Never has the prospect of "back to school" seemed so ominous as it does in 2020. As the number of COVID-19 cases climb steadily in nearly every state, the prospect of in-person classes are filling students, parents, and faculty alike with a corresponding sense of dread.
The notion that children are immune or resistant to SARS-CoV-2 is demonstrably untrue.
The decision to resume classes at primary, secondary, and collegiate levels is not one that should be regarded lightly, particularly as coronavirus cases skyrocket across the United States.
What should be a measured, data-driven discussion that weighs risks and benefits has been derailed by political talking points. President Trump has been steadily advocating for an unfettered return to the classroom, often through imperative "OPEN THE SCHOOLS!!!" tweets. In July, Secretary of Education Betsy DeVos threatened to withhold funding from schools that did not reopen for full-time, in-person classes, despite not having the authority to do so. Like so many public health issues, opening schools in the midst of a generational pandemic has been politicized to the point that the question of whether it is safe to do so has been obscured and confounded. However, this question still deserves to be examined based on evidence.
What We Know About Kids and COVID-19
Some arguments for returning to in-person education have focused on the fact that children and young adults are less susceptible to severe disease. In some cases, people have stated that children cannot be infected, pointing to countries that have resumed in-person education with no associated outbreaks. However, those countries had extremely low community transmission and robust testing and surveillance.
The notion that children are immune or resistant to SARS-CoV-2 is demonstrably untrue: children can be infected, they can become sick, and, in rare cases, they can die. Children can also transmit the virus to others, especially if they are in prolonged proximity to them. A Georgia sleepaway camp was the site of at least 260 cases among mostly children and teenagers, some as young as 6 years old. Children have been shown to shed infectious virus in their nasal secretions and have viral loads comparable to adults. Children can unquestionably be infected with SARS-CoV-2 and spread it to others.
The more data emerges, the more it appears that both primary and secondary schools and universities alike are conducive environments for super-spreading. Mitigating these risks depends heavily on individual schools' ability to enforce reduction measures. So far, the evidence demonstrates that in most cases, schools are unable to adequately protect students or staff. A school superintendent from a small district in Arizona recently described an outbreak that occurred among staff prior to in-person classes resuming. Schools that have opened so far have almost immediately reported new clusters of cases among students or staff.
This is because it is impossible to completely eliminate risk even with the most thoughtful mitigation measures when community transmission is high. Risk can be reduced, but the greater the likelihood that someone will be exposed in the community, the greater the risk they might pass the virus to others on campus or in the classroom.
There are still many unknowns about SARS-CoV-2 transmission, but some environments are known risks for virus transmission: enclosed spaces with crowds of people in close proximity over extended durations. Transmission is thought to occur predominantly through inhaled aerosols or droplets containing SARS-CoV-2, which are produced through common school activities such as breathing, speaking, or singing. Masks reduce but do not eliminate the production of these aerosols. Implementing universal mask-wearing and physical distancing guidelines will furthermore be extraordinarily challenging for very young children.
Smaller particle aerosols can remain suspended in the air and accumulate over time. In an enclosed space where people are gathering, such as a classroom, this renders risk mitigation measures such as physical distancing and masks ineffective. Many classrooms at all levels of education are not conducive to improving ventilation through low-cost measures such as opening windows, much less installing costly air filtration systems.
As a risk reduction measure, ventilation greatly depends on factors like window placement, window type, room size, room occupancy, building HVAC systems, and overall airflow. There isn't much hard data on the specific effects of ventilation on virus transmission, and the models that support ventilation rely on assumptions based on scant experimental evidence that doesn't account for virologic parameters.
There is also no data about how effective air filtration or UV systems would be for SARS-CoV-2 transmission risk reduction, so it's hard to say if this would result in a meaningful risk reduction or not. We don't have enough data outside of a hospital setting to support that ventilation and/or filtration would significantly reduce risk, and it's impractical (and most likely impossible in most schools) to implement hospital ventilation systems, which would likely require massive remodeling of existing HVAC infrastructure. In a close contact situation, the risk reduction might be minimal anyway since it's difficult to avoid exposure to respiratory aerosols and droplets a person is exhaling.
You'd need to get very low rates in the local community to open safely in person regardless of other risk reduction measures, and this would need to be complemented by robust testing and contact tracing capacity.
Efforts to resume in-person education depend heavily on school health and safety plans, which often rely on self-reporting of symptoms due to insufficient testing capacity. Self-reporting is notoriously unreliable, and furthermore, SARS-CoV-2 can be readily transmitted by pre-symptomatic individuals who may be unaware that they are sick, making testing an essential component of any such plan. Primary and secondary schools are faced with limited access to testing and no funds to support it. Even in institutions that include a testing component in their reopening plans, this is still too infrequent to support the full student body returning to campus.
Economic Conflicts of Interest
Rebecca Harrison, a PhD candidate at Cornell University serving on the campus reopening committee, is concerned that her institution's plan places too much faith in testing capacity and is over-reliant on untested models. Harrison says that, as a result, students are being implicitly encouraged to return to campus and "very little has been done to actively encourage students who are safe and able to stay home, to actually stay home."
Harrison also is concerned that her institution "presumably hopes to draw students back from the safety of their parents' basements to (re)join the residential campus experience ... and drive revenue." This is a legitimate concern. Some schools may be actively thwarting safety plans in place to protect students based on financial incentives. Student athletes at Colorado State have alleged that football coaches told them not to report COVID-19 symptoms and are manipulating contact tracing reports.
Public primary and secondary schools are not dependent on student athletics for revenue, but nonetheless are susceptible to state and federal policies that tie reopening to budgets. If schools are forced to make decisions based on a balance sheet, rather than the health and safety of students, teachers, and staff, they will implement health and safety plans that are inadequate. Schools will become ground zero for new clusters of cases.
Looking Ahead: When Will Schools Be Able to Open Again?
One crucial measure is the percent positivity rate in the local community, the number of positive tests based on all the tests that are done. Some states, like California, have implemented policies guiding the reopening of schools that depend in part on a local community's percent positivity rate falling under 8 percent, among other benchmarks including the rate of new daily cases. Currently, statewide, test positivity is below 7%, with an average of 3 new daily cases per 1000 people per day. However, the California department of health acknowledges that new cases per day are underreported. There are 6.3 million students in the California public school system, suggesting that at any given time, there could be nearly 20,000 students who might be contagious, without accounting for presymptomatic teachers and staff. In the classroom environment, just one of those positive cases could spread the virus to many people in one day despite masks, distancing, and ventilation.
You'd need to get very low rates in the local community to open safely in person regardless of other risk reduction measures, and this would need to be complemented by robust testing and contact tracing capacity. Only with rapid identification and isolation of new cases, followed by contact tracing and quarantine, can we break chains of transmission and prevent further spread in the school and the larger community.
None of these safety concerns diminish the many harms associated with the sudden and haphazard way remote learning has been implemented. Online education has not been effective in many cases and is difficult to implement equitably. Young children, in particular, are deprived of the essential social and intellectual development they would normally get in a classroom with teachers and their peers. Parents of young children are equally unprepared and unable to provide full-time instruction. Our federal leadership's catastrophic failure to contain the pandemic like other countries has put us in this terrible position, where we must choose between learning or spreading a deadly pathogen.
Blame aside, parents, educators, and administrators must decide whether to resume in-person classes this fall. Those decisions should be based on evidence, not on politics or economics. The data clearly shows that community transmission is out of control throughout most of the country. Thus, we ignore the risk of school outbreaks at our peril.
[Editor's Note: Here's the other essay in the Back to School series: 5 Key Questions to Consider Before Sending Your Child Back to School.]
Elaine Kamil had just returned home after a few days of business meetings in 2013 when she started having chest pains. At first Kamil, then 66, wasn't worried—she had had some chest pain before and recently went to a cardiologist to do a stress test, which was normal.
"I can't be having a heart attack because I just got checked," she thought, attributing the discomfort to stress and high demands of her job. A pediatric nephrologist at Cedars-Sinai Hospital in Los Angeles, she takes care of critically ill children who are on dialysis or are kidney transplant patients. Supporting families through difficult times and answering calls at odd hours is part of her daily routine, and often leaves her exhausted.
She figured the pain would go away. But instead, it intensified that night. Kamil's husband drove her to the Cedars-Sinai hospital, where she was admitted to the coronary care unit. It turned out she wasn't having a heart attack after all. Instead, she was diagnosed with a much less common but nonetheless dangerous heart condition called takotsubo syndrome, or broken heart syndrome.
A heart attack happens when blood flow to the heart is obstructed—such as when an artery is blocked—causing heart muscle tissue to die. In takotsubo syndrome, the blood flow isn't blocked, but the heart doesn't pump it properly. The heart changes its shape and starts to resemble a Japanese fishing device called tako-tsubo, a clay pot with a wider body and narrower mouth, used to catch octopus.
"The heart muscle is stunned and doesn't function properly anywhere from three days to three weeks," explains Noel Bairey Merz, the cardiologist at Cedar Sinai who Kamil went to see after she was discharged.
"The heart muscle is stunned and doesn't function properly anywhere from three days to three weeks."
But even though the heart isn't permanently damaged, mortality rates due to takotsubo syndrome are comparable to those of a heart attack, Merz notes—about 4-5% of patients die from the attack, and 20% within the next five years. "It's as bad as a heart attack," Merz says—only it's much less known, even to doctors. The condition affects only about 1% of people, and there are around 15,000 new cases annually. It's diagnosed using a cardiac ventriculogram, an imaging test that allows doctors to see how the heart pumps blood.
Scientists don't fully understand what causes Takotsubo syndrome, but it usually occurs after extreme emotional or physical stress. Doctors think it's triggered by a so-called catecholamine storm, a phenomenon in which the body releases too much catecholamines—hormones involved in the fight-or-flight response. Evolutionarily, when early humans lived in savannas or forests and had to either fight off predators or flee from them, these hormones gave our ancestors the needed strength and stamina to take either action. Released by nerve endings and by the adrenal glands that sit on top of the kidneys, these hormones still flood our bodies in moments of stress, but an overabundance of them could sometimes be damaging.
A recent study by scientists at Harvard Medical School linked increased risk of takotsubo to higher activity in the amygdala, a brain region responsible for emotions that's involved in responses to stress. The scientists believe that chronic stress makes people more susceptible to the syndrome. Notably, one small study suggested that the number of Takotsubo cases increased during the COVID-19 pandemic.
There are no specific drugs to treat takotsubo, so doctors rely on supportive therapies, which include medications typically used for high blood pressure and heart failure. In most cases, the heart returns to its normal shape within a few weeks. "It's a spontaneous recovery—the catecholamine storm is resolved, the injury trigger is removed and the heart heals itself because our bodies have an amazing healing capacity," Merz says. It also helps that tissues remain intact. 'The heart cells don't die, they just aren't functioning properly for some time."
That's the good news. The bad news is that takotsubo is likely to strike again—in 5-20% of patients the condition comes back, sometimes more severe than before.
That's exactly what happened to Kamil. After getting her diagnosis in 2013, she realized that she actually had a previous takotsubo episode. In 2010, she experienced similar symptoms after her son died. "The night after he died, I was having severe chest pain at night, but I was too overwhelmed with grief to do anything about it," she recalls. After a while, the pain subsided and didn't return until three years later.
For weeks after her second attack, she felt exhausted, listless and anxious. "You lose confidence in your body," she says. "You have these little twinges on your chest, or if you start having arrhythmia, and you wonder if this is another episode coming up. It's really unnerving because you don't know how to read these cues." And that's very typical, Merz says. Even when the heart muscle appears to recover, patients don't return to normal right away. They have shortens of breath, they can't exercise, and they stay anxious and worried for a while.
Women over the age of 50 are diagnosed with takotsubo more often than other demographics. However, it happens in men too, although it typically strikes after physical stress, such as a triathlon or an exhausting day of cycling. Young people can also get takotsubo. Older patients are hospitalized more often, but younger people tend to have more severe complications. It could be because an older person may go for a jog while younger one may run a marathon, which would take a stronger toll on the body of a person who's predisposed to the condition.
Notably, the emotional stressors don't always have to be negative—the heart muscle can get out of shape from good emotions, too. "There have been case reports of takotsubo at weddings," Merz says. Moreover, one out of three or four takotsubo patients experience no apparent stress, she adds. "So it could be that it's not so much the catecholamine storm itself, but the body's reaction to it—the physiological reaction deeply embedded into out physiology," she explains.
Merz and her team are working to understand what makes people predisposed to takotsubo. They think a person's genetics play a role, but they haven't yet pinpointed genes that seem to be responsible. Genes code for proteins, which affect how the body metabolizes various compounds, which, in turn, affect the body's response to stress. Pinning down the protein involved in takotsubo susceptibility would allow doctors to develop screening tests and identify those prone to severe repeating attacks. It will also help develop medications that can either prevent it or treat it better than just waiting for the body to heal itself.
Researchers at the Imperial College London recently found that elevated levels of certain types of microRNAs—molecules involved in protein production—increase the chances of developing takotsubo.
In one study, researchers tried treating takotsubo in mice with a drug called suberanilohydroxamic acid, or SAHA, typically used for cancer treatment. The drug improved cardiac health and reversed the broken heart in rodents. It remains to be seen if the drug would have a similar effect on humans. But identifying a drug that shows promise is progress, Merz says. "I'm glad that there's research in this area."
A highly contagious form of the coronavirus known as the Delta variant is spreading rapidly and becoming increasingly prevalent around the world. First identified in India in December, Delta has now been identified in 111 countries.
In the United States, the variant now accounts for 83% of sequenced COVID-19 cases, said Rochelle Walensky, director of the Centers for Disease Control and Prevention, at a July 20 Senate hearing. In May, Delta was responsible for just 3% of U.S. cases. The World Health Organization projects that Delta will become the dominant variant globally over the coming months.
So, how worried should you be about the Delta variant? We asked experts some common questions about Delta.
What is a variant?
To understand Delta, it's helpful to first understand what a variant is. When a virus infects a person, it gets into your cells and makes a copy of its genome so it can replicate and spread throughout your body.
In the process of making new copies of itself, the virus can make a mistake in its genetic code. Because viruses are replicating all the time, these mistakes — also called mutations — happen pretty often. A new variant emerges when a virus acquires one or more new mutations and starts spreading within a population.
There are thousands of SARS-CoV-2 variants, but most of them don't substantially change the way the virus behaves. The variants that scientists are most interested in are known as variants of concern. These are versions of the virus with mutations that allow the virus to spread more easily, evade vaccines, or cause more severe disease.
"The vast majority of the mutations that have accumulated in SARS-CoV-2 don't change the biology as far as we're concerned," said Jennifer Surtees, a biochemist at the University of Buffalo who's studying the coronavirus. "But there have been a handful of key mutations and combinations of mutations that have led to what we're now calling variants of concern."
One of those variants of concern is Delta, which is now driving many new COVID-19 infections.
Why is the Delta variant so concerning?
"The reason why the Delta variant is concerning is because it's causing an increase in transmission," said Alba Grifoni, an infectious disease researcher at the La Jolla Institute for Immunology. "The virus is spreading faster and people — particularly those who are not vaccinated yet — are more prone to exposure."
The Delta variant has a few key mutations that make it better at attaching to our cells and evading the neutralizing antibodies in our immune system. These mutations have changed the virus enough to make it more than twice as contagious as the original SARS-CoV-2 virus that emerged in Wuhan and about 50% more contagious than the Alpha variant, previously known as B.1.1.7, or the U.K. variant.
These mutations were previously seen in other variants on their own, but it's their combination that makes Delta so much more infectious.
Do vaccines work against the Delta variant?
The good news is, the COVID-19 vaccines made by AstraZeneca, Johnson & Johnson, Moderna, and Pfizer still work against the Delta variant. They remain more than 90% effective at preventing hospitalizations and death due to Delta. While they're slightly less protective against disease symptoms, they're still very effective at preventing severe illness caused by the Delta variant.
"They're not as good as they were against the prior strains, but they're holding up pretty well," said Eric Topol, a physician and director of the Scripps Translational Research Institute, during a July 19 briefing for journalists.
Because Delta is better at evading our immune systems, it's likely causing more breakthrough infections — COVID-19 cases in people who are vaccinated. However, breakthrough infections were expected before the Delta variant became widespread. No vaccine is 100% effective, so breakthrough infections can happen with other vaccines as well. Experts say the COVID-19 vaccines are still working as expected, even if breakthrough infections occur. The majority of these infections are asymptomatic or cause only mild symptoms.
Should vaccinated people worry about the Delta variant?
Vaccines train our immune systems to protect us against infection. They do this by spurring the production of antibodies, which stick around in our bodies to help fight off a particular pathogen in case we ever come into contact with it.
But even if the new Delta variant slips past our neutralizing antibodies, there's another component of our immune system that can help overtake the virus: T cells. Studies are showing that the COVID-19 vaccines also galvanize T cells, which help limit disease severity in people who have been vaccinated.
"While antibodies block the virus and prevent the virus from infecting cells, T cells are able to attack cells that have already been infected," Grifoni said. In other words, T cells can prevent the infection from spreading to more places in the body. A study published July 1 by Grifoni and her colleagues found that T cells were still able to recognize mutated forms of the virus — further evidence that our current vaccines are effective against Delta.
Can fully vaccinated people spread the Delta variant?
Scientists think it's unlikely that fully vaccinated individuals who have an asymptomatic infection are transmitting the Delta variant. That's because vaccinated people are thought to have relatively low levels of the virus in their respiratory tracts and therefore, they don't transmit as much virus.
Still, breakthrough infections can occur. If you have COVID-19 symptoms, even if you're fully vaccinated, you should get tested and isolate from friends and family because you could spread the virus.
What risk does Delta pose to unvaccinated people?
The Delta variant is behind a surge in cases in communities with low vaccination rates, and unvaccinated Americans currently account for 97% of hospitalizations due to COVID-19, according to Walensky. The best thing you can do right now to prevent yourself from getting sick is to get vaccinated.
Gigi Gronvall, an immunologist and senior scholar at the Johns Hopkins Center for Health Security, said in this week's "Making Sense of Science" podcast that it's especially important to get all required doses of the vaccine in order to have the best protection against the Delta variant. "Even if it's been more than the allotted time that you were told to come back and get the second, there's no time like the present," she said.
With more than 3.6 billion COVID-19 doses administered globally, the vaccines have been shown to be incredibly safe. Serious adverse effects are rare, although scientists continue to monitor for them.
Being vaccinated also helps prevent the emergence of new and potentially more dangerous variants. Viruses need to infect people in order to replicate, and variants emerge because the virus continues to infect more people. More infections create more opportunities for the virus to acquire new mutations.
Surtees and others worry about a scenario in which a new variant emerges that's even more transmissible or resistant to vaccines. "This is our window of opportunity to try to get as many people vaccinated as possible and get people protected so that so that the virus doesn't evolve to be even better at infecting people," she said.
Does Delta cause more severe disease?
While hospitalizations and deaths from COVID-19 are increasing again, it's not yet clear whether Delta causes more severe illness than previous strains.
How can we protect unvaccinated children from the Delta variant?
With children 12 and under not yet eligible for the COVID-19 vaccine, kids are especially vulnerable to the Delta variant. One way to protect unvaccinated children is for parents and other close family members to get vaccinated.
It's also a good idea to keep masks handy when going out in public places. Due to risk Delta poses, the American Academy of Pediatrics issued new guidelines July 19 recommending that all staff and students over age 2 wear face masks in school this fall, even if they have been vaccinated.
Parents should also avoid taking their unvaccinated children to crowded, indoor locations and make sure their kids are practicing good hand-washing hygiene. For children younger than 2, limit visits with friends and family members who are unvaccinated or whose vaccination status is unknown and keep up social distancing practices while in public.
While there's no evidence yet that Delta increases disease severity in children, parents should be mindful that in some rare cases, kids can get a severe form of the disease.
"We're seeing more children getting sick and we're seeing some of them get very sick," Surtees said. "Those children can then pass on the virus to other individuals, including people who are immunocompromised or unvaccinated."