4 min readAug 6, 2026 03:00 PM IST
A severe COVID-19 infection may do more than attack the body on its own. It can also awaken dormant viruses that have remained inactive for years, potentially worsening illness and increasing the risk of long COVID, according to a study published in Nature.
Researchers, led by The University of Texas at Austin, US, analysed samples from more than 1,000 people who were hospitalised with COVID-19 during the first waves of the pandemic. Nearly half showed evidence that common viruses lying dormant in their bodies had become active again during their illness.
These included viruses from the herpes family, such as Epstein-Barr virus (EBV), which causes infectious mononucleosis or “glandular fever”, and cytomegalovirus (CMV), a common virus that usually causes few or no symptoms in healthy people but can lead to serious illness in newborns and people with weakened immunity. The study also found reactivation of anelloviruses, a group of viruses that are widespread in humans and are generally considered harmless.
Most adults around the world carry one or more of these viruses. After the initial infection, they remain dormant inside the body for life, held in check by a healthy immune system.
Different viruses wake up at different times
The study found that these viruses did not reactivate simultaneously. Epstein-Barr virus and anelloviruses tended to become active early during COVID-19, peaking soon after patients were admitted to hospital. In contrast, cytomegalovirus and herpes simplex virus became active around three weeks later, largely in the lungs and respiratory tract.
Researchers believe the intense stress of a severe coronavirus infection may temporarily overwhelm the immune system, allowing these dormant viruses to re-emerge. Once reactivated, they may further amplify the inflammation already triggered by COVID-19, potentially making the illness more severe.
One of the study’s surprising findings was that viral reactivation occurred even in people with otherwise healthy immune systems. Earlier, many scientists believed this happened mainly in people with weakened immunity, such as those living with HIV or taking immunosuppressive medicines. However, the researchers found that patients receiving immunosuppressive drugs were no more likely to experience viral reactivation than others, suggesting that severe COVID-19 itself may be enough to overwhelm the body’s immune defences.
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Possible link to Long Covid
The researchers followed patients for a year after their initial infection and found that people in whom anelloviruses had reactivated were more likely to develop long COVID — a condition in which symptoms such as fatigue, breathlessness and brain fog persist for months or even years after the initial infection.
The findings also add to growing evidence that dormant viruses may not simply be innocent bystanders. Earlier research has linked Epstein-Barr virus to autoimmune diseases such as multiple sclerosis and lupus, raising the possibility that viral reactivation may contribute to prolonged illness in some people.
However, the authors caution that the study shows only an association. It does not prove that reactivated viruses directly cause long COVID. They could instead be a sign that the immune system has been severely stressed by COVID-19.
What this means for treatment
To determine whether viral reactivation itself was linked to worse outcomes, the researchers compared patients whose dormant viruses had reactivated with those whose viruses had remained inactive. Those with viral reactivation had higher levels of inflammation, greater immune activation and more evidence of cell damage.
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Researchers say existing antiviral medicines that work against herpesviruses could potentially help some patients if viral reactivation is found to contribute to severe disease or long COVID. Clinical trials are already on to evaluate whether antiviral drugs against herpesviruses can improve symptoms in people with long COVID.
The study also highlights the need to better understand dormant viruses that have long been regarded as harmless. Scientists say they may play a much bigger role in shaping the course of infectious diseases than previously recognised.
