It has been a while since a science story caught my eye. But here’s one that should at least catch your nose. It’s titled “How the Coronavirus Steals the Sense of Smell,” and it’s brought to us by a host of medical researchers from across the country: Columbia, NYU, and Mount Sinai in New York; Baylor in Texas; and UC Davis in California. Normally I’d just provide you with a link, which you’d ignore. But in this case I’m reprinting the bulk of the article below so you can at least pretend to have read it. Oh, and in case you care, the link to the story is here.
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Few of COVID-19’s peculiarities have piqued as much interest as the abrupt loss of smell that has become a well-known hallmark of the disease. COVID patients lose this sense even without a stuffy nose. The loss can make food taste like cardboard and coffee smell noxious. Occasionally it persists after other symptoms have resolved. Scientists are beginning to unravel the biological mechanisms of this process which until now have been something of a mystery. Neurons that detect odors lack receptors that the coronavirus uses to enter cells, and this has prompted a debate about whether they can be infected at all…
The new work settles the debate over whether the coronavirus infects nerve cells that detect odors: It does not. But the virus does attack other supporting cells lining the nasal cavity. Infected cells shed virus and die, while immune cells flood the region to fight the virus. Subsequent inflammation wreaks havoc on smell receptors on the nerve cells’ surface that detect and transmit information about odors. The process alters the sophisticated organization of genes in those neurons, essentially short-circuiting them.
This research significantly advances the understanding of how cells critical to the sense of smell are affected by this virus despite the fact that they are not directly infected. Indeed, many complications of COVID appear to be caused by the immune system’s friendly fire as it responds to infection, flooding the bloodstream with inflammatory proteins which can damage tissue and organs.
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Scientists examined golden hamsters and human tissue specimens from patients who succumbed to COVID. After the hamsters were infected with the original human coronavirus, scientists tracked damage to their olfactory systems over time. (How do you know a golden hamster has lost its sense of smell? You don’t feed it for several hours, then bury Cocoa Puffs in its bedding. Hamsters that can smell will find the cereal in seconds.)
The virus did not invade neurons, only cells that play supporting roles in the olfactory system. But that was enough to alter the function of nearby neurons, leading to a loss of smell. The immune response altered the architecture of genes in the neurons, disrupting production of odor receptors. The ability of the olfactory receptors to send and receive messages is altered, but the neurons don’t die. So the system can recover after the illness resolves.
Neurons that detect smells have complex genomic organizational structures that are essential to the creation of odor receptors. The receptor genes communicate among themselves intensively: There’s a signal released from the infected cells that’s received by the neurons that normally detect odors which tells them to reorganize and stop expression of olfactory receptor genes. This may represent an evolutionary adaptation that offers a form of antiviral resistance whose main purpose may be to prevent the virus from entering the brain. “That was a relief for us,” one of the paper’s authors commented. “It’s one piece of good news.”
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So now you know the answer to the question: “What role is played by Cocoa Puffs in olfactory research?” Make sure to write it down because I’m pretty sure it’s gonna be on the midterm.
