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Eian Kantor realized one Saturday in early April while making a cup of tea with fresh mint leaves: he had lost his sense of smell. The tea suspiciously smelled of nothing. Kantor began rummaging in the refrigerator, smelling jars of pickles, chili sauce, and garlic, nothing.
Ever since New York State was blocked at the end of March, Kantor, 30, and his girlfriend had been isolated in their Queens, New York apartment. So he didn’t suspect he had COVID-19 despite having a mild fever which he accused of seasonal allergies. When he was finally able to get tested for weeks in his loss of smell, or anosmia, he tested negative. But months later, he says, several tests showed his antibodies to the novel coronavirus were “off the scale, which he claimed I had.”
It is estimated that 80% of people with COVID-19 have smell disturbances, and many also have dysgeusia or ageusia (a disruption or loss of taste, respectively) or changes in chemesthesia (the ability to sense chemical irritants such as chillies spicy). Loss of smell is so common in people with the disease that some researchers have recommended its use as a diagnostic test because it may be a more reliable marker of fever or other symptoms.
One lingering mystery is how the novel coronavirus robs its victims of these senses. Early in the pandemic, doctors and researchers feared that COVID-related anosmia could signal that the virus makes its way into the brain through the nose, where it could cause severe and lasting damage. A suspicious path would be through the olfactory neurons that sense odors in the air and relay these signals to the brain. But studies have shown this probably isn’t the case, says Sandeep Robert Datta, a neuroscientist at Harvard Medical School. “My gestalt reading of the data to date suggests that the primary source of insult is actually in the nose, in the nasal epithelium,” the skin-like cell layer responsible for registering odors. “It appears that the virus predominantly attacks support cells and stem cells and not neurons directly,” Datta says. But that doesn’t mean neurons can’t be affected, he points out.
Olfactory neurons do not have receptors of the angiotensin converting enzyme 2 (ACE2), which allow the virus to enter cells on their surface. But the sustentacular cells, which support olfactory neurons in important ways, are studded with receptors. These cells maintain the delicate balance of salt ions in the mucus that neurons depend on to send signals to the brain. If this balance is disrupted, it could lead to a closure of neuronal signaling and therefore of smell.
Sustentacular cells also provide the metabolic and physical support needed to support finger-like cilia on olfactory neurons where odor-detecting receptors are concentrated. “If you physically cut off those lashes, you lose the ability to smell,” says Datta.
In a study in Brain, behavior and immunity, Nicolas Meunier, a neuroscientist at Paris-Saclay University in France, infected the nose of Syrian golden hamsters with SARS-CoV-2. Just two days later, about half of the hamster’s sustentacular cells were infected. But the olfactory neurons weren’t infected even after two weeks. And surprisingly, the olfactory epithelia were completely detached, which, Meunier says, resembled peeling of the skin after a sunburn. Although the olfactory neurons weren’t infected, their cilia had completely disappeared. “If you remove your lashes, you remove the olfactory receptors and the ability to detect odors,” he says.
The rupture of the olfactory epithelium could explain the loss of smell. However, it is unclear whether the damage is caused by the virus itself or by the invasion of immune cells, which Meunier observed after infection. Widespread reports of anosmia with COVID are not typical of other diseases caused by viruses. “We think it’s very specific to SARS-CoV-2,” Meunier says. In a previous study with other respiratory viruses in his lab, he found sustentacular cells only rarely infected, while with SARS-CoV-2, about half of the cells contained the pathogen. With other viruses, odor is usually compromised by a stuffy nose, but COVID does not usually cause nasal congestion. “This is very different,” Meunier says.
Researchers have found some clues to the loss of smell, but they are less sure how the virus causes a loss of taste. The taste receptor cells, which detect chemicals in saliva and send signals to the brain, do not contain ACE2, so they are likely not infected with SARS-CoV-2. But other supporting cells in the tongue carry the receptor, perhaps providing some indication of why the taste disappears. (Although taste may seem to disappear with anosmia because odors are a fundamental component of flavor, many people with COVID truly develop ageusia and are unable to detect sweet or salty taste either.)
Even the loss of chemical sensitivity – the burning of hot peppers or the refreshing sensation of mint – remains inexplicable and largely unexplored. These sensations are not tastes. Instead, their detection is transmitted by pain-sensitive nerves, some of which contain ACE2, throughout the body, including the mouth.
Further clues as to how the virus clears odor comes from people recovering from anosmia. “Most patients lose the smell like a light switch that goes off and quickly recovers it,” says Datta. “There is a fraction of patients who have much more persistent anosmia and recover over longer time scales.” The olfactory epithelium regenerates itself regularly. “This is how the body protects itself from the constant onslaught of toxins in the environment,” Meunier says.
However, more than seven months after experiencing anosmia for the first time, Kantor falls into the second group of patients: he has not yet detected any odors. “It’s hard because you don’t realize how much you relate to the smell until you lose it,” she says. “If the house was on fire, I wouldn’t know. It is very disturbing. “And then there’s what anosmia does to the joy of eating.” Foods that used to be good now taste ‘meh’, “says Kantor.
Carol Yan, a rhinologist at the University of California, San Diego, says anosmia poses a real health risk. “It actually increases mortality. If you can’t smell and taste food, you can predispose yourself to getting sick, such as spoiled food or a gas leak, “he says.” It can also cause social withdrawal or nutritional deficiencies.
The variation on sensory themes extends to another symptom called parosmia, a possible sign of healing in people with long-lasting anosmia. Freya Sawbridge, a 27-year-old New Zealand woman, is such a person. He got COVID-19 in March. After several weeks of anosmia and ageusia, when everything smelled of “ice cubes and cardboard,” he says, Sawbridge began to regain the most basic tastes – sweet, salty, sour – but no hint of flavor, which comes from the aromas of the food. . “Chocolate tastes like sweet gum,” he says.
Then, after about five months, some smells returned but not as expected. For a while, all the foods smelled of artificial strawberry flavor. But now “everything smells horrible and distorted,” says Sawbridge. “Nothing is accurate and the smells are all unpleasant.” The smell of onions, he says, is unbearable and a strange chemical taste permeates everything. “All my food tastes like it has been sprayed with glass cleaner,” adds Sawbridge.
Parosmia can occur when newly growing stem cells that develop into neurons in the nose attempt to extend their long fibers, called axons, through tiny holes at the base of the skull and connect with a structure in the brain called the olfactory bulb. Sometimes the axons connect in the wrong place, causing an uneven smell, but the wrong wiring can potentially correct itself, given enough time.
That news is welcome for people like Sawbridge. But the question he wants to answer is: how long will his anosmia last? “We don’t know the final recovery time course for those with anosmia,” Yan says, but it usually ranges from six months to a year. “With long-term postviral odor loss from the flu, after six months, there is a 30-50% chance of spontaneous recovery,” without any treatment, he adds. “There have been case reports of recovery after two years. But after that, we think regenerative capacity may be hampered. And the chances of recovery are rather slim, unfortunately. “
Kantor has tried every conceivable way to regain the sense of smell: a course of high-dose steroids to reduce inflammation; an olfactory training program with essential oils; beta-carotene supplements for nerve regeneration; acupuncture. Nothing made a difference. Yan recommends “irrigation” of the breasts with budesonide, a topical steroid that has been shown to improve results in a Stanford University study of people with postfluid loss of smell for more than six months. Another promising treatment that Yan and others are studying is platelet-rich plasma, an anti-inflammatory mixture isolated from the blood that has been used to treat certain types of nerve damage. But with any treatment, Yan says, the results “are not surprising. It’s not like you wake up and say, “Wow, I can smell again.” But if you can smell the soap again or enjoy the taste of some foods, that’s a big plus. “
There is a final worrying note about anosmia: it has been identified as a risk factor for some neurodegenerative diseases. “After the 1919 flu pandemic, we have seen an increase in the prevalence of Parkinson’s disease,” Meunier says. “It would be really worrying if something like this happened here.”
But Yan thinks the fear is exaggerated. “There is certainly a link between anosmia and disease, but we think virus-induced anosmia is [working by] a completely different mechanism, “he says.” Having postviral anosmia does not put you at greater risk of disease. These are two completely separate phenomena. ” This should reassure Sawbridge and Kantor and the millions of others around the world affected by the COVID-related odor loss.
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