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Cover your nose: Johns Hopkins research suggests that’s how coronavirus gains foothold

The cells that allow people to smell are a key entryway for the coronavirus, making nose coverings crucial, suggests new research from the Johns Hopkins University.

The nose already had been emerging as a main door for the virus and related respiratory disease. But this research specifically points to the olfactory cells because they have a very large number of receptors on their surface called ACE2 that have been shown to be vulnerable to coronaviruses.

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“My main takeaway for now would be wear your mask properly and cover your nose,” said the lead researcher, Dr. Andrew Lane, professor of otolaryngology and director of the Hopkins School of Medicine’s Division of Rhinology and Skull Base Surgery.

“You could get infected by breathing in your nose,” he said. “You could infect other people by breathing out of your mouth or your nose.”

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Lane stressed that the findings are preliminary, but if proven to be the main entryway for COVID-19, the disease caused by the coronavirus, then Lane said better preventive measures and treatments could be developed.

They could be drugs, or something as simple as soapy washes or topical creams to smear inside the nostrils, Lane said. Their use could cut transmission of the virus as an effective vaccine is developed, though he said any measure would take careful study to ensure that it didn’t accelerate spread of the virus.

Lane said the research may help explain another coronavirus-related mystery: Why do so many people with COVID-19 lose their sense of smell? The cells may be temporarily damaged by the infection and unable to do their job.

There also are clues about why some people with COVID-19 have no symptoms in the research, a summary of which appeared Aug. 19 in the European Respiratory Journal. Lane said the cells in some people may serve as a sufficient reservoir for the virus, which never moves to other parts of the body.

For the research, the scientists looked at tissue taken from surgeries that had both the olfactory cells and other cells side-by-side and found the olfactory cells lining the upper part of the nose contained up to 700 times more ACE2 receptors than cells lining the rest of the nose and windpipe that leads to the lungs.

The scientists used fluorescent stains and a high-resolution imaging of the nasal and tracheal airways to see all the receptors.

That’s significant because those receptors, formally called angiotensin-converting enzyme 2 receptors, are present on many types of human cells and already had been found to be vulnerable to covoraviruses.

They’re in the lungs, for example, which tend to bear the brunt of COVID-19 infection in a lot of people.

A study released in April by a consortium of global researchers found two receptors, ACE2 and another called TMPRSS2, that were good hooks for coronaviruses.

They found the receptor combination most heavily in eyes, intestines and noses, though they focused on cells associated with mucus production in the nose rather than olfactory cells. The results from the Human Cell Atlas Lung Biological Network were published April 23 in the journal Nature Medicine.

“This is the first time these particular cells in the nose have been associated with COVID-19,” said Dr Martijn Nawijn, from the University Medical Center Groningen in the Netherlands, said in a statement at the time.

“While there are many factors that contribute to virus transmissibility, our findings are consistent with the rapid infection rates of the virus seen so far,” he said. “The location of these cells on the surface of the inside of the nose make them highly accessible to the virus, and also may assist with transmission to other people.”

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Back at Hopkins, the researchers will continue closing in on the exact cells that attract and transmit the virus.

The next step for the scientists is to allow the coronavirus to infect human nasal tissue in the lab. Then researchers plan to move onto hamsters.

“We’ll see if they infect these olfactory cells more,” Lane said. “Then we’ll need to see if they infect these cells more in real world exposure.”

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