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 Table of Contents  
Year : 2020  |  Volume : 11  |  Issue : 1  |  Page : 74

Why children are less likely to contract COVID-19 infection than adults?

Department of Pediatrics, Division of Nephrology, Rush University Medical Sciences, Chicago, Illinois, USA

Date of Submission17-Apr-2020
Date of Acceptance18-Apr-2020
Date of Web Publication19-Jun-2020

Correspondence Address:
Farahnak Assadi
Department of Pediatrics, Division of Nephrology, Rush University Medical Sciences, !804 E. North Water Street, Suite 1804, Chicago, Illinois 60611
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpvm.IJPVM_199_20

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How to cite this article:
Assadi F. Why children are less likely to contract COVID-19 infection than adults?. Int J Prev Med 2020;11:74

How to cite this URL:
Assadi F. Why children are less likely to contract COVID-19 infection than adults?. Int J Prev Med [serial online] 2020 [cited 2021 Jun 21];11:74. Available from: https://www.ijpvmjournal.net/text.asp?2020/11/1/74/287177

The novel coronavirus disease of 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).[1] The reported cases of COVID-19 among children have been less severe than those in adults.[2] Dong et al.,[3] in a recent clinical study of more than 2000 infants and preschool-aged children with suspected COVID-19, found that 4% of virologically confirmed cases were symptomatic and among children who were symptomatic, 5% experienced dyspnea and hypoxemia, and only 0.6% progressed to acute respiratory distress syndrome, a substantially lower percentage rate than has been reported in adults.

The findings of children that are less likely than adults to become severely ill from COVID-19 are challenging to discern.[4]

Previous data from clinical trials suggest that children and adults who are healthy have a balanced renin-angiotensin system (RAS)––both the angiotensin-converting enzyme (ACE)/angiotensin II and angiotensin-converting enzyme 2 (ACE2)/angiotensin (1–7) pathways.[5],[6] However, as we age and/or develop disease (hypertension, chronic kidney disease, diabetes, cardiovascular disease), we have relatively more ACE/angiotensin II compared to ACE2/angiotensin (1–7).[7],[8] The ACE2 pathway increases to compensate, but only to a point, at which time the ACE pathway is essentially unopposed.[9],[10]

Remember ACE2 degrades angiotensin II (“bad”) into angiotensin (1–7) (“good”).

We definitely have data that this shift in the RAS occurs more in children than in adults with hypertension, chronic kidney disease, and cardiovascular disease.[11]

In COVID-19, the hypothesis is that children have plenty of ACE2 but it easily counteracts the ACE pathway. Thus, children have the same (or higher) risk of infection with SARS-CoV-2, but are protected (in part) from the (likely) angiotensin II-mediated acute lung (and possibly heart/kidney/brain) injury that we see in COVID-19.

For sure, there are many other factors, which may play major role in the pathogenesis of COVID-19 disease. This is just one theory that could be involved.

  References Top

CoronavirIdae Study Group of the International Committee on Taxonomy of Viruses. The species severe acute respiratory syndrome-related coronavirus: Classifying 2019-nCov and naming it SARS-Cov-2. Nat Microbiol 2020;5:536-44.  Back to cited text no. 1
Cruz AT, Zeichner SL. COVID-19 in children: Initial characterization of the pediatric disease. Pediatrics 2020;145:e20200834.  Back to cited text no. 2
Dong Y, Mo X, Hu Y, Qi X, Jiang F, Jiang Z, et al. Epidemiology of COVID-19 among children in China. Pediatrics 2020;145:e20200702. doi: 10.1542/peds.2020-0702.  Back to cited text no. 3
Jenco M. COVID-19 less severe in children than adults: Study. AAP News Content Editor. 2020. Available from: http://www.aappublications.org/ne ws/2020/01/28/coronavirus.  Back to cited text no. 4
Ferrario CM. ACE2: More of Ang-(1-7) or less Ang II? Curr Opin Nephrol Hypertens 2011;20:1-6.  Back to cited text no. 5
Varagic J, Ahmad S, Ferrario CM. ACE2: Angiotensin II/Angiotensin-(1-7) balance in cardiac and renal injury. Curr Hypetens Rep 2014;16:420.  Back to cited text no. 6
Souza Dos Santo RA, Passaglio KT, Pesquero JB, Bader M, Simoes E Silva AC. Interactions between angiotensin-(1-7), kinins, and angiotensin II in kidney and blood vessels. Hypertension 2001;38:660-4.  Back to cited text no. 7
Chappell MC, Allred AJ, Ferrario CM. Pathways of angiotensin-(1-7) mechanism in the kidney. Nephrol Dial Transplant 2001;16:22-6.  Back to cited text no. 8
Santos RAS, Ferreira AJ, Simoes e Silva AC. Recent advances in the angiotensin-converting enzyme 2-angiotensin-(-7) Mas axis. Exp Physiol 2008;93:519-27.  Back to cited text no. 9
Brant Pinheiro SV, Simons e AC. Angiotensin converting emzyme 2, angiotensin-(1-7), and receptor Mas axis in the kidney. Int J Hpertens 2012;414128. doi: 10.1155/2012/414128.  Back to cited text no. 10
Fernandez-Atucha A, Izagirre A, Fraile-Bermudez AB, Kortajarena M, Larrinaga G, Martinez-Lage P, et al. Sex differences in the aging pattern of renin-angiotensin system serum peptidases. Biol Sex Differ 2017;8:5.  Back to cited text no. 11


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