
Researchers show children are silent spreaders of virus that causes Covid-19 - InInteraction
https://www.eurekalert.org/pub_releases/2020-08/mgh-rsc081720.php
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InInteraction
BOSTON - In the most comprehensive study of COVID-19 pediatric patients to
date, Massachusetts General Hospital (MGH) and Mass General Hospital for
Children (MGHfC) researchers provide critical data showing that children play
a larger role in the community spread of COVID-19 than previously thought. In
a study of 192 children ages 0-22, 49 children tested positive for SARS-CoV-2,
and an additional 18 children had late-onset, COVID-19-related illness. The
infected children were shown to have a significantly higher level of virus in
their airways than hospitalized adults in ICUs for COVID-19 treatment.

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InInteraction
Related Journal of Pediatrics Article: Pediatric SARS-CoV-2: Clinical
Presentation, Infectivity, and Immune Responses
[https://www.jpeds.com/article/S0022-3476(20)31023-4/fulltext](https://www.jpeds.com/article/S0022-3476\(20\)31023-4/fulltext)

Results A total of 192 children (mean age 10.2 +/\- 7 years) were enrolled.
Forty-nine children (26%) were diagnosed with acute SARS-CoV-2 infection; an
additional 18 children (9%) met criteria for MIS-C. Only 25 (51%) of children
with acute SARS-CoV-2 infection presented with fever; symptoms of SARS-CoV-2
infection, if present, were non-specific. Nasopharyngeal viral load was
highest in children in the first 2 days of symptoms, significantly higher than
hospitalized adults with severe disease (P = .002). Age did not impact viral
load, but younger children had lower ACE2 expression (P=0.004). IgM and IgG to
the receptor binding domain (RBD) of the SARS-CoV-2 spike protein were
increased in severe MIS-C (P<0.001), with dysregulated humoral responses
observed.

Conclusion This study reveals that children may be a potential source of
contagion in the SARS-CoV-2 pandemic in spite of milder disease or lack of
symptoms, and immune dysregulation is implicated in severe post-infectious
MIS-C.

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lbeltrame
From the methods:

> SARS-CoV-2 viral load quantification: SARS-CoV-2 RNA levels were quantified
> with a quantitative viral load assay using the US CDC 2019-nCoV_N1 primers
> and probe set as previously described(10).

RNA. This _can_ mean that they have a higher viral load, but high level of
viral RNA does not necessarily equate with live virus. Why didn't they try to
infect Vero E6 cells with the swab samples? (My guess: lack of equipment).
Given the day of sampling, it may be still related, but given studies in
children are far and few between, this is an IMO glaring omission.

I checked the paper for cell cultures or in vitro assays for live virus, no
dice.

I'm kind of disappointed. We're well into the pandemic and we still rely on
the presence of RNA alone to infer infectiousness? Why didn't the reviewers
ask for that?

