Do you experience running nose with nasal obstruction leading to loss of smell??
Almost we all isn’t?
But a majority of COVID-19 patients experience some level of acute anosmia, without rhinitis or nasal obstruction most often temporary.
This become one of the earliest and most commonly reported indicators of COVID-19. Studies suggest it better predicts the disease than other well-known symptoms such as fever and cough.
Now it become 27 times more likely to have smell loss but are only around 2.2 to 2.6 times more likely to have fever, cough or respiratory difficulty in COVID 19.
So, what is the cause ??
Is there any effect on sensory neurons that detect and transmit the sense of smell to the brain
Surprisingly….not!!
It is Olfactory support cells, not neurons, are vulnerable to novel coronavirus infection
Now, an international team of researchers led by neuroscientists at Harvard Medical School has identified the olfactory cell types in the upper nasal cavity most vulnerable to infection by SARS-CoV-2, the virus that causes COVID-19.
On July 24, the research team found that olfactory sensory neurons do not express the gene that encodes the ACE2 receptor protein, which SARS-CoV-2 uses to enter human cells.
Instead, ACE2 is expressed in Olfactory support cells that provide metabolic and structural support to olfactory sensory neurons, as well as certain populations of stem cells and blood vessel cells.
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The findings suggest that infection of nonneuronal cell types may be responsible for anosmia in COVID-19 patients and help inform efforts to better understand the progression of the disease.
“Our findings indicate that the novel coronavirus changes the sense of smell in patients not by directly infecting neurons but by affecting the function of supporting cells,” said senior study author Sandeep Robert Datta, associate professor of neurobiology in the Blavatnik Institute at HMS.
This implies that in most cases, SARS-CoV-2 infection is unlikely to permanently damage olfactory neural circuits and lead to persistent anosmia, Datta added, a condition that is associated with a variety of mental and social health issues, particularly depression and anxiety.
“I think it’s good news, because once the infection clears, olfactory neurons don’t appear to need to be replaced or rebuilt from scratch,” he said. “But we need more data and a better understanding of the underlying mechanisms to confirm this conclusion.”
Some studies have hinted that anosmia in COVID-19 differs from anosmia caused by other viral infections, including by other coronaviruses.
For example, COVID-19 patients typically recover their sense of smell over the course of weeks—much faster than the months it can take to recover from anosmia caused by a subset of viral infections known to directly damage olfactory sensory neurons. In addition, many viruses cause temporary loss of smell by triggering upper respiratory issues such as stuffy nose. Some COVID-19 patients, however, experience anosmia without any nasal obstruction.
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The team focused on the gene ACE2, widely found in cells of the human respiratory tract, which encodes the main receptor protein that SARS-CoV-2 targets to gain entry into human cells. They also looked at another gene, TMPRSS2, which encodes an enzyme thought to be important for SARS-CoV-2 entry into the cell.
The analyses revealed that both ACE2 and TMPRSS2 are expressed by cells in the olfactory epithelium—a specialized tissue in the roof of the nasal cavity responsible for odor detection that houses olfactory sensory neurons and a variety of supporting cells.
Neither gene, however, was expressed by olfactory sensory neurons. By contrast, these neurons did express genes associated with the ability of other coronaviruses to enter cells.
These included sustentacular cells, which wrap around sensory neurons and are thought to provide structural and metabolic support, and basal cells, which act as stem cells that regenerate the olfactory epithelium after damage. The presence of proteins encoded by both genes in these cells was confirmed by immunostaining.
Yet,“We don’t fully understand what those changes are yet, however,” Datta said.
However, depending on the true distribution of ACE2, virulence potential, and resulting immune and inflammatory response, olfactory dysfunction may indicate a peripheral injury of the first cranial nerve and branches or a harbinger of a more global neurological manifestation of the disease.
Long-term follow-up studies on patients with isolated sudden onset anosmia will be important because this symptom may indicate the onset of neuroinvasion that could result in chronic neurodegenerative disease.
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