Severe COVID-19 may trigger the reactivation of dormant viruses already present in the body, according to a new study involving researchers from Boston Children's Hospital and over 20 other biomedical institutions in the U.S. and Canada. The study analyzed more than 200,000 biological samples from 1,154 hospitalized COVID-19 patients over one year.
Researchers identified 11 different dormant viruses that reactivated within 40 days of hospital admission for SARS-CoV-2, the virus that causes COVID-19. Among these were several herpes viruses, including Epstein-Barr virus, cytomegalovirus, and herpes simplex virus-1, as well as Anelloviridae, a family of viruses for which no human disease has been proven.
These viruses commonly exist in a dormant state in healthy individuals and can reactivate during periods of illness or stress. The study found that reactivation of Anelloviridae, a virus carried by most adults, was associated with long-term physical disability and long COVID, a condition characterized by persistent symptoms at least four weeks after initial infection.
The research also indicated that Epstein-Barr virus and cytomegalovirus appeared to reactivate in response to inflammation rather than immune suppression, suggesting a potentially new mechanism of viral reactivation during severe illness.
Dr. Ofer Levy, a co-author of the study and director of the Precision Vaccines Program at Boston Children's Hospital, expressed surprise at the findings, noting that the extent to which viral reactivation might associate with COVID-19 severity and outcome was not previously understood in such detail. The findings could offer insights for understanding long COVID and aid in developing future diagnostic tests and treatments.
However, the study's authors caution that because it focused solely on hospitalized patients with severe COVID-19, the results may not be applicable to individuals with mild or moderate infections. The study demonstrated an association between viral reactivation and severe COVID-19 but did not establish a causal link between the reactivated viruses and the development of long COVID or long-term disability.
Dr. William Schaffner, a professor of preventive medicine at Vanderbilt University Medical Center who was involved in the study, stated that more research is needed to determine the significance of these findings, emphasizing that the study does not attribute any disease, including long COVID, to the reactivated viruses. He suggested that the observed reactivation might be coincidental. Levy also highlighted the need for further investigation into anelloviruses, which have typically been considered harmless, to understand if they might contribute to disease.
Levy further noted that even though the pandemic has subsided, SARS-CoV-2 continues to cause infections with both acute and long-term consequences. He estimated that in recent years, COVID-19 has caused tens of thousands of deaths annually and affected millions with long COVID, underscoring the continued importance of immunization for vulnerable populations to prevent severe outcomes and the ongoing need for research into better prevention methods.