own genetic material, DNA, that produces copied fragments of itself in RNA form. These are continuously copied and sent into the main body of the cell, where they provide instructions for how to make the proteins that carry out all the functions of the cell. It’s like Santa’s workshop, where the elves, dutifully hammering out the toys on Santa’s instructions, are complexes of RNA and protein called ribosomes.

As soon as the viral RNA encounters a ribosome, that ribosome begins reading it and building viral proteins. These proteins then help the viral RNA to copy itself, and these copies then hijack more of the cell’s ribosomes. Other viral proteins block the cell from fighting back. Soon the cell’s normal business is completely overwhelmed by the demands of the viral RNA, as its energy and machinery are occupied with building the components of countless replica viruses.

As they are churned out, these components are transferred on a kind of cellular conveyor belt toward the surface of the cell. The virus membrane and spike proteins wrap around RNA strands, and a new particle is ready. These collect in internal bubbles, called vesicles, that move to the surface, burst open, and release new virus particles into your body by the tens and hundreds of thousands.

Meanwhile, spike proteins that haven’t been incorporated into new viruses embed themselves directly into the host cell’s membrane so that it latches onto the surface of an adjacent cell, like a pirate ship lashing itself to a helpless merchantman. The two cells then fuse, and a whole host of viral RNA swarms over into the new host cell.

All up and down your lungs, throat, and mouth, the scene is repeated over and over as cell after cell is penetrated and hijacked. Assuming the virus behaves like its relative, SARS, each generation of infection takes about a day and can multiply the virus a millionfold. The replicated viruses spill out into the mucus, invade the bloodstream, and pour through the digestive system.

You don’t feel any of this. In fact, you still feel totally fine. If you have any complaint at all, it’s boredom. You’ve been a dutiful citizen, staying at home to practice social distancing, and after two day of bingeing on the Fast & Furious franchise, you decide that your mental health is at risk if you don’t get outside.

You call up an ex, and she agrees to meet you for a walk along the river. You’re hoping that the end-of-the-world zeitgeist might kindle some afternoon recklessness, but the face mask she’s wearing kills the vibe. Also she tells you that she’s decided to move in with a guy she met at Landmark. You didn’t even know she was into Landmark. She gives you a warm hug as you say good-bye, and you tell her it was great to see her, but you leave feeling deflated. What she doesn’t know is that an hour before, you went to the bathroom and neglected to wash your hands afterward. The invisible fecal smear you leave on the arm of her jacket contains 893,405 virus particles. Forty-seven seconds after she gets home, she’ll hang up her coat and then scratch an itch at the base of her nose just before she washes her hands. In that moment, 9,404 viral particles will transfer to her face. In five days, an ambulance will take her to Mount Sinai.

Like a retail chain gobbled up by private equity, stripped for parts, and left to die, your infected cells spew out virus particles until they burn themselves out and expire. As fragments of disintegrated cells spread through your bloodstream, your immune system finally senses that something is wrong. White blood cells detect the fragments of dead cells and release chemicals called cytokines that serve as an alarm signal, activating other parts of the immune system to swing into action. When responding immune cells identify a cell that has become infected, they attack and destroy it. Within your body, a microscopic Battle of the Somme is raging with your immune system leveling its Big Berthas on both the enemy trenches and its own troops. As the carnage mounts, the body’s temperature rises and the infected area becomes inflamed.

Two days later, sitting down to lunch, you realize that the thought of eating makes you feel nauseated. You lie down and sleep for a few hours. When you wake up, you realize that you’ve only gotten worse. Your chest feels tight, and you’ve got a dry cough that just won’t quit. You wonder: Is this what it feels like? You rummage through your medicine cabinet in vain and ultimately find a thermometer in the back of your linen closet. You hold it under your tongue for a minute and then read the result: 102. Fuck, you think, and crawl back into bed. You tell yourself that it might just be the regular flu, and even if worse comes to worst, you’re young(-ish) and otherwise healthy. You’re not in the high-risk group.

You’re right, of course, in a sense. For most people infected with the coronavirus, that’s as far as it goes. With bed rest, they get better. But for reasons scientists don’t understand, about 20 percent of people get severely ill. Despite your relative youth, you’re one of them.

After four days of raging fever and feeling sore all over, you realize that you’re sicker than you’ve ever been in your life. You’ve got a dry cough that shakes you so hard that your back hurts. Fighting for breath, you order an Uber and head to the nearest emergency room. (You leave 376,345,090 virus particles smeared on various surfaces of the car and another 323,443,865 floating in aerosols in the air.)

At the ER, you’re examined and sent to an isolation ward. As doctors wait for the results of a test for the coronavirus, they administer a CT scan of your lungs, which reveals tell-tale “ground-glass opacities,” fuzzy spots caused by fluid accumulating where the immune-system battle is the most intense. Not only have you got COVID-19, but it’s led to a kind of intense and dangerous pneumonia called acute-respiratory-distress syndrome, or ARDS.

With all the regular beds already occupied by the many COVID-19 sufferers, you’re given a cot in a room alongside five other patients. Doctors put you on an intravenous drip to supply your body with nutrients and fluids as well as antiviral medicine. Within a day of your arrival, your condition deteriorates. You throw up for several days and start to hallucinate. Your heart rate slows to 50 beats a minute. When a patient in the next room dies, doctors take the ventilator he was using and put you on it. By the time the nurse threads the endotracheal tube down your throat, you’re only half-conscious of the sensation of it snaking deeper and deeper toward your lungs. You just lie there as she places tape over your mouth to keep the tube in place.

You’re crashing. Your immune system has flung itself into a “cytokine storm” — an overdrive of such intensity that it is no longer fighting just the viral infection but the body’s own cells as well. White blood cells storm your lungs, destroying tissue. Fluid fills the tiny alveolar sacs that normally let the blood absorb oxygen. Effectively, you’re drowning, even with the ventilator pumping oxygen-enriched air into your lungs.

That’s not the worst of it. The intensity of the immune response is such that under its onslaught, organs throughout the body are shutting down, a process known as multiple-organ-dysfunction syndrome, or MODS. When your liver fails, it is unable to process toxins out of your blood, so your doctors rush to hook you up to a round-the-clock dialysis machine. Starved of oxygen, your brain cells begin to expire.

You’re fluttering on the edge between life and death. Now that you’ve slipped into MODS, your odds are 50-50 or worse. Owing to the fact that the pandemic has stretched the hospital’s resources past the breaking point, your outlook is even bleaker

Lying on your cot, you half-hear as the doctors hook you up to an extracorporeal-membrane-oxygenation (ECMO) machine. This will take over the work of your heart and lungs and hopefully keep you alive until your body can find its way back to equilibrium.

And then, you are flooded with an overwhelming sense of calm. You sense that you have reached the nadir of your struggle. The worst of the danger is over. With the viral attack beaten, your body’s immune system will pull back, and you’ll begin the slow, painstaking journey to full recovery. Some weeks from now, the doctors will remove the tube from your throat and wheel away the ventilator. Your appetite will come back, and the color will return to your cheeks, and on a summer morning you’ll step out into the fresh air and hail a cab for home. And later still, you’ll meet the girl who will become your wife, and you’ll have three children, two of whom will have children of their own, who will visit you in your nursing home outside Tampa.

That’s what your mind is telling itself, anyway, as the last cells of your cerebral cortex burst in starburst waves, like the glowing algae in a midnight lagoon. In the isolation ward, your EKG goes to a steady tone. The doctors take away the ventilator and give it to a patient who arrived this morning. In the official records of the COVID-19 pandemic, you’ll be recorded as victim No. 592.

This story appeared in New York magazine on March 18, 2020.

35 thoughts on “New York: How the Coronavirus Could Take Over Your Body (Before You Ever Feel It)”

  1. Wow. This should be printed on leaflets and air dropped over every spring break beach.

  2. I read this yesterday and it messed me up; came back to read it again today to twist the knife further. It’s really such beautiful, devastating writing.

  3. This is such a well-written piece, so amazing and crazy at the same time… and will possibly haunt me in my dreams.

  4. This is a really well researched piece Jeff. Also of course it’s well written. The medical terminology is spot on. And yes the mechanism of death with COVID-19 seems to be cardiac arrest over and above the inability to oxygenate properly. The thickening of the alveolar endothelial barrier due to the immune response causes a diffusion barrier for oxygen transfer. This produces the ground glass appearance you describe.

    As a doctor working in a busy public in Australia in the front line for intubating these patients this is all concerning stuff. But while exponential functions rise quickly they also tend to dissipate quickly too.

  5. Jeff, I was looking at your random numbers of virus particles hoping to find a 370 or a 777 but alas I didn’t. Fantastic piece, albeit a brutal and harrowing read.

  6. Are you a journalist or a muckraker? On one hand, journalists tell people to be calm but careful and the statistics show, that in most cases, people do get better.

    Then, in your story, emotion-based scare tactics are used, with two young people (judging from the descriptions of their interactions) going to the hospital and one dying. And the dying is presented in a gut-wrenching way. Stories of worst-case scenarios, used to convince people to take something seriously, are not journalism. Journalists should inform us, using the best evidence at hand, and give us the ability to make the best choices. You have written a short-story. It would make a good movie of the week.

    Why do people go out and buy all the toilet paper, while stocking up on guns and ammunition? Fear, which is also the driver for the labeling of the disease as foreign. Your story, while well written and certainly “correct”, as to possible outcomes, stokes that fear.

    It should certainly get clicks, as it did from me. So, that is good for you at least.

  7. @Sunken Deal, Ha! Actually that hadn’t occurred to me, I don’t know how I pulled those numbers out the air. Maybe next time… Anyway, thanks for the kind words.

  8. Hi. Please can you tell me how true this is? I haven’t seen anything else like it and so it makes me wonder how much is fact and how much is fiction.

    Thank you

  9. @Emma Doyle, The story is fiction–an imagined scenario–but it’s based on actual science. So the number of virus particles in a sneeze, for instance, is purely imagined. (I thought that would be obvious but apparently some people took it as an actual counted number.) But the description of the proteins in the virus coat, for instance, is real.

    I should acknowledge that the actual risk of death from COVID-19 among people under 50 with no complications is very low, less than 1 percent. Of course, I don’t say that the character doesn’t have any pre-existing conditions, or even necessarily that he’s under 50. Or maybe he’s one of the very unlucky ones…

  10. Jeff, upon another careful read, I see that your story’s victim (#592) met the same tragic fate as those unfortunate souls on a 1996 Valujet flight from MIA.

  11. @JeffWise

    Yes we certainly have been looking after COVID-19 patients but there hasn’t been a flood yet. To date a lot of these are suspected, or at risk cases only. Aggressive curve flattening by our Parliament has had an effect. Though by all accounts ICU’s in Sydney are receiving more ventilated patients. We are yet to reach the situation in Spain and Italy where operating theatres are used to ventilate COVID-19 patients. Certainly in London you can move in a couple of days from no patients to ICUs being filled with COVID-19. Most patients improve but some die from hypoxia or cardiac arrest – presumably viral myocarditis. The mechanism you describe – attack via the angiotensin II receptor – is spot on. Elderly hypertensive patients are therefore at risk because of upregulation or proliferation of these receptors, particularly if on ACEI or ARBs.

    The pneumonia from COVID-19 seems much worse compared to seasonal flu.

  12. Hope you guys keep the curve flattened… here in the States we obvious have a lot to learn from success stories like yours (knock on wood)

  13. @ jeff wise
    thank you for the well written article. Feels like watching a tsunami wave coming right at us and feeling totally helpless.
    BTW, what are your thoughts on the Trump administration calling the coronavirus the ‘Chinese virus’ and insisting the outbreak began in Nov 2019 according a draft resolution at the UN Sec. Council?
    Here are some curious aspects of this outbreak:
    – it affects mainly senior citizens. China has a large population of senior citizens due to the one child policy. But many western countries also have large populations of seniors. Senior citizens tend to have conservative views
    – it can be spread by asymptomatic carriers
    – the outbreak may have started in Nov 2019, unrelated to the Wuhan wild animals market
    – pangolins may have been the intermediate species but the original reservoir is still unknown, although bats are suspected
    – trafficked pangolins from Malaysia are found to have the virus, but it’s not known how they got the virus
    – Saudi Arabia & Russia start an oil price war to coincide with this pandemic related economic downturn
    – Chinese biomedical researchers working in top security labs in USA & Canada have recently been removed from their posts for security reasons

  14. @CliffG, The administration called it the “Chinese virus” is naked race-baiting and is demonstrative of the moral rot that has taken hold of the United States. It’s amazing to see how quickly a incompetent, morally bankrupt leader and his party can exploit the lazy, self-regarding citizenry to bring a superpower to its knees.

  15. An excellent example of reckless journalism, and a great service to the American conservatives who are trying to reduce this emergency to fear-mongering and collective hysteria. With articles like this, they can undoubtedly find some ground to defend for their views, however mistaken they are. Also inaccurate in taking for granted infection via suspended aerosol (no certainty about this at the moment in the scientific community) and in throwing in that 20% without pointing out what that precisely means.

  16. Good to know that good and helpful stories spread even faster than the virus. This article reached me in rural Austria from Finland today. Thanks to all people infected by it spreading it.

  17. Hi Jeff

    As I understand it from your article in the Daily Mail in the uk dated 28 March 2020 this virus destroys your lung surfaces to the extent that they can’t take in oxygen. If that is the case then what is the obsession with ventilators – there is no point. There is not enough of them and we can’t produce them fast enough.

    If oxygen cannot get into the body we are dead anyway so we could perhaps look at a transfusion method of treatment with oxygenated blood. Problem is that keeps the body alive but the lungs are gone and the virus will spread through the cells.

    Just a thought but electric blankets are cheaper than ventilations and if you can externally force a bodies core temperature to a level higher than the virus likes or can tolerate, I think it may give some people a chance. OK so you might sweat a bit but what’s the option.

    Crazy maybe, but where are the expert’s in all this – yeah, let’s wait for a vaccine -really – I am not convinced. Besides, what harm would it do to try.


  18. @Geoff, Interesting idea! Definitely not knowledgeable myself to know whether such a scheme might work. I would point out that it’s not the virus’ destruction of lung tissue that causes the flooding of the lungs, but the reaction of the immune system.

  19. @SteveBarrett
    As a fellow Australian I would like to thank you and all of Australia’s frontline workers who are putting their own health in danger to assist those in need. Keep up the great work!!!

    We are extremely lucky here to have a government that listened to the medical advise from experts and, put in force movement restrictions fairly early on in the global pandemic.

    There seems to have been a rise in covid-19 cases in medical personnel, is this due to lack of ppe in our hospitals?
    We definitely don’t want a situation like we’re seeing elsewhere in the world.

  20. @Geoff Moden

    Now that we know that ventillators are not going to be effective – we need to help the immune system to overcome the viruses. The suggestion from you is practical and effective, which can work from a home too. I can endorse it, because this is how I always cut down the virus cycle, whenever I get affected by serious bout of common cold. I welcome the natural rise in temperature and infact increase it further by wrapping myself in warm sweaters and blankets till I am sweating. A slight rise in temperature is all that is required to tilt the battle in favor of the immune system. This is opposed to the common practice of trying to lower the temperature through some tablets (I don’t know which as I never take them).

  21. Dear Jeff Wise,

    Hats off to you. I had been searching for some fundamental information about the virus and how it replicates and affects. Nobody could have described it more lucidly than you have. There are people who would have liked the scary parts to be diluted, but its better to be scared and prepared than wishful and ill fated.

    I earlier tried to simplify an eye opening medical article from the Irish vascular Surgeon, Prof. Sherif Sultan. You must have gone through it. Here is a link.

    Following is a summary of his new discoveries about the prime aggravation occuring through the blood stream and not the lungs.

    The fundamental new notion is that the virus is hijacking the red blood cell, by throwing out its iron and lodging itself out there. The existing white blood cells are able to do nothing about it. So the immune system increases its trigher to henerate more macrophages (bigger white blood cells). This can cause a overdrive and lead to excess of inflammation which itself becomes dangerous.

    The lack of blood cells with iron now causes severe symptoms because of oxygen deprivation in organs – leading to multi organ failure.

    On the other hand the iron ions dumped in the blood stream causes its own problem of oxidation stress in the lungs.

    The traditional ventillator solutions create a severe stress in the alveolar sacs, which can cause them to burst. The hyperbaric chambers with 100% oxygen are supposed to allow the fewer blood cells to carry more oxygen

    What is perhaps needed is somehow supplying sufficient oxygen to the body organs while the immune system is trying to eliminate the dead red blood cell and free iron ions. And till the bone marrows can generate new blood cells. Here is where the blood transfusion can help.


    Is the above research right. If so, can you incorporate in your vivid scenario to tell the story as we know till now.

    Mohan Tambe

  22. Papain is known for its ability to break proteins and is available from papaya. If one scratches raw papaya, white milk like liquid ozzes out. That is papain.

    Papain is used by beer industry to help digestion to break molecules of proteins into smaller proteins.

    Can having raw papaya salads help countering corona virus because it has potential to break proteins.

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