COVID-19 may be capable of waking up dormant viruses that hide in the human body, according to a new study from the University of Texas. The research indicates that infection with SARS-CoV-2 could reactivate latent viruses such as Epstein-Barr virus and certain herpesviruses, and this can occur even in people who were otherwise healthy before their COVID-19 illness.
The findings, published in the journal Microbiology Spectrum, suggest that the reactivation of these hidden viruses might contribute to some of the lingering symptoms and complications seen after COVID-19, sometimes referred to as long COVID. The study team analyzed blood samples from a group of patients who had recovered from mild or moderate COVID-19 and compared them with samples from uninfected controls. They looked for markers of reactivation of several viruses known to establish lifelong latency in the body after an initial infection.
Results showed that a significant proportion of the COVID-19 patients had evidence of reactivation of Epstein-Barr virus, which is best known as the cause of infectious mononucleosis, and also of human herpesvirus 6, a virus that infects most people in childhood and then remains dormant. The reactivation was detected even in patients who had not been hospitalized and who had no known immune deficiencies, indicating that the effect is not limited to severe cases.
The researchers caution that their study does not prove that COVID-19 directly causes the reactivation, but the association is strong and biologically plausible. SARS-CoV-2 is known to cause immune dysregulation and inflammation, and such disturbances are thought to create conditions that allow latent viruses to become active again. The team notes that reactivation of these viruses has been observed in other stressful conditions, including critical illness and immunosuppression, but the new data suggest that even a routine COVID-19 infection might trigger the same process.
If confirmed, the reactivation could help explain why some people experience persistent fatigue, cognitive difficulties, and other symptoms after COVID-19. Epstein-Barr virus reactivation, for instance, has been linked to chronic fatigue syndrome, and human herpesvirus 6 has been associated with neurological symptoms. The authors suggest that testing for reactivation of these viruses in patients with long COVID might open new avenues for treatment, possibly using antiviral drugs that target the reactivated viruses.
The study is observational and based on a relatively small sample, so larger and longer-term studies are needed to confirm the findings and to determine whether reactivation actually causes the symptoms or is merely a marker of immune disturbance. The researchers also note that they did not measure viral load directly but relied on antibody responses that indicate reactivation, which is a standard but indirect method.
Despite these limitations, the study adds to a growing body of evidence that COVID-19 can have effects on the body that go beyond the acute respiratory illness. Understanding these effects is important for developing strategies to prevent and treat long-term complications. The University of Texas team plans to continue following the patients to see whether reactivation persists and whether it correlates with the development of long COVID symptoms.
The findings also raise broader questions about the long-term consequences of viral infections in general. Many viruses, including herpesviruses, are never fully cleared from the body and can remain dormant for decades. If a common infection like COVID-19 can disrupt that dormancy, it could have implications for public health far beyond the immediate pandemic.
