A new study challenges long-held theories of why a common virus can reactivate and become a life-threatening infection in people with a compromised immune system, including blood cancer patients undergoing bone marrow transplantation.
The research looks at cytomegalovirus (CMV) and used a newly developed mouse model. It is hoped to pave the way for cheaper, safer therapies to protect patients from CMV.
Previous research on CMV reactivation has focused on T cells – the celebrated disease fighters of the immune system.
There had been occasional hints that the 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.
But the new research revealed 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.
Dr Geoffrey Hill, paper co-author, said: “This is a big deal for the bone marrow transplantation field.
“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.”
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