Epstein-Barr: A new antibody could block a virus that 95% of us carry
Epstein-Barr virus stays hidden in our immune systems, only to reactivate decades later. New research could point to a solution.
- 11 May 2026
- 4 min read
- by Priya Joi
At a glance
- Epstein-Barr virus (EBV) infects around 95% of adults globally and is associated with about 358,000 new cancer cases each year. So far, there is no treatment or vaccine.
- A team has produced antibodies against EBV that prevented infection in 100% of 13 mice models of the human immune system across three separate experiments.
- This finding could be especially important in stopping EBV reactivation in people with compromised immune systems.
There’s a 95% chance that you’ve got Epstein-Barr virus.
But for most of us, the virus lies dormant for life and we never know we have it.
Some of us may have a bout of glandular fever. But for some, the virus reactivates and has been linked to serious disease including multiple sclerosis, lupus and rheumatoid arthritis, as well as a range of cancers.
The most recent global estimates suggest EBV is associated with around 358,000 new cases of cancer and 209,000 deaths every year, but there are still no specific vaccines or treatments licensed against it.
Now, a team at the Fred Hutchinson Cancer Center and the University of Washington in Seattle has developed a fully human antibody that, in mice with humanised immune systems, blocked EBV infection in every animal that received it.
Their work was published in Cell Reports Medicine in February 2026.
This finding could be especially important in stopping EBV reactivation in people with compromised immune systems.
Blocking EBV from taking hold
The virus’s reach is what has made it so hard to treat.
EBV does not infect a niche population of cells. It binds to nearly every B cell, the white blood cell that drives a large part of the immune response, which has historically made it almost impossible to find the rare human immune cells producing useful antibodies against it that wouldn’t also attack our own immune system.
The Seattle team got around the problem by going sideways. Rather than trying to fish the right antibodies out of human samples, they used genetically modified mice that produce human antibodies.
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The mice were exposed to two key proteins on the surface of EBV: gp350 and gp42, both of which allow the virus to hook onto our B cells. The researchers collected ten new antibodies that resulted from that infection.
The team ran three separate experiments in which the mice received a single dose of one of the candidate antibodies. They were then infected with EBV a day later and were monitored for around three months while they looked for detectable levels of the virus.
One of the gp42 antibodies performed extremely well. Across all three experiments combined, EBV was undetectable in every one of the 13 mice that received it. In the control group, meanwhile, 10 of 12 mice had detectable virus.
The lead gp350 antibody did less well. It prevented enlarged spleens in every mouse that received it, but did not always stop the virus from reaching the spleen.
The authors say this might be because EBV could still infect B cells without gp350 protein and this antibody also disappeared from the bloodstream faster, so the mice may simply have run out of antibody before the experiment ended.
The patients who could benefit first
Around 128,000 people in the US alone undergo a solid organ or bone marrow transplant every year. To stop their bodies rejecting the new tissue, they take drugs that suppress the immune system.
That leaves them vulnerable to infections, and EBV is one of the most dangerous. In some recipients, latent virus inside donor cells reactivates and goes unchecked, driving an aggressive cancer called post-transplant lymphoproliferative disorder, or PTLD.
Children awaiting transplants are especially exposed because many have not yet been infected with EBV at all, leaving them with no prior immunity if the donor passes the virus along.
Rachel Bender Ignacio, an infectious disease physician at Fred Hutch and the University of Washington, who wasn’t an author, said that preventing EBV from replicating in transplant patients has strong potential to reduce the incidence of PTLD and limit the need to lower immunosuppression, helping preserve the function of the transplanted organ. Effective prevention of EBV in this group, she said, remains a significant unmet need in transplant medicine.
The team is working with an industry partner to advance the antibodies toward a potential therapy. The next stage is human safety testing in healthy adult volunteers, and if that goes well, clinical trials in transplant patients.
“After many years of searching for a viable way to protect against Epstein-Barr virus, this is a significant stride for the scientific community and the people at the highest risk of complications from this virus,” said co-author Andrew McGuire, Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center.
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