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The last word: I volunteered to get sick
To unlock the secrets of the common cold, author Jennifer Ackerman made herself miserable
Choosing to get sick in order to get better
Choosing to get sick in order to get better
Corbis
O

NE MONDAY IN October, against the counsel of friends, I applied to catch a cold. Five weeks later, I am about to be tucked away on the seventh floor of a three-star hotel in order to open up my nose to assault by a virus.

I am a member of a select group of subjects taking part in a cold study at the University of Virginia. We are checking into the hotel on a Friday. The plan is to 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. One friend dubs it my weekend "frolic at the rhinovirus festival." 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?

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 university students—most of them male—who are all in cold pursuit of three free meals a day, a clean bed, and a $600 fee.

After we’re settled into our rooms, the study’s chief investigator, Birgit Winther, in a white lab coat and blue gloves, comes around to infect us. 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. 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 COMMON COLD is as common as it is because it 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), parainfluenza viruses, and influenza viruses (yes, those influenza viruses). With so 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 an 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 hundreds of other 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.

But here’s the weird thing: Though none of the members of our study group have antibodies to T39, only 75 percent of us will actually come down with cold symptoms after being infected. The other 25 percent will have virus growing in our noses but will get off pretty much scot-free. This is what’s known as asymptomatic infection. Why some people get infected and never suffer symptoms while others experience the full cold syndrome seems utterly illogical, and it’s one of the great mysteries gripping cold science. "There are so many things we still don't know about the common cold," says Winther. "As a mother with children, I think we deserve a better understanding."

WE DO KNOW some things. As little as a single particle of the rhinovirus is enough to get you infected. Normally, the virus has 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 tear duct from the eye to the nose). Inside the nose, they encounter the thick, sticky mucus lining your nasal passages, which traps viruses and other foreign particles before they can enter the lungs.

Oddly enough, the nose assists the viruses in their journey to the back of the throat and to the large lymph glands there, known as adenoids. Cells lining the nasal passages carry tiny hairs that beat vigorously in unison, driving the mucus that coats them. 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.

Once the rhinoviruses have reached the soft tissue of the adenoids, the tiny invaders approach the substantially larger body cells like pirates in a speedboat approaching a tanker. Once on board, they take over the controls. Each virus slips into the jelly of a cell and releases a little stitch of genetic material, RNA. The RNA hijacks the machinery of the cells, using it to produce hundreds of copies of the virus. Eventually, the 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 throat that so often heralds a cold.

At the hotel, nurses knock on our doors three times a day to monitor our symptoms. We sit on chairs in our 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 subjects seem to think, but viruses. This is why antibiotics have no effect on colds. Zip. Nil. This is also why those antibacterial soaps and lotions have no effect on cold transmission.

Strangely, though, it’s not all that easy in the real world to catch a cold. Colds appear to spread only grudgingly—at least compared with diseases such as tuberculosis or flu. In the 1970s and ’80s, a professor at the University of Wisconsin, Elliot C. Dick, threw together groups of people, half healthy, half heavy with cold, in various situations, including living together in dormitory rooms for 36 hours and giving one another a lingering kiss. Only 8 percent or 9 percent of the healthy people living together with infected people or kissing them came down with colds.

One school of thought proposes that cold viruses wing their way through the world by airborne means, launched by coughs and sneezes. This is the main route of spread for influenza viruses. But the most common cold viruses appear to trace a more plodding route, by way of contact with hands and surfaces. People with colds typically carry the cold virus on their hands (most probably as a result of nose blowing or wiping) and can pass it to other hands, even after only brief hand-to-hand contact. Studies by Winther’s colleague Owen Hendley have shown that rhinovirus remains alive on the skin, capable of infecting another person, for at least two hours. It readily transfers from the hands of the sufferer to the hand of a potential new victim, even if the contact is a brief handshake.

Inanimate objects can also become passive carriers of contagion. Not long before I signed up for Winther’s cold study, she and Hendley revealed that guests checking out of hotel rooms leave behind more than just loose change. The researchers’ 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.

BY DAY THREE of my weekend in the rhinovirus hotel, about half the participants have most of the early symptoms of a cold—including me. There’s no agreement about which symptoms are the worst. Some can’t abide the sore throat. Others despise the runny nose and congestion that blocks or floods the harbor of our nostrils. Many are dreading the impending cough that annihilates sleep. We all know these woes—and that points to a striking feature of colds: There may be more than 200 cold viruses, but once any cold bug launches an infection, the resulting spectrum of symptoms is pretty much the same. How can this be?

Until a couple of decades ago, science assumed that symptoms from any disease arose from the bugs themselves or from the toxins they produced. "We all just assumed that when you had a terrible cold, your nose was falling apart inside," Winther says. A cold’s miseries were thought to be the upshot of the cold virus’ destruction of the innocent cells lining your nose—just as the miseries of flu arose from the flu virus’ devastating effect on cells of the respiratory tract. That was before Winther and some colleagues, then studying at the University of Copenhagen, began taking nasal biopsies and discovered that there was "absolutely no evidence of damage to the nasal lining" in any of the samples from cold sufferers. "Rhinoviruses are not ripping up cells as we suspected," explains Jack Gwaltney Jr., a professor emeritus at the University of Virginia. "Rather, they turn on processes in the body that under normal conditions are not active.” Some of those so-called inflammatory processes help fend off or demolish viruses—but they also make us miserable.

This was a blow to one of the nose’s deepest secrets as well as the start of new cold theory: Cold symptoms do not result from the destructive effects of viruses but from the body’s response to the intruders. Confronted by a virus, the body’s cells release a complex brew of chemicals called inflammatory mediators, and these chemicals inflame cells and tissues from the throat and nose to the brain itself—which may explain the headaches and lethargy associated with colds. This also means that if you’re keen on tamping down a cold, "boosting" your immune system may be the last thing you want to do. Doing so, in fact, could result in more exaggerated symptoms.

It’s not even true that the stuffy, blocked feeling that stifles breathing during a cold is the product, as one might expect, of excess mucus in the nasal passages. Instead, it’s the result of swelling blood vessels in the turbinates—spongy shelves inside the nasal passages that help trap particles entering the nose. Though the urge is great to forcefully expel whatever’s causing the blockage with a hard snort, 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.

NONE OF THIS new knowledge offers much relief to the suffering study participants, of course, as we sit in our doorways on Monday morning sniffling, sneezing, coughing, and awaiting our discharge. I’m told that once 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 offer to scrub us. But they do ask that we wash our hands before joining the complimentary buffet breakfast downstairs.



Adapted from Ah-Choo! The Uncommon Life of Your Common Cold ©2010 by Jennifer Ackerman. Reprinted by permission of Twelve Books/Hachette Book Group, New York, N.Y. All rights reserved.

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