A new study in Science challenges long-held theories of why a common virus — cytomegalovirus, or CMV — can reactivate and become a life-threatening infection in people with a compromised immune system, including blood cancer patients undergoing bone marrow transplantation.
The discovery, to be published in Science’s Jan. 18 issue, used a newly developed mouse model and could pave the way for cheaper, safer therapies to protect patients from CMV.
“This is a big deal for the bone marrow transplantation field,” said Dr. Geoffrey Hill, the paper’s senior co-author and director of Hematopoietic Stem Cell Transplantation at Fred Hutchinson Cancer Research Center. “Our study shows for the first time that antibodies can play a dominant role in controlling CMV reactivation. This is turning dogma on its head.”
Previous research on CMV reactivation has focused on T cells, the celebrated disease fighters of the immune system. There had been occasional hints that antibodies produced by immune system B cells played some role against CMV, but it seemed to be a supporting role. Clinical trials using antibodies to fight the virus were disappointing, Hill said.
But Hill and his research team found that strain-specific antibodies made from B cells are responsible for keeping CMV suppressed in mice, without the need for any other immune cells.
A future therapy could work by collecting the CMV-thwarting antibodies from patients who have been exposed to the virus and who are undergoing bone marrow transplant. The antibodies would be purified and multiplied in the lab, then returned to the patient after transplant.
