Severe COVID may reactivate dormant viruses, study finds
KEY DEVELOPMENTS:
- A study of 1,154 hospitalized COVID-19 patients found evidence of reactivation of several chronic viruses during severe SARS-CoV-2 infection.
- Persistent Anelloviridae activity during recovery was associated with physical deficits among some people experiencing long COVID.
- Researchers stressed that the findings establish associations, not causation, and that further studies are needed before the findings can guide clinical testing or treatment.
LONDON (News Medical Life Sciences) — August 08, 2026: Severe COVID-19 may trigger the reactivation of viruses that normally remain under control in the body, according to a study published in Nature that examined more than 1,100 hospitalized patients.
The research found evidence of reactivation involving viruses from the Herpesviridae and Anelloviridae families during acute COVID-19. Viral activity was also detected during the recovery period, with persistent Anelloviridae activity showing an association with physical deficits among some patients with long COVID.
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The study analyzed data from 1,154 hospitalized COVID-19 patients enrolled in the Immunophenotyping Assessment in a COVID-19 Cohort (IMPACC) study. Participants were followed through multiple biological samples during hospitalization and for up to 12 months afterward.
Viral Reactivation linked to Disease Severity
Researchers detected SARS-CoV-2 alongside other viral transcripts, including Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex viruses and Anelloviridae.
The patterns varied depending on the virus and the type of sample analyzed. EBV, CMV and HSV-1, among others, were detected during the early stages of hospitalization, while some viral activity continued at lower levels during recovery.
The researchers reported that viral reactivation was associated with the severity of COVID-19 and several adverse clinical outcomes.
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Patients with more severe disease were more likely to show evidence of certain viral reactivations. In some severely ill patients, detection of CMV, EBV or HSV-1 was also associated with a higher likelihood of death within one year.
However, the researchers emphasized that these associations do not establish that viral reactivation directly caused the complications.
Findings Challenge earlier Assumptions
The study also challenges the assumption that reactivation of chronic viruses occurs primarily in people with weakened immune systems.
The researchers found evidence of viral reactivation in patients who were not overtly immunosuppressed, suggesting that severe illness and the immune response associated with SARS-CoV-2 infection may influence the activity of viruses already present in the body.
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Recent reporting on the research similarly highlighted that the findings involved patients who had not received COVID-19 vaccination when they entered the study and were largely exposed to earlier SARS-CoV-2 strains. These factors limit how directly the results can be applied to people with later variants, vaccination histories or milder infections.
Possible Link with Long COVID
One of the study’s notable findings involved Anelloviridae during the recovery period.
Researchers found that Anelloviridae transcripts were more frequently detected among participants classified as having physical deficits during convalescence. The association remained after accounting for factors including age, sex, immunosuppressive medication use and the severity of the initial COVID-19 illness.
The finding may provide another avenue for investigating the biological mechanisms behind long COVID, but the researchers did not establish that Anelloviridae reactivation causes persistent symptoms.
The study’s authors said further research is needed to determine whether identifying and treating reactivated viruses could improve outcomes.
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More Research Needed before Clinical Use
The researchers suggested that established laboratory techniques such as quantitative PCR could potentially be used in future monitoring strategies. However, no specific clinical protocols have yet been established on the basis of these findings.
The study also noted several limitations. Participants were hospitalized, unvaccinated at study initiation and primarily exposed to ancestral SARS-CoV-2 strains. The results therefore cannot automatically be generalized to vaccinated populations, people with mild infections or infections caused by newer variants.
The findings add to growing research into the biological mechanisms behind long COVID. Earlier studies have also reported associations between chronic viral reactivation and COVID-19 severity, but researchers continue to investigate whether such reactivation is a driver of disease or a consequence of the body’s response to severe illness.
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The authors concluded that future research should examine the causal relationship between chronic virus reactivation and clinical outcomes, while also studying whether viral activity differs in vaccinated people and those experiencing milder SARS-CoV-2 infections.
The research was published in Nature under the title “Virus reactivation in acute and long COVID-19.”
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