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For These 17 COVID Long Haulers, Reactivated Viruses May Be to Blame

0 2 years ago

We carry our histories in our bodies: the broken bone that never properly healed, the burn from a baking mishap, the crown over a root canal.

But history tends to repeat itself—and for COVID-19 long-haulers, reactivated viruses are part of that story.

New research is shining a light on how latent viral reactivations occur in long-haulers, the nearly 30% of COVID-19 patients who are left with lingering diseases and disabilities following their infections.


A latent viral infection is when a virus remains inactive (dormant) in the body after the initial infection.

It cannot replicate or cause symptoms in this state, but external events—such as co-infection with another pathogen, physiological stress, or immunosuppression—can trigger the virus to switch to an active, replicating state (a lytic infection).

Scientists already knew that interactions between different viruses can trigger the reactivation of dormant viruses, as the cells responsible for keeping them at bay become preoccupied with the new invader.

However, COVID-19’s long-term inflammatory and immunosuppressive qualities are allowing these reactivations to turn into chronic infections, only adding to the host of symptoms long-haulers are forced to endure.

Which Viruses Cause the Infections?

The viruses at play here mainly fall under the Herpesviridae family. Most Americans carry a dormant version of herpesviruses. An estimated 87.4% of U.S. adults aged 14 to 49 years infected with HSV-2 remain asymptomatic with no clinical diagnosis. Likely over 95% of adults carry Epstein-Barr virus (EBV). After our immune system defeats any virus in the herpes virus family, that virus will burrow into our nerves and go into a dormant (latent) state.

Makeda Robinson, MD, PhD, an infectious disease specialist currently studying COVID-19 at Stanford University, told Verywell that what keeps the herpesviruses in that latent state are the body’s T cells.

“If you have fewer T cells, it can be more difficult to control these viruses,” Robinson said. “We know that during COVID-19, our level of T cells is reduced significantly and our ability to fight these Herpesviruses if they become more active may be impaired.”

In other words, when COVID gets into the body it depletes our T cells, which can allow for reactivation of a herpes virus during the acute phase of a COVID infection.

“If you’re infected with another virus, that’s a stress to the body and immune system and that may be enough of a stress to trigger replication of these dormant viruses,” said Robinson, adding that research has shown that with EBV, specifically, “there is active replication in those cells post-COVID.”

Under normal circumstances, our T-cells would show up to fight off EBV. But Robinson said that in the case of COVID, that does not happen because there are not as many of them circulating in the blood.


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