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Airborne transmission of covid-19

BMJ 2020; 370 doi: https://doi.org/10.1136/bmj.m3206 (Published 20 August 2020) Cite this as: BMJ 2020;370:m3206

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Rapid Response:

Re: Airborne transmission of covid-19

Dear Editor

Given the poor correlation of "viral load" as measured on a pharyngeal swab with infectivity ( https://jamanetwork.com/journals/jamapediatrics/fullarticle/2768952 ), and that aerosolised virus is now recognised as being a potent driver of infections, then we need to look beyond the pharynx to figure out the source of aerosolisation.

Given knowledge of superspreading events in "phonation-loud" settings such as choirs, meatpacking plants, noisy pubs & bars, then this raises suspicion that the larynx is somehow involved.

Given that young children appear to be almost a dead-end host for SARS-CoV-2, yet will often demonstrate high "viral loads" on pharyngeal swabs ( https://jamanetwork.com/journals/jamapediatrics/fullarticle/2768952 ) then perhaps infectivity is tied to the number of viral receptors in the LOWER respiratory tract. There are far fewer ACE2 receptors in the lower respiratory tract of children compared to adults ( https://www.sciencedirect.com/science/article/pii/S2329050120301005 ). A lack of ACE2 receptors will also reconcile with the scarcity of lung disease in young children.

So what might tie this together more precisely is a posit that "aerosolisation of virus is in fact a process which occurs from larynx to lungs (i.e. it occurs within the lower respiratory tract, not the upper respiratory tract)".

In fact, this posit, when taken with another posit that "the infectious dose of virus is organ-specific and correlates inversely with the density of viral receptors", will go a long way towards explaining important epidemiological aspects of Covid-19 disease.

Competing interests: No competing interests

13 September 2020
Robert Stephens
Consultant Dermatologist
North West Sydney Dermatology
Suite 1, The Terrace, 40 Panmure St, Rouse Hill, NSW 2155, AUSTRALIA