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 <a href="https:&#x2F;&#x2F;www.jpeds.com&#x2F;article&#x2F;S0022-3476(20)31023-4&#x2F;fulltext" rel="nofollow">https:&#x2F;&#x2F;www.jpeds.com&#x2F;article&#x2F;S0022-3476(20)31023-4&#x2F;fulltext</a><p>Results A total of 192 children (mean age 10.2 +&#x2F;- 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&lt;0.001), with dysregulated humoral responses observed.<p>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:<p>&gt; 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).<p>RNA. This <i>can</i> mean that they have a higher viral load, but high level of viral RNA does not necessarily equate with live virus. Why didn&#x27;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.<p>I checked the paper for cell cultures or in vitro assays for live virus, no dice.<p>I&#x27;m kind of disappointed. We&#x27;re well into the pandemic and we still rely on the presence of RNA alone to infer infectiousness? Why didn&#x27;t the reviewers ask for that?