It was dawn when Eian Kantor brewed tea from fresh mint leaves on Saturday in early April. He had lost his sense of smell. The tea suspiciously did not smell anything. Cantor rifleed through the fridge and sniffed a bottle of pickles, chili sauce and garlic. There was nothing.
Since the blockade of New York In late March 30-year-old Cantor and his girlfriend remained isolated in a Queens apartment in New York. So he didn’t think he had COVID-19, even though he performed a slight fever chalked on seasonal allergies. He was negative on the test when he was finally able to be tested weeks after loss of odor or anosmia. But a few months later, he says, in some tests, his antibody against the new coronavirus was “off the chart”, which confirmed that I had it. ..
An estimated 80% of people with COVID-19 have dysgeusia, many of whom have dysgeusia or ageusia (disorder or loss of taste, respectively) or altered chemosensation (ability to detect chemical stimulants such as hot peppers). ) Also has. Because olfactory loss is common in people with this disease, it may be a more reliable marker than fever and other symptoms, and some researchers recommend using it as a diagnostic test.
One of the remaining mysteries is how the new coronavirus deprives victims of these sensations. Early in the pandemic, doctors and researchers worried that COVID-related anosmia might indicate that the virus could invade the brain through the nose and cause serious and permanent damage. was doing. The suspicious pathway is through olfactory neurons, which sense air odors and transmit these signals to the brain. However, research has shown that this is probably not the case, says Sandeep Robert Datta, a neuroscientist at Harvard Medical School. “Gestalt readings of the data so far suggest that the main cause of seizures is actually the nose, the epithelium of the nose,” says the skin-like layer of cells involved in odor recording. “The viral attack appears to primarily support cells and stem cells rather than neurons,” says Datta. But that fact does not mean that neurons are unaffected, he emphasizes.
Olfactory neurons do not have angiotensin converting enzyme 2 (ACE2) receptors on their surface that allow the virus to invade cells. However, the persistent cells that support olfactory neurons in an important way are studded with receptors. These cells maintain a delicate balance of salt ions in the mucus that neurons rely on to signal the brain. When that balance is lost, neuronal signaling can cease, thus odor arrest.
Persistent cells also provide the metabolic and physical support needed to maintain finger-like cilia on olfactory neurons where odor-detecting receptors are concentrated. “Physically destroying these cilia makes it impossible to smell,” says Datta.
In the study of Brain, behavior and immunityNicolas Meunier, a neuroscientist at the University of Paris-Sacre, France, infected the nose of a golden hamster with SARS-CoV-2. Just two days later, about half of the hamster’s persistent cells became infected. However, the olfactory neurons were not infected even after 2 weeks. And surprisingly, the olfactory epithelium was completely exfoliated, which was similar to exfoliation of the skin after sunburn, says Meunier. The olfactory neurons are uninfected, but the cilia are completely gone. “When you remove the cilia, you lose your ability to detect olfactory receptors and odorants,” he says.
Destruction of the olfactory epithelium may explain the loss of olfaction. Still, it is unclear whether the damage was due to the virus itself or the invasion of immune cells, which Meunier observed after infection. Extensive reports of anosmia due to COVID are not typical of other diseases caused by the virus. “We think it’s very specific to SARS-CoV-2,” says Meunier. Previous studies with other respiratory viruses in his laboratory found that persistent cells were rarely infected, but SARS-CoV-2 contained pathogens in about half of the cells. Was there. With other viruses, stuffy nose usually damages the odor, but COVID usually does not cause stuffy nose. “This is very different,” says Meunier.
Researchers have found some clues about odor loss, but are less confident about how the virus causes taste loss. Taste receptor cells that detect chemicals in saliva and signal the brain do not contain ACE2 and may not be infected with SARS-CoV-2. However, other supporting cells in the tongue carry receptors and probably provide some indication of why the taste disappears. (Smell is an important element of taste, so it may appear to disappear in anosmia, but many people with COVID really develop ageusia and cannot detect sweet or even salty tastes. )
The loss of chemical perception (burns of peppers and the refreshing sensation of mint) is also unexplained and almost unexplored. These sensations are not taste. Instead, their detection is transmitted by nerves that sense pain throughout the body, including the mouth, some of which contain ACE2.
More clues as to how the virus eliminates odors come from people recovering from anosmia. “The majority of patients lose the odor of turning off the lamp and recover quickly,” says Datta. “Some patients have much more persistent anosmia and recover on a longer time scale.” The olfactory epithelium regenerates regularly. “It’s a way of the body to protect against the constant onslaught of toxins in the environment,” says Meunier.
Still, more than seven months after he first experienced anosmia, Cantor still falls into the second group of patients. He has not yet detected any odor. “It’s difficult because you don’t know how much it’s related to the smell until you lose it,” he says. “If the house was on fire, I didn’t know it. I’m very worried.” And there’s what anosmia does to the joy of eating. “You can now enjoy food that was good before,” says Canter.
Carol Jan, a nasalist at the University of California, San Diego, says anosmia poses a real health risk. “It actually increases mortality. Failure to smell or taste food can cause harm, such as rotten food and gas leaks,” she says. “It can also cause social withdrawal symptoms or undernourishment.”
Variations in sensory themes extend to another symptom called parosmia. This can be a sign of recovery in people with long-lasting anosmia. Freya Sawbridge, a 27-year-old New Zealand woman, is such an individual. She became infected with COVID-19 in March. After a few weeks of anosmia and ageusia, when everything tasted “ice and cardboard”, Sawbridge began to regain its most basic taste (sweet, salty, sour), but food. There was no flavor nuance derived from the aroma of. “Chocolate tastes like sweet rubber,” she says.
About five months later, some odors returned, but not as expected. For a while, all foods smelled like artificial strawberries. But now, “everything smells horribly distorted,” says Sawbridge. “Nothing is accurate and all the odors are unpleasant,” she says, with the onion odor unbearable and the strange chemical flavors permeating everything. “All my food tastes like a spray of window cleaner,” Sawbridge adds.
Parosmia can occur when newly grown stem cells that develop into neurons in the nose try to stretch long fibers called axons through small holes in the base of the skull to connect to structures in the brain called the olfactory bulb. .. Axons can connect to the wrong place and cause offensive odors, but if you have enough time, miswiring can automatically fix them.
The news is welcomed by people like Sawbridge. But the question she wants to answer is how long her olfactory dysfunction will last. “We don’t know the final time course for recovery in people with anosmia,” says Yan, but it’s usually six months to a year. “Due to the long-term post-viral odor loss caused by the flu, there is a 30 to 50 percent chance of spontaneous recovery without treatment after 6 months,” she adds. “There are case reports of recovery after two years. However, I suspect that regenerative capacity will be impaired after that. Unfortunately, the chances of recovery are very low.”
Kantor has tried every conceivable means of regaining his sense of smell. A high-dose steroid course to reduce inflammation. Smell training program using essential oils. Beta-carotene supplements for nerve regeneration; acupuncture. There is no difference. Yang recommends “cleansing” the sinuses with budesonide. This is a topical steroid that has been shown to improve results in studies of people at Stanford University who have been odorless after influenza for more than 6 months. Another promising treatment that Yang et al. Are investigating is platelet-rich plasma. It is a blood-separated anti-inflammatory drug that has been used to treat certain types of nerve damage. But with any treatment, the result is “not surprising. It doesn’t mean that you get up and” smell again. ” But if you can smell the soap and enjoy the taste of food, that’s a big advantage. “
There is one last concern about anosmia. It has been identified as a risk factor for several neurodegenerative diseases. “After the 1919 influenza pandemic, the prevalence of Parkinson’s disease increased,” says Meunier. “I’m really worried if something similar is happening here.”
But Yang thinks the fear is exaggerated. “There is certainly a link between anosmia and illness, but virus-induced anosmia [working by] It’s a completely different mechanism, “she says. “Post-viral anosmia does not increase the risk of illness. These are two completely separate phenomena.” It is affected by the loss of Sawbridge and Cantor, and COVID-related odors. It should reassure millions of people around the world.
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The mystery of COVID odor loss finally yields some answers
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