Once inside the body, the virus moves around by attaching to the same ACE2 protein on other tissues deep in the lungs, the heart, and the kidneys. The receptor can also be found in the lining of blood vessels, and possibly even the taste buds on our tongues. This is one reason why Covid-19 patients may present such a diverse set of symptoms.
A paper recently published in JAMA examines one measure of the amount of receptors in the noses of children and adults. I say one measure because what is measured is not the protein responsible for attachment, but rather the RNA which directs its production. Usually but not always, the amount of RNA in cells determines the amount of the corresponding protein. The authors assume that is the case, and their conclusion depends on that assumption.
With that caveat in mind, they report finding less ACE2 RNA in cells scraped from the noses of children than in those from adults. Participants in the study were divided into four age groups: less than ten, 10-17, 18-24, and older than 24.
The first conclusion is there was no difference in the amount of ACE2 RNA detected according to gender or those with or without asthma. The second conclusion is that the amount of ACE2 RNA increases with each age group.
The differences are relatively small and the error bars large. The average relative amount of RNA ranges from 2.4 for those less than 10 to 3.09 for those 25 and older. However, when the probable range is included, the results from the three older groups overlap, as do the results from the three younger groups.
Can we conclude that such differences imply a difference in overall susceptibility to infection? Possibly, but not certainly. We do not know how many receptors are needed for the SARS-CoV-2 virus to successfully infect us. Clearly children, even very young children, can be infected.
Additionally, we do not know the efficiency of the conversion of RNA to the stable ACE2 protein that serves as a receptor. Also unknown is whether or not there are age related biological and behavioral factors other than ACE2 which determine susceptibility to infection.
Such is science. We must collect data, analyze it for accuracy, and infer its meaning. Our job is to do our best to disprove our favorite hypothesis, so that it remains the only explanation left standing. Does this paper “prove” children are less susceptible to Covid-19 infection? Alas, no. Does it advance our understanding of ACE2 expression in the noses of different age groups? Marginally, yes.