The new coronavirus still holds many secrets, one of which is how it can cause loss of smell -- even in infected people who have no other COVID-19 symptoms. Image is in the public domain.
Summary: ACE2 and TMPRSS2, two proteins required for SARS-CoV-2 entry, are produced in cells in the nasal cavity that contribute to odor detection. The findings may explain why people with coronavirus often describe the loss of the sense of smell as a symptom of the virus.
Doctors have reported that partial or total loss of the sense of smell is often an early symptom of infection with SARS-CoV-2, the virus that causes COVID-19. Now, researchers reporting in ACS Chemical Neuroscience have shown that in mice, two proteins required for SARS-CoV-2 entry are produced by cells of the nasal cavity that contribute to odor detection. Moreover, larger amounts of the proteins are made in older animals than in younger ones.
The new coronavirus still holds many secrets, one of which is how it can cause loss of smell — even in infected people who have no other COVID-19 symptoms. SARS-CoV-2 hijacks two proteins to invade human cells: the cell surface receptor ACE2 and the protease TMPRSS2. However, scientists still aren’t sure which cells in the olfactory epithelium (the tissue lining the nasal cavity) express these proteins and could potentially be infected by the virus. Finding out could help explain symptoms and aid in the development of more accurate diagnostic tests. So Rafal Butowt and colleagues studied the proteins’ expression in mice and how their levels change with age.
Using several methods, the researchers found that ACE2 and TMPRSS2 are expressed in sustentacular cells — cells of the nose that help transfer odors from the air to neurons. Older mice made more of the two proteins in nasal cells than younger mice. If also true in humans, this result could explain why older people are more susceptible to SARS-CoV-2, the researchers say. They also note that future studies should examine whether sustentacular cells can pass the virus to neurons, which could provide SARS-CoV-2 a route to infect the brain.
Funding: The authors acknowledge funding from the National Science Centre of Poland and the National Institute of General Medical Sciences of the National Institutes of Health.
About this coronavirus research article
Source: ACS Media Contacts: Katie Cottingham – ACS Image Source: The image is in the public domain.
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The Covid-19 pandemic revealed that there is a loss of smell in many patients, including in infected, but otherwise asymptomatic individuals. The underlying mechanisms for the olfactory symptoms are unclear. Using a mouse model, we determined whether cells in the olfactory epithelium express the obligatory receptors for entry of the SARS-CoV-2 virus by using RNAseq, RT-PCR, in situ hybridization, Western blot, and immunocytochemistry. We show that the cell surface protein ACE2 and the protease TMPRSS2 are expressed in sustentacular cells of the olfactory epithelium, but not, or much less, in most olfactory receptor neurons. These data suggest that sustentacular cells are involved in SARS-CoV-2 virus entry and impairment of the sense of smell in COVID-19 patients. We also show that expression of the entry proteins increases in animals of old age. This may explain – if true also in humans – why individuals of older age are more susceptible to the SARS-CoV-2 infection.