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COVID-19 study shows similar nasal SARS-CoV-2 antigen levels in children and adults: JAMANETWORK– Pediatrics. Opening schools will spread the virus even faster.

photo by nastya_gepp courtesy of

This study came out on JAMANETWORK July 30, and it is devastating for the accepted notion that children do not pose a COVID-19 risk to adults. The study shows high levels of SARS-COV-2 antigen in swabs from the noses of small children presenting with symptoms or exposure to the virus. Children under five have more virus, and children 5-17 have the same amount of virus as adults.

It is worth quoting extensively; here is an excerpt from Methods:

This cohort included all individuals aged younger than 1 month to 65 years who tested positive for SARS-CoV-2. Patients with symptoms suggestive of a COVID-19–compatible illness and/or high-risk exposures were tested. We included the first sample tested for patients with multiple samples. Because patients with severe infection have lower CT values [reference 4] we excluded 7 children who required supplemental oxygen support. We also excluded 7 asymptomatic patients, 29 patients with unknown duration of symptoms, and 19 patients whose symptoms started more than 1 week prior to testing.

Here is an excerpt from the results section:

Our final cohort included 145 patients with mild to moderate illness within 1 week of symptom onset. We compared 3 groups: young children younger than 5 years (n = 46), older children aged 5 to 17 years (n = 51), and adults aged 18 to 65 years (n = 48). We found similar median (interquartile range) CT values for older children (11.1 [6.3-15.7]) and adults (11.0 [6.9-17.5]). However, young children had significantly lower median (interquartile range) CT values (6.5 [4.8-12.0]), indicating that young children have equivalent or more viral nucleic acid in their upper respiratory tract compared with older children and adults (Figure). The observed differences in median CT values between young children and adults approximate a 10-fold to 100-fold greater amount of SARS-CoV-2 in the upper respiratory tract of young children.

In other words, in 46 children under 5 compared to 48 adults (18-65 y/o), samples taken from the nasopharynx (back of the nose) showed higher median virus levels and children aged 5-17 had similar virus levels (CT means amplification cycle thresholds, the inverse of virus numbers; lower CT means more virus, or: “lower values indicating higher amounts of viral nucleic acid.”)

In fact, “younger children had significantly lower median CT values” and this means “approximate[ly] a 10-fold to 100-fold greater amount of SARS-CoV-2 in the upper respiratory tract of young children.”

So younger children had roughly 10-100 times as much virus as adults in their noses, on average. The report concludes:

Thus, young children can potentially be important drivers of SARS-CoV-2 spread in the general population, as has been demonstrated with respiratory syncytial virus, where children with high viral loads are more likely to transmit.6 Behavioral habits of young children and close quarters in school and day care settings raise concern for SARS-CoV-2 amplification in this population as public health restrictions are eased. In addition to public health implications, this population will be important for targeting immunization efforts as SARS-CoV-2 vaccines become available.

This result contrasts with previous studies that supposedly showed less transmission to and from children. This report was actually “accepted for publication on May 31”– a two month delay in some very important news. There is a contradiction here that needs to be examined closer.

Previous research on children:

Let us look at the studies that supposedly showed less transmission in children.

This review, titled “Children are unlikely to be the main drivers of the COVID‐19 pandemic – A systematic review” from Acta Pediatrica dated May 19, asserts that “Data on viral loads were scarce, but indicated that children may have lower levels than adults, partly because they often have fewer symptoms, and this should decrease the transmission risk.”

Whatever else it says, this review is already obsolete– and the data it is missing (viral loads) was “accepted for publication” nine days before this one was published.

Another review, titled “Role of children in the transmission of the COVID-19 pandemic: a rapid scoping review” from BMJ (British Medical Journal) Open, says it was “received May 1” but also says it included studies “from 1 December 2019 until 28 May 2020. ” It states that, of 14 (1099 were considered) studies finally included, these statistics were found:

Although no complete data were available, between 15% and 55%–60% were asymptomatic, and 75%–100% of cases were from family transmission. Studies analysing school transmission showed children as not a driver of transmission.

Children are not transmitters to a greater extent than adults. There is a need to improve the validity of epidemiological surveillance to solve current uncertainties, and to take into account social determinants and child health inequalities during and after the current pandemic. … There is also insufficient information on the child population as a source of transmission of the infection. Despite this, in the majority of countries, one of the first measures adopted has been the closure of schools…

One reason schools were closed is that influenza is known to be widely spread through schools to adults. While the novel coronavirus is not thought to be as contagious as influenza, it seemed a wise precaution at the time. Now the pressure to reopen schools seems to be ignoring that wisdom.

Since schools have been closed, there is little surprise in studies finding that most infected children got the virus from adults in their households.

Next, we have a report titled “COVID-19 in children: the link in the transmission chain” and published online March 25 in Lancet Infectious Diseases. (This is actually an analysis of a study written up by Chinese doctors; the original is available here.) It includes 36 children (1-16 y/o), about half of whom had pneumonia on CT scan but all of whom had clinically mild disease. It concludes thusly:

The most important finding to come from the present analysis is the clear evidence that children are susceptible to SARS-CoV-2 infection, but frequently do not have notable disease, raising the possibility that children could be facilitators of viral transmission. If children are important in viral transmission and amplification, social and public health policies (eg, avoiding interaction with elderly people) could be established to slow transmission and protect vulnerable populations. There is an urgent need to for further investigation of the role children have in the chain of transmission.

This would suggest caution in light of the possibility that children could transmit infection without appearing to be sick.

Then there is this Medscape article from July 10, titled “Children Rarely Transmit SARS-COV-2 Within Households”… It quotes a Swiss study that collected all patients identified by Geneva University Hospital surveillance between March 10 and April 10. Of 4310 patients with COVID-19, only 40 were under 16. The mild illnesses of these children is shown in this quote from the Results:

 29 (74%) patients were previously healthy; the most frequently reported comorbidities were asthma (10%), diabetes (8%), obesity (5%), premature birth (5%), and hypertension (3%). Seven patients (18%) were hospitalized to the ward, for a median duration of 3 days (IQR: 2–4); reasons for admission were surveillance for nonhypoxemic viral pneumonia (n = 2), fever without source (n = 2), apparent life-threatening event (n = 1), and sepsis-like event (n = 1); 1 paucisymptomatic child admitted because both parents had severe COVID-19 (n = 1). No patient required ICU admission or SARS-CoV-2–specific therapies. The others 32 patients were managed as outpatients. All patients had a complete resolution of symptoms by day 7 after diagnosis.

The familial clustering of cases was apparent from this data, headed Familial Clusters:

Familial cluster evaluation revealed a t number of 4 household members per family (IQR: 3–4). Among the 111 HHCs of study children, mothers predominated (n = 39), followed by fathers (n = 32), pediatric siblings (n = 23), adult siblings (n = 8), and grandparents (n = 7) (Fig 1). Adult HHCs were suspected or confirmed with COVID-19 before the study child in 79% (31/39) of cases. In only 8% (3/39) of households did the study child develop symptoms before any other HHC (Fig 1). Interestingly, 85% (75/88) of adult HHCs developed symptoms at some point, compared with 43% (10/23) of pediatric HHCs (P < .001). Also, 92% (36/39) of mothers developed symptoms, compared with 75% (24/32) of fathers (P = .04).

Note that it appears that 79% of child cases appeared to be preceded by, probably brought on by, adult cases. From the Discussion section:

In 79% of households, ≥1 adult family member was suspected or confirmed for COVID-19 before symptom onset in the study child, confirming that children are infected mainly inside familial clusters.6 Surprisingly, in 33% of households, symptomatic HHCs tested negative despite belonging to a familial cluster with confirmed SARS-CoV-2 cases, suggesting an underreporting of cases. In only 8% of households did a child develop symptoms before any other HHC, which is in line with previous data in which it is shown that children are index cases in <10% of SARS-CoV-2 familial clusters10; however, with our study design, we cannot confirm that child-to-adult transmission occurred.

This study does NOT show that children don’t transmit infections to adults. It shows that most children detected with infection caught it from adult family members. As the authors noted at the end:

This study has some limitations. The study sample likely does not represent the total number of pediatric SARS-CoV-2 cases during this time period. Indeed, patients with milder or atypical presentation might not have sought medical attention. Moreover, the recall of symptom onset among HHCs might be inaccurate, although this seems for once less likely because of the confinement measures and anxiety in the community.

An editorial in the same issue of Pediatrics quotes a Chinese study, which is well worth quoting again. From its Results section:

RESULTS: A total of 74 pediatric patients with COVID-19 were included in this study. Of the 68 case patients whose epidemiological data were complete, 65 (65 of 68; 95.59%) were household contacts of adults. Cough (32.43%) and fever (27.03%) were the predominant symptoms of 44 (59.46%) symptomatic patients at onset of the illness. Abnormalities in leukocyte count were found in 23 (31.08%) children, and 10 (13.51%) children presented with abnormal lymphocyte count. Of the 34 (45.95%) patients who had nucleic acid testing results for common respiratory pathogens, 19 (51.35%) showed coinfection with other pathogens other than SARS-CoV-2. Ten (13.51%) children had real-time reverse transcription polymerase chain reaction analysis for fecal specimens, and 8 of them showed prolonged existence of SARS-CoV-2 RNA.

Again, most (over 95%) of the 74 patients in this study got their virus from adults in their households.

Another fascinating finding was that 34 children were checked for other pathogens and about half of them showed “coinfection”– meaning that they also had another virus besides SARS-COV-2 in their systems. We’ll see coinfection again in a ski chalet, below.

Also, 13% of the children had the new virus in their stools and most of them had “prolonged” presence of virus in the stool. Fecal-oral transmission of SARS-COV-2 has not been studied and is unlikely in sanitary countries; this route is more likely to be important in places like India and Mexico where sanitary precautions are not universal.

The Medscape article mentions a letter about contact tracing. A French chalet where an English case infected 75% (12 of 15) of his chalet-mates includes a single pediatric case (who had a triple infection):

One pediatric case, with picornavirus and influenza A coinfection, visited 3 different schools while symptomatic. …

All [chalet] cases were negative for other viruses except for the pediatric case, who had a SARS-CoV-2 + picornavirus (rhinovirus or enterovirus) + influenza A(H1N1)pdm09 coinfection. His 2 siblings were negative for SARS-CoV-2, but had an influenza A(H1N1)pdm09 infection and an influenza A(H1N1)pdm09 + picornavirus coinfection, respectively. …  At school C, 30% (3/10) of contacts of the pediatric case had a picornavirus infection. … In addition, “classical” human coronaviruses such as HUK1 and NL63 were detected in 16% of contacts without any cross-reactivity with SARS-CoV-2 molecular diagnostics. …  the infected child, despite interactions with a large number of contacts in different schools, did not transmit the disease, as evidenced by the large number of negative results of his tested contacts. …  It is also possible that the very low viral load of the pediatric case and the subsequent lack of transmission might be related to his coinfection and the co-circulation of respiratory viruses. Viral load was only tested 8 days after his onset of symptoms. The child continued his normal activities and interactions as his symptoms were mild.

We could go on, but I’m out of time.

Cutting off debate due to time

That’s enough. There is a lack of information on the important question: will opening schools for in-person attendance during an uncontrolled outbreak of a novel disease cause more people to get sick?

There is a reason to think that the answer is yes: what we already know about influenza. When schools are closed, influenza morbidity and mortality goes down.

There is no data on the novel coronavirus that would contradict this observation. There is only unfounded optimism, based on the unusual behavior of this pathogen, which seems to cause less serious clinical manifestations in younger patients.

The new study mentioned at the head of this post shows that, despite mild or inapparent disease, children have equal or greater amounts of virus to spread when they are infected. This turns unfounded optimism into blind “polyanna-ism.”

I suggest keeping schools closed except for children with no internet access and to pick up the meals usually handed out to poor children. Teachers and staff can be first in line, with bus drivers and other essential personnel like health care workers, when a vaccine becomes available in January (I just picked that date because I’m a semi-founded optimist.) Then we can re-open schools in February, after the vaccine has time to take effect.

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