One Monday in October, against the counsel of friends, I applied to catch a cold. Five weeks later, on Friday, the 13th of November, tucked away on the seventh floor of a three-star hotel, I open up my nose to assault by a virus and wait.
It’s the peak of the swine flu epidemic. Colleagues, friends, and family are succumbing one after another to the feverish misery of H1N1. After weeks of scrupulously avoiding the sniffling masses, I actually invite infection, opting to join a select group of subjects taking part in a cold study at the University of Virginia. The plan is to check in to a local hotel on a Friday afternoon, have a common strain of cold virus injected into the nose, and then hunker down for the weekend, waiting for cold symptoms to develop.
My family thinks I’ve gone off the deep end. My plan elicits this merry note from my dour sister: “You know our family. It’ll go straight to your chest.” One friend dubs it my weekend “frolic at the rhinovirus festival.” “Chin up!” he says. “That way your nose won’t drip.” Another friend takes a darker view. “I’ll keep you in my prayers: Death by cold is one of my greatest anxieties.”
Death by cold?
It’s a strange thing to anticipate even mild illness, to know that in a few days viral lightning will strike. It’s like awaiting the arrival of a massive snowstorm or a hurricane. There’s that sense of urgency, of the need to get things done before you’re under the weather and not feeling like doing much more than hanging around in your bathrobe, nursing a cup of hot tea. What kind of people normally go in for this form of weekend entertainment? As far as I can tell, mostly young male students.
The researchers have set up shop in Room 726. Oddly enough, there are no signs in the lobby, “WELCOME VIRUS STUDY SUBJECTS!” But when I reach the seventh floor, the hall is lined with boys and their backpacks in cold pursuit of three free meals a day, a clean bed, and a $600 fee. I look around for one young man I met earlier at the screening for this study, a big guy with tattoos and what sounded like serious congestion. The screening took place at around 9 a.m. on a Monday morning. When the nurse asked this fellow if he had a cold, he said no, he wasn’t sick; he had just been “playing outside in the cold all morning, since 3:30 a.m.”
Oh, and what was the game?
“Setting traps for animals.”
There are a few outliers. As we’re checking in with the study nurse, I ask the middle-aged woman in line ahead of me whether her family thinks she’s crazy to be participating in this study. “Oh no,” she says cheerily. “In fact, I’ve brought my 18-year-old daughter”—the dark-haired beauty sitting with the nurse to the right of us, awaiting the results of the routine pregnancy test. “This will take care of Christmas. My husband would have come, too, but he works for Student Health, and that created some kind of conflict of interest.” A couple of years ago, she joined another such study in order to give her daughter a bang-up sweet sixteen party.
With the help of willing subjects such as these, researchers can probe the basics of a disease and also try out remedies. At a hotel up the road from ours, similar studies produced the flu drugs Relenza and Tamiflu. The flu studies are the really lucrative gigs. Nine days of isolation in a hotel room with a nasty case of flu will net you $1,750. One such opportunity recently drew a married couple who participated sequentially. First the wife got the flu (while the husband cared for their three boys) and then her spouse did. This—18 days of combined illness—so the whole family could take a $3,500 vacation.
It’s money hard earned. There’s the sledgehammer of the flu itself. Then there’s the isolation in a hotel room. Nine days is a long time in one room, even under perfect conditions. And conditions are not always perfect. Once, lightning struck the hotel, and the electricity went out for three days. No lights, no television, no coffee pot. The hotel staff had to carry food for 80 subjects up five flights of stairs from the kitchen in the basement; meals were a little less than punctual and a lot less than hot. For entertainment, younger subjects resorted to saving up their fruit from dinner and bowling with it in the halls.
Another time, a fire in the elevator shaft prompted a hotelwide evacuation. The study participants stood around in the icy parking lot in their slippers and pajamas, wearing masks, while the rest of the hotel guests gawked.
Our three-day stay is easy by comparison. Still, it feels strangely surreal, like a hybrid of holiday, hospital, and prison. During these three days, we can’t leave the hotel for any reason (unless we drop out of the study and forsake our fee), which prompts young Tom Jackson in the room next door to mutter from his doorway, “I feel like I’m in The Shining.” We’re not even supposed to wander down to the end of the floor, where regular guests are lodged (one would hope at a deep discount). And, of course, we have to submit to a litany of nasal exams, nasal washes, and nasal sprays at all hours of the day and night.
This study is testing the effects of a new nasal spray, one of the latest shining hopes of cold treatment. The spray contains a synthetic version of a compound the body’s own immune system uses to kill microbes. In this nasal form, it’s designed to murder a virus before it can do its dirty work in the nose. But it’s also effective against bacteria and fungi and has been used effectively as a treatment for conjunctivitis and impetigo. The study is carefully designed as a so-called randomized, placebo-controlled, double-blind experiment. Half of us picked at random will get spritzed with the real McCoy, the active-ingredient spray; half with a placebo saline spray. No one knows which group they’re in; not even the scientists conducting the study—hence the expression “double blind.” I’m secretly hoping the roll of the dice put me in the placebo group; I’m not sure I want up my nose what may turn out to double as a cure for toe fungus.
After we’re settled into our rooms, the study’s chief investigator, Birgit Winther, in white lab coat and blue gloves, comes around to infect us. Winther is an associate professor of otolaryngology (often called ENT for ear, nose, and throat) at the University of Virginia and a pioneer in cold research. Not long ago, she and her colleague Owen Hendley revealed the deeply disappointing news that guests checking out of hotel rooms leave behind more than just loose change. Their now-infamous hotel studies showed that people with colds may bestow little deposits of cold viruses on surfaces throughout a room and that these germs linger long after the sniffling guest is gone.
Winther asks me to lie with my head hanging over the foot of my hotel bed and administers the virus in a saline suspension, two sprays per nostril. It’s not unlike a nasal vaccine, she tells me. It’s produced the same way, with all of the safety precautions, except that it contains a live virus, a common strain of cold virus in experimental form. Into the nose is the ideal way to deliver the bug for the same reason it’s a good avenue for vaccines: it offers the most direct route to the body’s immune response. “The nose is set up to sample viruses that come in from the outside and to alert the immune system,” Winther explains.
The common cold is caused by at least 200 different viruses. The experimental one now making its way through my nasal passages—affectionately known as T39—belongs to the largest family, the rhinoviruses, which account for 40 percent of all colds. There are at least five families of cold viruses, among them the picornaviruses (which includes rhinoviruses), adenoviruses, coronaviruses, parainfluenza viruses, and influenza viruses. Yes, those influenza viruses. Something like 15 percent of colds are caused by flu viruses. (This gave me pause once, when I was considering deliberately catching a cold from a friend in order to participate in another cold study. What if she was infected by something more insidious than a simple rhinovirus?) With this many flavors, you can catch one new cold virus after another and never run out—which is precisely what happens. After your body encounters a particular strain of virus and mounts a proper immune response, it dutifully produces antibodies to that virus, which will disable that strain the next time you’re exposed to it. But this still leaves you susceptible to the hundreds of other remaining circulating strains. That colds are caused by this enormous menagerie of cold bugs is what has made creating a vaccine thus far impossible.
As Winther injects the cold-virus solution into my nostrils, I imagine the little beasties getting straight to work. The nose has virtually no protection against the virus once it is deposited on the nasal mucosa. Nearly everyone exposed to a cold virus in this direct fashion will get infected, provided they don’t have antibodies. (And none of the study subjects do. We were tested earlier for the presence of antibodies to this strain and found wanting—which means that our bodies have never been exposed to it.)
But here’s the weird thing: Though all the members of our study group will get infected and none of us has immunity to this virus, only 75 percent of us will actually come down with a cold. The other 25 percent will have virus growing in our noses but will get off pretty much scot-free, with no symptoms—whether or not we receive treatment. This is what’s known as asymptomatic infection. Why some people get infected and never suffer symptoms (but still make antibodies) while others experience the full knock-down, drag-out syndrome of a cold seems utterly illogical, and it’s one of the great mysteries gripping cold science. “We really don’t know why this is,” says Winther, “but it could be the key to colds”—why we get them and how we can avoid them. “There are so many things we still don’t know about the common cold,” Winther remarks later. “As a mother with children, I think we deserve a better understanding.”
Just a tiny smack of rhinovirus—as little as a single particle—is enough to give you an infection. But just to be sure, the saline solution Winther delivers contains 100 particles. These experimental buggers are getting a free ride. Normally, rhinoviruses have to steal into your nasal passages, often by way of a contaminated finger probing a nose or rubbing an eye. It was Winther and her team who discovered that cold viruses can travel down the lacrimal (or tear) duct from the eye into the nose. There, they encounter the thick, sticky mucus lining your nasal passages, which traps viruses and other foreign particles before they enter the lungs. Some viruses inevitably escape this viscous barrier and travel on to the big lymph glands known as adenoids at the back of your throat.
Oddly enough, they’re assisted in their journey by the nose itself. Cells lining the nasal passage carry tiny hairs that beat vigorously in unison, driving the mucus that coats them. Under a scanning electron microscope, these hairs look like nothing so much as a shag carpet. Normally, they act as a kind of nasal hausfrau, sweeping dust, pollen, and other particles toward the back of the throat to be swallowed and destroyed by the acids of the stomach. But the tiny hairs can also act like a little moving sidewalk for the virus, bearing it toward the back of the nose.
Within some 10 to 15 minutes, the rhinoviruses are deposited in the nasopharynx, what the 19th-century physician Sir William Osler called the “garbage dump” of the throat. There, in the soft tissue of the adenoids (aptly described as “crypts”), the tiny invaders approach body cells a thousand times their size, like pirates in a small speedboat approaching an oil tanker. They get onboard by wily means, pretending to be something they’re not. (Coast Guard? Tourists?) Cold viruses have evolved a specialized device for docking on a target host cell: little canyonlike grooves on their surface that fit perfectly with specialized receptors on the surface of your body cells (called ICAM-1 receptors). The fit is tight, like lock and key.
Once the virus particles are docked, the sedition begins. They fool a body cell into thinking they’re something useful, so the cell readily takes them in. And once they’re onboard, like pirates, they take over the controls. That is, unless you’re lucky enough to have been exposed to this strain of virus before and possess antibodies against it. In that case, the antibodies neutralize the viral particles by binding to their surface, obstructing their ability to dock with your body cells. Otherwise, the virus slips into the jelly of a cell and releases its little stitch of genetic material, RNA. The RNA hijacks the machinery of your own cells, using it to produce hundreds of copies of the virus. Eventually your body cell starts to destroy itself, and the mother lode of fresh virus particles is released to infect surrounding cells.
This part of the infection is the genesis of that scratchy sore throat that so often heralds a cold, the uncomfortable feeling like a pair of pants too tight at the waist or the faintly itchy sensation of a wool sweater on a warm day.
“From the time a cold virus enters your nose, it takes around 8 to 12 hours for the virus to complete its reproductive cycle and for new cold virus to be released into nasal secretions,” says Ron Turner, a cold expert and colleague of Winther’s at the University of Virginia. This is what’s known as the incubation period.
You have to admire how something so small and so simple can be so ingenious. “Rhinovirus infection is not only very efficient, it proceeds very rapidly,” says Turner. Only 24 hours after a single virus particle enters your nose, Bam! Infected cells have been coerced into making millions of new viruses, which are then sent out to infect other healthy cells. The sneezing, snuffling misery tends to begin within 12 hours of infection but typically peaks at around 48 to 72 hours.
At the hotel, nurses knock on our doors three times a day to monitor our symptoms: any fever, sneezing, runny nose, nasal obstruction, sore or scratchy throat, cough, headache, feverishness, chilliness, malaise. We sit in chairs in our hotel room doorways like unadopted pets at the pound. From the chatter, it’s clear there’s some confusion about the nature of the bugs now flourishing in our noses. They’re not bacteria, as some of the boys seem to think, but viruses. This is why antibiotics have no effect on colds. Zip. Nil. Antibiotics kill bacteria by preventing them from building their cell walls. Viruses are not cells and have no cell walls, so they’re utterly unaffected by the drugs. This is also why those antibacterial soaps, shampoos, and lotions have no effect on cold germs. Promotional claims notwithstanding, these products will do nothing to protect you, your friends, or your family from contracting a cold.
After the first 12 hours, most of us are still symptom-free. (Come to think of it, I do feel a kind of creeping crumminess. But that might be on account of having our nasal spray delivered late last night and then again at 6:30 this morning.)
Early on the morning of the second day, I take an informal survey of my fellow patients and hear about a range of complaints, from mild to severe. Colds don’t usually cause fever in adults, but some subjects tell me they are registering a “normal” 98.6 degrees Fahrenheit in the morning. This is in fact not a normal morning temperature. Body temperature varies over the course of the day by as much as two degrees Fahrenheit. It’s lowest in the morning, usually around 97 degrees or so, and rises to as high as 99 degrees in the evening. So at 6:30 a.m., a temperature registering 98.6 degrees could actually be considered a low-grade fever.
What do the study participants view as the worst of cold symptoms? Some can’t abide that heraldic sore throat at the start of a cold that sabotages swallowing—with its sharp reminder every time our throat opens and closes. Others despise the congestion and runny nose that blocks or floods the harbor of our nostrils, disrupting the sweet pleasures of breathing and tasting. Many are dreading the impending cough that annihilates sleep.
This is what makes colds so irritating and distracting—they make those basic body functions of which we’re normally blissfully unaware suddenly leap into unpleasant consciousness.
The sore, scratchy throat that makes a trial of downing spit results when the body sends blood rushing to the infected cells at the back of the throat, releasing chemicals that make the blood vessels in the surrounding tissue swell. The swelling pressures nerve endings in the throat, causing pain every time you do what you have to do so you won’t choke on your own saliva. (Lest you think we’re the only species that suffers so, a new study suggests that the seven-ton Tyrannosaurus rex at the Field Museum in Chicago, nicknamed Sue, actually died of a sore throat. Scientists suspect that a parasite that also infects pigeons made it difficult for the dinosaur to swallow, leading to starvation. So we’re in splendid company.)
Rarely do colds produce lasting throat soreness. But neither is it a temporary, acute pain, like a hammer blow to the thumb. This is unfortunate, as it means that for sore throats, we can’t call on what science tells us is an accessible and convenient form of painkiller for acute pain, such as stove burn or stubbed toe: swearing. A 2009 study at Keele University’s School of Psychology in England found that channeling your inner sailor can actually diminish pain. Swearing, it seems, triggers both an emotional and a physical response that together raise heart rate and reduce pain. Alas, it’s more effective for the sudden, hammer-nailing-thumb sort of hurt than the swollen grip of a sore throat. The only real relief for the latter comes from the messier but less profane remedy of a saltwater gargle. (But more on that later.)
As for congestion: The job of the nose is nothing less than making air fit for your lungs to breathe. It’s hardly a simple task. Air flows into the nose not in a straightforward rivulet but in whirls and eddies more complex than the airstream over the wings of a plane or blood flow through the heart, while the nose warms, filters, and humidifies it. No wonder we suffer when a cold runs interference. Our mouths are not nearly as deft at air-conditioning. And since 75 percent of flavor is aroma, a blocked sense of smell obliterates taste—among the most egregious of a cold’s sins, at least in my book. (Also in Charles Lamb’s. “I inhale suffocation,” wrote poor, cold-ridden Lamb. “I can’t distinguish veal from mutton.”)
But don’t blame mucus for the nasal blockage. The problem is more fundamental.
Or architectural.
There’s a sort of Roman nobility to the nose, both inside and out. Its interior is composed of two large air passages, separated by the thin wall of the septum. These passages lead to four sinus cavities just above, behind, and below your eyes. Spongy shelves called turbinates line the sidewalls of the nasal passages and help trap particles entering the nose. They also heat and humidify the air so it’s warm and almost completely saturated with moisture by the time it reaches the lungs.
The stuffy, blocked feeling that stifles breathing during a cold is not the product, as one might expect, of excess mucus but the result of swelling blood vessels in the turbinates. The turbinates are designed to engorge this way, just like other erectile tissues in the body. They normally swell in a rhythmic, alternating cycle—first one side, then the other—so that one nasal passage always has a little less airflow than the other. It’s not clear why they do this, but the cycling may rest one nasal chamber while the other fulfills the duty of air-conditioning. Colds tend to exaggerate the asymmetry of the rhythm, completely closing one nasal passage, so breathing becomes a labored affair. Though the urge is great to forcefully expel whatever’s causing the blockage with a good hard snort, one should try to resist the temptation. Blowing out the mucus isn’t going to make your nose feel less stuffy. And you don’t particularly want to blow out your turbinates, even if you could.
Though it has not yet shown up as a symptom among my cold compatriots, within a few days, coughing may be the bane of many on this sick hall. First, there’s the quick inspiration of breath, followed by an involuntary squeeze of the diaphragm. The glottis—that cap on the larynx at the back of the throat—suddenly pops open, releasing a turbulent blast of air from the lungs traveling at more than 80 feet per second. Coughing is a reflex that protects the airways in the throat and chest. It helps to eject any foreign substance that might be tickling the larynx or the trachea (the tube leading to your lungs). Its sound depends on the site of irritation. The barking seal sound of croup, for instance, arises from an irritated voice box.
Naturally, it’s a good idea to eject foreign matter. But when you have a cold, the chemicals your body produces may continuously tickle the nerve endings in the larynx or trachea, making them think there’s something there—phantom foreign material—to expel. Coughing becomes, as Ogden Nash once wrote, “like the steps of a moving stair, there is always another cough there.”
By day three, I have most of the usual early symptoms, as do about half of the study participants. And my dour sister was right—the blasted bug will eventually give me a chest cough that’s hard to shake. This scientifically induced cold may have been designed to be mild, but for me, it turns out to be a humdinger, and it’s almost 10 days before I finally get over the residual, nagging hack.
Either there isn’t much to this new nasal spray product or I and my fellow cold sufferers were the recipients of the placebo saline solution. I’m guessing it’s the latter. Birgit Winther has seen a lot of drugs come and go, and she’s genuinely optimistic about this new one. She likes it because it’s designed to work the way the body’s own compounds work to fight viruses—and does so early in the process of infection. Winther thinks it could be used prophylactically, to stave off the spread of colds in a family if a child comes home with a doozy. But it will be some time before we know whether the spray is really effective. Even if this study shows positive results, these must be confirmed by other, larger studies. As scientists are quick to point out, a single study does not a finding make. It’s just a start.
Early Monday morning, everyone is packed up and sitting in the doorways to our hotel rooms, awaiting discharge. We’re all keenly aware that we’re about to go home with a little more microbial baggage than we had when we arrived. Colds are most contagious during the first two to four days after symptoms appear, so at this point, we’re all walking Typhoid Marys. After we leave, the study staff will have to scrub our hotel rooms with alcohol and bleach to kill any critters we’ve left behind on sink handles, TV remotes, light switches, and phones.
They don’t scrub us, but they do ask us to wash our hands.
When I hear that we’re all invited for a buffet breakfast in the lobby before we leave, I make a mental note to avoid brunch at this hotel. It turns out, however, that the staff has exercised caution here, too, assigning us to a private breakfast room of our own. Still I have to wonder: How thoroughly did the boys wash up—or any of us for that matter? What are the chances of passing some residual little T39s to the waitress, along with our basket of sweet rolls or jam knife?
Just how does one normally catch cold?
Excerpted from Ah-Choo! by Ackerman, Jennifer Copyright © 2010 by Ackerman, Jennifer. Excerpted by permission.
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