A recently published report in Nature Medicine by a group of British epidemiologists concludes that children are half as likely to be infected by SARS-CoV-2 as adults. The conclusion is based primarily on publicly available data from Wuhan and from five other countries including Canada, Italy, Japan, Singapore, and South Korea.
Specifically, they estimate that those under the age of 20 have half the chance of infection as those 20 and older. They estimate that Covid-19 symptoms occur in about 20 percent of infections in children between the ages of 10 and 20 as compared to about 70 percent for those 70 and older.
The conclusions are based solely on data analysis. The work does not describe direct observation of adult to adult, adult to child, and child to child transmission. Although the analytical methods may be sound, the conclusions may be affected by factors other than age-related differences in infection susceptibility. For example, detection of infection in children may be influenced by what is already know about the absence of any disease symptom in children also documented in here, with the result that the actual number of children infected in undercounted.
However another recent study provides more detail on whether and why the incidence of SARS-CoV-2 infection is lower in children than adults. The research seeks to confirm the hypothesis that the difference is due to a lower density of ACE2 receptors in the nasal epithelium of children as compared to adults. The reported relative densities of the ACE2 receptors are:
Age Relative ACE2 Density
The significant difference in this study is reported to be between those under 17 and those aged 18-60.
The authors speculate that this difference may account for the apparent difference in infection of children and adults.
Several caveats to consider:
How sure are we that there is an inherent difference in infection rates between adults and children? Many factors affect infection in adults which but not children confounding such studies.
The authors acknowledge a weakness in the study as no one over 60 was included. Those 60 and above are those most affected by Covid-19.
The density of ACE2 receptors may not be uniform throughout the nasal mucosa. Perhaps there are fewer differences in regions unlikely to have been sampled.
SARS-CoV-2 may infect via the nasal mucosa by routes other than via attachment the ACE2 receptor, specifically via M cell transcytosis or via attachment to the exterior of migrating dendritic macrophages. Other respiratory viruses initiate infection by both alternative methods.
I do not believe the literature shows that children are less susceptible to the NL63 cold-causing coronaviruses that also infects via the ACE2 receptor.
No mention is made of oral/fecal transmission of SARS-CoV-2 which is also a confounding variable.
Considerably more research is needed to validate both hypotheses: That children are indeed less infectable and that the reason for the difference is the density of nasal ACE2 receptors.
What is clear is that the policy implications of the distinction between disease prevalence and age for susceptibility to infection are profound, as these observations may have implications relevant to school closings and to other public health control measures.