COVID-19 may do more than cause an acute respiratory infection. A new study has found that SARS-CoV-2 infection can trigger the reactivation of several viruses that normally remain dormant in the body, including Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex viruses and anelloviruses. The findings could provide new clues about why some people develop prolonged symptoms after COVID-19.
Published in Nature, the study analysed longitudinal data from 1,154 people who had been hospitalised with COVID-19. Researchers used blood, nasal swabs and respiratory samples along with viral, immune, metabolic and protein analyses to track changes during acute infection and for up to 12 months after hospitalisation.
The researchers found evidence of chronic viral reactivation in almost half of the participants during acute COVID-19. Overall, 47.9% of participants had evidence of at least one virus becoming active during the acute phase of the illness. Most people with reactivation had only one virus detected rather than several viruses becoming active simultaneously.
Why do dormant viruses reactivate?
Many people carry viruses that remain inside the body after the initial infection. Epstein-Barr virus and other members of the herpesvirus family can persist for years, generally being kept under control by the immune system. Anelloviruses are also widespread and are usually considered harmless.
The new findings suggest that the physiological stress caused by COVID-19 may disrupt this balance. Different viruses appeared to reactivate at different stages of the illness. EBV and anelloviruses tended to become active early, while CMV and herpes simplex viruses were more commonly detected later, particularly in respiratory samples.
Importantly, the researchers found that viral reactivation was not restricted to people with severely weakened immune systems. Reactivation also occurred in people who were not receiving immunosuppressive medication. This suggests that the intense immune and inflammatory response associated with COVID-19 itself may contribute to the process. However, the study does not prove that SARS-CoV-2 directly causes these viruses to reactivate or that reactivation itself causes long COVID.
Could this explain long COVID?
The study raises an important possibility. Researchers found that persistent reactivation of anelloviruses during recovery was associated with post-acute COVID-19 symptoms, including problems with physical function and fatigue. The findings add to previous research linking EBV reactivation with symptoms such as fatigue and cognitive difficulties in some people with long COVID.
However, long COVID is a complex condition and viral reactivation is unlikely to be the only explanation. Researchers say further studies are needed to determine whether reactivated viruses actively contribute to prolonged symptoms or are simply a consequence of the immune disruption caused by COVID-19.
The findings could eventually help scientists identify people at higher risk of prolonged illness and explore whether targeting specific viral reactivations could become part of future treatments. For now, the study offers another piece of the puzzle surrounding the long-term effects of COVID-19 and highlights the complex relationship between SARS-CoV-2, the immune system and viruses that have been quietly living inside the body.
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