COVID Reactivates Dormant Viruses Behind Long COVID
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- Boston Children's Hospital researchers published a Nature study showing COVID-19 can reactivate dormant viruses in hospitalized patients, tracking 1,154 patients across 20 U.S. biomedical research hospitals and 15 collaborating institutions
- Within the first 40 days of hospital admission, the team identified 11 reactivated viruses, with Epstein-Barr, herpes simplex 1, cytomegalovirus, and Anelloviridae the most frequently detected
- Anelloviridae reactivation — a poorly understood viral family latent in roughly 90% of the population — showed a prominent association with long-term physical disability and long COVID, according to site principal investigator Ofer Levy, MD, PhD
- Blood sample analysis revealed that Epstein-Barr and cytomegalovirus appeared to reactivate in response to systemic inflammation rather than immunosuppression, challenging the prevailing theory that chronic viral reactivation stems mainly from a weakened immune system
- The study generated more than 1 billion data points from over 200,000 samples collected over a year, funded by the NIH, with Joann Diray Arce, PhD, leading the Clinical and Data Coordinating Center
- Levy noted up to 50,000 Americans died of COVID in the 2025–2026 respiratory season and that some estimates put U.S. long COVID sufferers at over 10 million adults, calling for better diagnostics and treatments
- Researchers next plan to study how the immune system responds to reactivated viruses across the course of COVID-19 to identify effective treatments and optimal timing for interventions
Why it matters: The Anelloviridae-long COVID link gives researchers a concrete molecular target to chase in an estimated 10 million U.S. adults with long COVID, while the inflammation-not-immunosuppression finding overturns the leading mechanism theory and may reshape how clinicians monitor viral reactivation in severe illness.
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