According tomedia BGR reported that fever, cough, shortness of breath is a common symptom of new coronary pneumonia. Since then, doctors have observed unusual symptoms in patients with COVID-19, including heart and nervous system symptoms, skin lesions, and gastrointestinal symptoms. But the most unusual symptoms associated with COVID-19 are sudden loss of smell (smell disorder) and taste (taste disorder).
Several studies have shown that patients who show these symptoms are most likely infected, and the CDC has updated its website to include loss of smell and taste on its list of possible COVID-19 symptoms. But not all people infected with the disease lose their sense of smell and taste, so these symptoms are not enough to diagnose the new disease without actual testing. Researchers have offered a potential explanation for why viruses bind to olfactory epithelial cells, and new research offers more details about the symptoms of this strange new coronavirus.
In an unpeerly study from Harvard University published in early April, researchers found that SARS-CoV-2 is likely to bind to non-neuronal cells that support neurons in olfactory epithelial cells. The researchers analyzed the genes involved in the perception of the sense of smell and the transfer of information to the various cells in the brain and concluded that new viruses could bind to them.
Another study from researchers at the University of Tolenco-Perni in Poland was published in mid-April in the journal ACS Chemical Neuroscience. The paper attempts to accurately explain why the virus may infect olfactory cells and suggests that tests should be detected in that particular area to detect the virus early — even in asymptomatic patients. The researchers also warn that further research is needed to determine whether the virus can attack the brain with olfactory cells, as the SARS-CoV virus did nearly 20 years ago.
“We suggest that the olfactory epithelial from the nasal cavity may be a better tissue to detect SARS-CoV-2 virus in patients before symptoms occur, even in asymptomatic patients, than commonly used nasopharyngeal swabs,” the researchers wrote. The olfactory epithelial may be “a possible part of sars-CoV-2’s enhanced binding.” “A variety of non-neuronal cell types present in olfactory epithelial cells express two host receptors, ACE2 and TMPRSS2 proteases, which promote the binding, replication and accumulation of SARS-CoV-2. “
Anyone who has followed COVID-19 news in recent months knows that the S protein of the new coronavirus binds to ACE2 cell receptors. Once this link is established, the virus invades cells and turns them into “factories” that can replicate the virus. The replica is then ejected from the damaged cells, infecting other nearby cells and repeating the process. TMPRSS2 is not a frequent reference in COVID-19 news reports, but it appears in a different study that says a specific type of prostate cancer treatment regulates TMPRSS2 in the prostate and lungs and has the potential to reduce the severity of COVID-19 disease in men.
In the new study, the researchers found that older mice had higher levels of ACE2 and TMPRSS2 than younger mice. If this conclusion is correct for humans, it may explain why older people are more susceptible to infection and then complications. However, the study did not take into account the various medical conditions associated with old age, which reduce the body’s ability to handle unknown pathogens.
The scientists cited other studies that suggest edgy ACE2 receptors appear in non-neuronal olfactory cells in humans and mice, which appears to be consistent with the Harvard study. TMPRS2 is present in both neurons and non-neurons.