COVID-19 may have done more harm to your body than just a stubborn fever and long-standing fatigue. Scientists are increasingly investigating whether a SARS-CoV-2 infection can disturb viruses that have been quietly dormant inside the body for years, and, in some cases, decades.

A large multi-omic study involving 1,154 hospitalised COVID-19 patients found evidence of reactivation across several families of viruses during the acute phase of infection. The researchers detected significant reactivation involving Herpesviridae, Enteroviridae and Anelloviridae, with viral activity particularly evident during the first 40 days after hospitalisation. Importantly, the study also found that viral reactivation was associated with COVID-19 severity and certain clinical outcomes.

Some viruses do not completely disappear after the first infection. Instead, they can enter a latent state, essentially remaining under control of the immune system. Epstein-Barr virus (EBV), for example, infects the vast majority of adults and can remain dormant in the body. Under certain circumstances, including significant immune stress, it can begin replicating again.

An earlier study examining EBV found that 27.1% of EBV reactivations detected among COVID-positive samples came from the COVID-positive group, compared with 12.5% among the COVID-negative group. The researchers concluded that COVID-19 patients experienced increased EBV reactivation compared with COVID-negative patients.

More recent research has added another layer to the story. A 2025 study involving people with persistent symptoms after COVID-19 found EBV reactivation in 40 of 140 patients (28.6%), compared with 9 of 80 controls (11.3%). The authors concluded that EBV reactivation ‘plays a role’ in Long COVID, although this was an observational study and cannot by itself establish that EBV reactivation causes Long COVID.

Other research has found similar signals. A 2025 Cell Reports study reported that recent EBV reactivation was more common in people with Long COVID and linked higher latent EBV levels with long-term lung impairment.

But there is an important catch: this does not mean everyone who has had COVID will experience viral reactivation.

The evidence is also not completely consistent. A separate study of people who had asymptomatic or mild COVID-19 found no detectable EBV DNA in participants with post-COVID symptoms and concluded that their symptoms could not be attributed to EBV reactivation. Researchers are therefore looking at several possible explanations. COVID-19 can cause substantial inflammation and changes in immune function, potentially making it harder for the body to keep latent viruses suppressed. The newest research is also examining whether persistent viral or inflammatory signals could contribute to some Long COVID symptoms.

For now, the message is not to panic. ‘Dormant virus reactivation’ does not automatically mean a dangerous new infection or serious disease. It is a biological phenomenon that can occur when the immune system is under stress, and scientists are still working out when it matters clinically.

What is becoming clearer is that COVID-19 is not simply a respiratory infection for everyone. In some people, its effects may involve a much more complicated interaction between SARS-CoV-2, the immune system and viruses that were already present in the body, a relationship researchers are only beginning to understand.