Coronavirus (CoV) pandemics are nothing new to humans. Another member of the coronavirus family, SARS-CoV, caused the severe acute respiratory syndrome (SARS) outbreak over portions of Asia in 2003, same as SARS-CoV-2 (the virus that causes COVID-19).
However, it propagated far more quickly than COVID-19. So, what is it about SARS-CoV-2 that makes it so contagious?
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Both SARS-CoV and SARS-CoV-2 viruses include “spike proteins” that enter our cells via attaching to angiotensin-converting enzyme 2 (ACE2), a protein abundant in our cells.
The SARS-CoV-2 spike (S) protein, on the other hand, has been discovered to have a greater affinity for ACE2 (10 to 20 times that of SARS-CoV), suggesting a connection between the virus and the protein.
Patients with COVID-19 who have rhinosinusitis (inflammation of the nose) had a reduced risk of hospitalization, according to recent research. Furthermore, in patients with rhinosinusitis, ACE2 expression was decreased.
Another study found that short-chain fatty acids (SCFAs), which are generated by bacteria in the gut, can help with allergies and viral infections.
Scientists at the University of Fukui in Japan, led by Dr Tetsuji Takabayashi, investigated the impact of SCFAs in the nasal cavity against SARS-CoV-2 infection.
The researchers tried to investigate the effect of SCFAs on ACE2 expression in the nasal tube, as well as the possible influence on COVID-19 infection, in a recent study published in the American Journal of Rhinology & Allergy.
Dr. Takabayashi says, “This is the first report that short-chain fatty acids (SCFAs) effectively reduce the ACE2 levels in human airway epithelial cells.”
The researchers investigated the levels of ACE2 in the inner lining of the nose in patients with seasonal allergic rhinitis caused by Japanese cedar pollen (SAR-JCP) and chronic rhinosinusitis to better understand the status of ACE2 expression in allergy patients (CRS).
Researchers observed no increase in ACE2 expression in patients with SAR-JCP, but a reduction in individuals with CRS, using techniques like real-time PCR to measure the expression of ACE2.
To better understand the effect of SCFAs on ACE2 expression, the team cultivated nasal epithelial cells and subjected them to either SFCA or double-stranded RNA to better understand the influence of SCFAs on ACE2 expression (similar to the nuclear material found in some viruses and known to enhance ACE2 expression). When the researchers looked at the expression of ACE2, they discovered that the SFCAs inhibited ACE2 expression even when the RNA was present.
These findings imply that SFCAs might be useful in the treatment of COVID-19. According to Dr Takabayashi,
“The nasal mucosa exhibits the highest ACE2 expression among human organs and hence is a prominent target of original infection. Therefore, the development of strategies to downregulate ACE2 expression in nasal epithelial cells could reduce SARS-CoV-2 transmission and be useful as a novel therapeutic approach.”
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The team’s timely results will undoubtedly help us combat COVID-19.
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