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Few features of Covid-19 have aroused as much interest as anosmia, the sudden loss of smell that has become a well-known feature of the disease. Covid patients lose this feeling even without nasal congestion; The loss can make food taste detrimental, such as the smell of cardboard and coffee, and can sometimes persist after other symptoms have resolved.

Scientists are now starting to unravel the biological mechanisms that are somewhat of a mystery: Neurons that sense odors lack the receptors the coronavirus uses to enter cells, sparking a long debate over whether they’re infected.

Insights from new research can shed new light on how the coronavirus can affect other types of brain cells, leading to conditions such as “brain fog,” and possibly help explain the biological mechanisms behind the protracted Covid. initial infection.

The new study, along with previous studies, resolves the debate over whether the coronavirus infects nerve cells that detect odors: It doesn’t. However, the researchers found that the virus attacked other supporting cells lining the nasal cavity.

As the infected cells shed the virus and die, immune cells populate the area to fight the virus. The ensuing inflammation damages odor receptors, proteins on the surface of nerve cells in the nose that detect and transmit information about odors.

The researchers reported that the process alters the complex organization of genes in these neurons, essentially shorting them out.

Associate professor of neurobiology at Harvard Medical School, Dr. Sandeep Robert Datta said their paper has significantly improved the understanding of how cells critical to the sense of smell are affected by the virus, even though they are not directly infected. not included in the study.

Dr. “Indirectly, it’s clear that a lot of bad things will happen if you affect the support cells in the nose,” Datta said. Inflammation in adjacent cells triggers changes in sensory neurons that prevent them from working properly.

Indeed, many of the complications of Covid seem to be caused by friendly fever of the immune system as it responds to the infection by flooding the bloodstream with inflammatory proteins called cytokines that can damage tissues and organs.

Dr. “This may be a general principle: Much of what the virus does to us is a result of its ability to create inflammation,” Datta said.

The new study builds on research conducted at the Zuckerman Institute and Irving Medical Center at Columbia University in New York; New York University Grossman School of Medicine; Icahn School of Medicine at Mount Sinai, New York; Baylor Genetics in Houston; and University of California, Davis School of Medicine. Research Published online on Cell At the beginning of February.

Scientists examined golden hamsters and human tissue samples from 23 patients who succumbed to Covid. After hamsters were infected with the original coronavirus, scientists tracked damage to their olfactory systems over time.

(How do you know when a golden hamster has lost its sense of smell? “How do you know if a golden hamster has lost its sense of smell? You don’t bury Cocoa Puffs in its bed after you’ve fed it for a few hours,” said Benjamin tenOever, professor of microbiology at NYU Langone Health. hamsters will find the cereal in seconds.)

Researchers learned that the virus does not invade neurons, but only cells that play a supporting role in the olfactory system. However, this was enough to alter the function of nearby neurons, leading to loss of smell.

Marianna Zazhytska, a postdoctoral researcher at the Zuckerman Institute and one of the first authors of the paper, said, along with graduate student Albana Kodra, that the immune response changes the structure of genes in neurons and disrupts the production of olfactory receptors.

Dr. “It’s not the virus itself that’s causing all this rearrangement — it’s the systemic inflammatory response,” said Zazhytska. “The nerve cells do not harbor the virus, but they are not doing what they did before.”

The ability of the olfactory receptors to send and receive messages is impaired. However, neurons do not die so that the system can recover after the disease has healed.

Stavros Lomvardas, one of the paper’s corresponding authors, said that previous work at the Zuckerman Institute has shown that neurons that detect odors have complex genomic organizational structures necessary for the creation of olfactory receptors, and that the receptor genes communicate very intensely among themselves.

Dr. “Early upon infection, we found that the genomic organization of these neurons completely changed – they are unrecognizable compared to what they normally are,” Lomvardas said.

“There’s a signal released from infected cells that is picked up by neurons that normally detect odors and tell them to upregulate and stop the expression of their olfactory receptor genes,” he said.

He suggested that this may represent an evolutionary adaptation that offers some form of antiviral resistance and whose main purpose may be to prevent the virus from entering the brain. “It was a relief for us,” he said. “That was a good piece of news.”