Researchers show children are silent spreaders of virus that causes Covid-19

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.

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

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.

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?