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But why would patients show these symptoms in the first place? There are three potential explanations, Munger said.
In one scenario, SARS-CoV-2 could infect the inner lining of the nasal cavity, triggering localized inflammation. Inflammation in the nose can prevent incoming odors from reaching the cells that detect them, "basically just gumming up the works," Munger told Live Science. For example, chronic inflammation in the sinuses and nasal cavity — a condition known as chronic rhinosinusitis — is one of g the leading causes of smell loss, Hummel added.
Alternatively, the virus might specifically target cells in the nose that react to incoming odors. Receptors on these cells serve as docking stations for smelly chemicals, which once bonded to the receptor, jump-start a chemical and electrical reaction that passes information on to the brain. If the cells bearing smell receptors become infected and can't generate signals, a person could temporarily lose their sense of smell. Thankfully, because these sensory cells are often damaged by chemicals and pathogens, the body replaces them every 30 to 60 days, Munger said.
Beyond infecting nerve tissue in the nasal cavity, the virus could theoretically "also penetrate the cribriform plate, the bone between the nose and the brain, and infiltrate the olfactory bulb," the brain region where cells in the nose send smell information to be processed, Hummel said. A 2008 study of the SARS-CoV virus, which caused an outbreak of severe acute respiratory syndrome in 2002-2003, revealed that the coronavirus could penetrate the olfactory bulbs of transgenic mice.
From there, SARS-CoV went on to infect deeper structures in the mouse brains, causing extensive damage. Several review papers have suggested that SARS-CoV-2 may do the same in humans and potentially infect regions of the brain that support breathing and heart rate. If this proves to be the case, "some of the purely respiratory symptoms that you might attribute to the disease, the inability to get air into the lungs, might actually be defects in respiration controlled by the nervous system," Matthew Anderson, a neuropathologist at Beth Israel Deaconess Medical Center in Boston, told The Scientist.
But again, these hypotheses have yet to be supported with hard data.
In one scenario, SARS-CoV-2 could infect the inner lining of the nasal cavity, triggering localized inflammation. Inflammation in the nose can prevent incoming odors from reaching the cells that detect them, "basically just gumming up the works," Munger told Live Science. For example, chronic inflammation in the sinuses and nasal cavity — a condition known as chronic rhinosinusitis — is one of g the leading causes of smell loss, Hummel added.
Alternatively, the virus might specifically target cells in the nose that react to incoming odors. Receptors on these cells serve as docking stations for smelly chemicals, which once bonded to the receptor, jump-start a chemical and electrical reaction that passes information on to the brain. If the cells bearing smell receptors become infected and can't generate signals, a person could temporarily lose their sense of smell. Thankfully, because these sensory cells are often damaged by chemicals and pathogens, the body replaces them every 30 to 60 days, Munger said.
Beyond infecting nerve tissue in the nasal cavity, the virus could theoretically "also penetrate the cribriform plate, the bone between the nose and the brain, and infiltrate the olfactory bulb," the brain region where cells in the nose send smell information to be processed, Hummel said. A 2008 study of the SARS-CoV virus, which caused an outbreak of severe acute respiratory syndrome in 2002-2003, revealed that the coronavirus could penetrate the olfactory bulbs of transgenic mice.
From there, SARS-CoV went on to infect deeper structures in the mouse brains, causing extensive damage. Several review papers have suggested that SARS-CoV-2 may do the same in humans and potentially infect regions of the brain that support breathing and heart rate. If this proves to be the case, "some of the purely respiratory symptoms that you might attribute to the disease, the inability to get air into the lungs, might actually be defects in respiration controlled by the nervous system," Matthew Anderson, a neuropathologist at Beth Israel Deaconess Medical Center in Boston, told The Scientist.
But again, these hypotheses have yet to be supported with hard data.
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