Silent spread

New study shows why temperature checks aren't enough to open schools safely

"I think we'll see a little bit more of the role kids can potentially play in spreading the virus."

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When schools shuttered in March, the United States had only just recognized the threat posed by the novel coronavirus. Now, school season is back and we're living in a different world.

We know more about how the virus spreads, who's most at-risk, and making headway toward a vaccine. However, we've left one critical question unanswered: Do kids really spread Covid-19? And what does that mean for the communities where schools are set to reopen?

A new study on 192 children conducted at Massachusetts General Hospital shows that children are capable of harboring high viral loads — the amount of SARS-CoV-2 detected someone's blood samples or nasal swabs.

During early infection, typically within two days, viral loads in children were higher than in hospitalized adults monitored over a week. The study also found that only 51 percent of the 49 children who were diagnosed with Covid-19 had fevers. That complicates things: One way that schools are monitoring students for coronavirus is a temperature check.

The study stops short of tracing cases of Covid-19 from children from adults and doesn't indicate that children transmit the virus more so than adults do. However, the study does suggest that children, regardless of age, can carry a high viral load and may act as silent spreaders – especially if they only show very mild symptoms.

Ultimately, the research points to the role that kids could play in spreading the virus to those who suffer more severely, explains Lael Yonker, the study's first author and the co-director of Massachusetts General Hospital's Cystic Fibrosis Center.

"We found that symptoms really didn't differentiate between who had Covid-19 or who didn't, but those who have Covid-19 had a very high viral load in their respiratory secretions," Yonker tells Inverse. "The more virus that you have in respiratory secretions, the more likely somebody else is going to pick it up."

"I think we'll see a little bit more of the role kids can potentially play in spreading the virus because they do have viral loads and they're going to be out more in the larger group settings in schools," she continues.

The study was published Thursday in The Journal of Pediatrics.

Kindergarteners in China have their temperatures checked to monitor them for coronavirus, but new research suggests that kids may not show temperatures when they are harboring SARS-CoV-2.

Getty Images/STR / Contributor

Children and coronavirus

It seems counterintuitive that kids might spread Covid-19 differently than adults do. But studies that focus on transmission, not viral load as this study does, have published mixed findings.

A study of 109 people (23 families) living in Greece found that the adult represented the first case of Covid-19 in the household in 91 percent of cases. The authors suggested that there was "no evidence of child-to-adult" and "child-to-child" transmission. A study in Switzerland also argues that "children most frequently acquire COVID-19 from adults, rather than transmitting it to them."

Other studies have suggested that there may be nuances as to how children do, or do not, spread Covid-19. Age appears to be one of them: A widely cited study in South Korea first reported that children between the ages of 10 were less likely to spread Covid-19. Newer data on older children has clarified that study's message – suggesting that the risk of transmitting the virus increases as children get older, but that older children probably don't transmit the virus more so than adults do.

"If they do get infected, they have the same capability of any age range of having a very high viral load."

Yonkers' study analyzed children from newborns to 22-years-old, though most of the patients were between 11 and 16. She found that younger kids were just as likely to have high viral loads as older kids were. However, the team did find that kids younger than ten had fewer ACE2 receptors (the landing pad for coronavirus on cells) in their upper airways than older kids. Overall, ACE2 receptors increased with age.

That does suggest that younger children may be less susceptible to the virus than older kids, Yonker says. But that may not make them less likely to transmit the virus once they have it:

"There is some protection from catching Covid-19 with younger age, but it's not black and white," she says. "If they do get infected, they have the same capability of any age range of having a very high viral load."

Importantly, having a high viral load doesn't necessarily mean that kids are transmitting the virus. However, the study underscores the possibility that transmission could happen as schools reopen, affecting the wider community.

What happens if we open schools too early? 

Kids don't always suffer severe consequences of the disease, though some do end up with a Multisystem Inflammatory Syndrome in Children (MIS-C). This can lead to hospitalization.

What's more of a concern, currently, is whether gathering in-person at school will negatively affect school staff or those within the student's household. An estimated 24 percent of teachers, roughly 1.5 million people, may be at risk for severe disease. People who live in multi-generational homes, where an older parent or grandparent is around kids, may also suffer severe disease if they get Covid-19.

Yonker's study found that only 51 percent of the children examined had fevers; other symptoms were "non-specific." Temperature checks and self-monitoring of symptoms are "unreliable," says Yonker.

"Parents are going to really have to pay attention to mild symptoms," she says.

That may not be enough to catch a case of Covid-19, especially in the early stages. As the study notes, the viral loads detected in children were the highest in the first two days of the illness, suggesting that this is the period when they're most contagious.

Right now, there are no easy answers, says Yonker. It's still unclear whether children are playing a large role in actually spreading the virus. But what this study does make clear is that we need to be even more careful as we start reopening.

"We have to be careful in opening the schools, not only to keep the kids healthy but also to protect the larger community and keep everybody healthy," Yonker says.

Abstract:
Objectives: As schools plan for re-opening, understanding the potential role children play in the coronavirus infectious disease 2019 (COVID-19) pandemic and the factors that drive severe illness in children is critical.
Study design: Children ages 0-22 years with suspected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection presenting to urgent care clinics or being hospitalized for confirmed/suspected SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) at Massachusetts General Hospital (MGH) were offered enrollment in the MGH Pediatric COVID-19 Biorepository. Enrolled children provided nasopharyngeal, oropharyngeal, and/or blood specimens. SARS-CoV-2 viral load, ACE2 RNA levels, and serology for SARS- CoV-2 were quantified.
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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