Scientists claim to have finally discovered how the coronavirus can cause patients to lose their sense of smell.
Until now, researchers have been puzzled as to why some infected patients were stripped of their senses.
Researchers at Harvard Medical School investigated the ‘devastating’ symptom and say it is ‘good news’ because the loss of smell does not appear to be permanent.
They found that sensory neurons, the ones that detect odor and send it to the brain, are not vulnerable to Covid-19.
Instead, it is the cells that provide key structural support for the sensory neurons infiltrated by the virus, which explains the loss of smell.
But experts say it means that sensory neurons don’t need to be ‘built from scratch,’ which could take months or never happen.
It offers hope to those who had feared that their loss of smell was permanent. Research has suggested that this could be a problem for 10 percent of sufferers.
Covid-19’s loss of smell doesn’t seem to be permanent, scientists say, after discovering crucial cells in the nose are still intact (stock).
The study, published in the journal Science Advances, was written by lead author Dr. Sandeep Robert Datta, an associate professor of neurobiology.
He said: ‘I think that is good news, because once the infection clears up, the olfactory neurons don’t seem to need to be replaced or rebuilt from scratch.
“But we need more data and a better understanding of the underlying mechanisms to confirm this conclusion.”
Temporary loss of smell, or anosmia, is recognized as one of the main symptoms of Covid-19, along with fever and persistent cough.
A dysfunction in smell can cause indirect taste problems, since the two senses are linked.
Dr. Datta said: ‘Anosmia seems like a curious phenomenon, but it can be devastating for the small fraction of people in whom it is persistent.
“It can have serious psychological consequences and it could be a major public health problem if we have a growing population with permanent loss of smell.”
He and an international team of scientists tried to answer whether the anosmia was permanent by analyzing thousands of individual cells found in the noses of humans, mice, and primates.
Academics looked at which genes each cell expressed, information they already had at the disposal of previous studies.
They focused on ACE-2, which controls receptors of the same name that act as a gateway for the virus to enter cells in the respiratory tract.
They also looked for the TMPRSS2 gene, which encodes an enzyme that is considered important for the SARS-CoV-2 virus to enter cells.
Neither gene was expressed by olfactory sensory neurons, which detect and transmit information about odors to the brain.
Both ACE-2 and TMPRSS2 are expressed by two specific support cells that help transmit odors to the brain and are found in the olfactory epithelium, on the roof of the nasal cavity..
The two types of cells are sustainability cells, which wrap around sensory neurons and are believed to provide structural support, and basal cells, which act as stem cells that regenerate the olfactory epithelium after damage.
Both types expressed ACE-2 at levels similar to those observed in cells of the lower respiratory tract, the most common targets of SARS-CoV-2.
This suggests that they are the most vulnerable to infection because the virus is better able to enter.
People would lose their smell because a temporary loss of support cell function would indirectly cause changes in olfactory sensory neurons, but not damage.
Dr. Datta said: ‘We still don’t fully understand what those changes are.
Sustain cells have been largely ignored, and it seems we need to pay attention to them.
“Our findings indicate that the new coronavirus changes the sense of smell in patients by not directly infecting neurons but by affecting the function of supporting cells.”
Dr. Datta and colleagues also analyzed gene expression in nearly 50,000 individual cells in the mouse olfactory bulb.
This structure in the forebrain receives signals from olfactory sensory neurons and is responsible for the initial processing of a new odor.
Neurons in the olfactory bulb did not express the ACE-2 or TMPRSS2 gene, supporting the findings.
In most cases, SARS-CoV-2 infection is unlikely to permanently damage the cells needed to detect odor, according to the study.
It was feared that the coronavirus pandemic would lead millions of people worldwide to never regain their scent.
According to a study in a small group of Italians, one in ten people with mild illnesses still have difficulty smelling or tasting a month after the illness.
The study found that only half of the people with the symptom had fully recovered their sense of taste and smell a month after their recovery.
Dr Claire Hopkins, one of the researchers and president of the British Rhinological Society, told the BBC: ‘The data for other viral diseases, and some of the new data we are collecting, suggest that the vast majority of people It will improve, but for some, recovery will be slow.
‘For people who recover faster, the virus likely has only affected the cells that line their nose.
‘For people who recover more slowly, the virus may also have affected the nerves involved in the smell. It may take longer for these nerve cells to repair and regenerate. ”
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