Abstract
COVID-19 pandemic has given rise to a collective scientific effort to study its viral causing agent SARS-CoV-2. Research is focusing in particular on its infection mechanisms and on the associated-disease symptoms. Interestingly, this environmental pathogen directly affects the human chemosensory systems leading to anosmia and ageusia. Evidence for the presence of the cellular entry sites of the virus, the ACE2/TMPRSS2 proteins, has been reported in non-chemosensory cells in the rodent’s nose and mouth, missing a direct correlation between the symptoms reported in patients and the observed direct viral infection in human sensory cells. Here, mapping the gene and protein expression of ACE2/TMPRSS2 in the mouse olfactory and gustatory cells, we precisely identify the virus target cells to be of basal and sensory origin and reveal the age-dependent appearance of viral entry-sites. Our results propose an alternative interpretation of the human viral-induced sensory symptoms and give investigative perspectives on animal models.
Highlights
COVID-19 pandemic has given rise to a collective scientific effort to study its viral causing agent SARS-CoV-2
We revealed that the emergence of viral entry sites in sensory and basal cells only occurs with age, which could explain both, the observed COVID-19 long-lasting effects and the age-dependent sensory-symptomatology in human
Ace[2] is strongly expressed in a specific area of the main olfactory epithelium (MOE), the dorsal part (MOED) which is directly exposed to the environment and specialized in sensing volatile chemical cues[14,15]
Summary
COVID-19 pandemic has given rise to a collective scientific effort to study its viral causing agent SARS-CoV-2. The target cells of the virus share a molecular signature: the concomitant cellular expression of the angiotensin-converting enzyme 2 (ACE2) and of its facilitating transmembrane serine protease 2 (TMPRSS2), which plays a crucial role for the interaction of viral spike proteins with the host cell[11,12,13] These entry sites seem to be lacking in sensory cells[14,15,16,17,18], while a direct SARS-CoV-2 contamination has been observed both in humans and rodents[19,20], requesting further investigations to explain the sensory-associated symptoms[21,22,23,24]. We revealed that the emergence of viral entry sites in sensory and basal cells only occurs with age, which could explain both, the observed COVID-19 long-lasting effects and the age-dependent sensory-symptomatology in human
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