A recent study¹ has unveiled an association between SARS-CoV-2 infections and the development of autoantibodies in children, even among those who experienced mild or asymptomatic cases. This study challenges the prevailing narrative that COVID-19 poses minimal risk to younger populations and underscores the need for renewed public health vigilance.

Over half of the children who contracted COVID-19 were found to have developed autoantibodies, immune proteins that mistakenly target the body's own tissues. In contrast, only 14% of uninfected children exhibited such antibodies. The autoantibodies identified are linked to a range of autoimmune conditions, including type 1 diabetes, thyroid disorders, and connective tissue diseases. Notably, the presence of autoantibodies was observed regardless of the severity of the initial infection, indicating that even mild cases can trigger immune dysregulation. We’ve previously written about commonly held but misguided views on immunity and the role of infection in triggering autoimmunity² and this study provides yet more evidence of the risks involved.

The presence of autoantibodies in childhood is very unlikely to be a benign finding and as the authors suggest, more research is urgently needed. Decades of immunological research have shown that these immune markers often precede clinical autoimmune disease by years or even decades. Children who produce antibodies against thyroperoxidase, insulin-producing cells, or nuclear proteins are statistically more likely to go on to develop disorders such as type 1 diabetes, Hashimoto’s thyroiditis, systemic lupus erythematosus, and other chronic inflammatory conditions.

Despite growing evidence that no SARS-CoV-2 infection is benign³, children are being repeatedly exposed to the virus with little to no mitigation in schools or public settings. Each reinfection is another chance for further dysregulation, antibody imprinting, or escalation of autoreactivity. While public discourse has largely moved on, mounting evidence suggests we should be taking action to reduce transmission. Preventive measures such as improved ventilation, air filtration, masking, and rapid testing and isolation should be used to protect children from the long-term effects this virus is leaving in its wake³.

We’ve previously written about how government response to SARS-CoV-2 echoes the decades-long failure seen with tobacco⁴. Early warnings were dismissed, tax revenue and industry interests were prioritised, and the slow accumulation of harm was downplayed until it became undeniable. Just as officials once insisted there was no conclusive evidence linking smoking to cancer, despite conclusive evidence being published and reviewed by governments in the 1950s, today we see a similar denialism around the long-term impacts of COVID-19. We have been encouraged to believe COVID-19 is just a cold. Just as with smoking, harm is framed as individual rather than systemic, shifting responsibility away from policymakers and towards personal choice. And as with tobacco, it may take a generation of suffering before the truth becomes politically inconvenient enough to acknowledge.

While we wait for governments to recognise the need for action, we recommend people do whatever is reasonably possible to reduce the number of SARS-CoV-2 infections they and their loved ones experience over their lifetime. Click here for advice on how to reduce your risk.