New Antibody Breakthrough Helps Stop Common EBV Infections

EBV Antibody

Researchers at the Fred Hutch Cancer Center have built a new tool to fight Epstein‑Barr virus (EBV). This virus touches almost everyone on Earth and can cause cancers, brain problems, and other long‑term illnesses.

By using special mice that make human antibodies, the team produced several monoclonal antibodies. These tiny proteins stop the virus from grabbing onto and entering our immune cells. In tests, one of the antibodies blocked the virus completely in mice that carry a human‑like immune system.

How the Antibodies Work

EBV sticks to our B‑cells with a protein called gp350 and then fuses with the cell using another protein called gp42. The scientists searched for antibodies that could grab these two proteins without causing the body to attack the therapy itself.

They found two antibodies that target gp350 and eight that target gp42. One gp42‑targeting antibody stopped infection 100 %, while a gp350 antibody gave partial protection.

Why This Matters for Transplant Patients

Every year more than 128,000 people in the U.S. receive organ or bone‑marrow transplants. To keep the new organ from being rejected, patients take drugs that lower their immune defenses. This makes it easier for EBV to reactivate and cause a serious lymphoma called post‑transplant lymphoproliferative disorder (PTLD).

Stopping EBV from spreading could lower the chance of PTLD, help keep the transplanted organ working, and reduce the need to lower immunosuppressive medicines.

Looking Ahead

The research team hopes to turn these antibodies into an infusion that can be given before or after a transplant. By blocking the virus early, the treatment could keep high‑risk patients safe.

Fred Hutch has filed patents on the antibodies and is now working with partners to test safety in healthy volunteers, followed by trials in transplant recipients.

“After many years of searching for a way to protect people from EBV, this discovery is a big step forward,” said lead scientist Andrew McGuire.