ACR: Epstein-Barr Virus May Be New Therapeutic Target in SLE

There are additional differences between SLE patients and healthy controls in terms of response to EBV infection. Patients with SLE have 15- to 40-fold higher EBV loads, 10-100 times more EBV-infected B cells, and defective CD8 T-cell responses against EBV.

In an interview, Dr. Harley predicted that as EBV’s role in the pathogenesis of SLE becomes more fully understood, “there will be new opportunities for treatment.” For example, once the specific T-cell responses to the virus in SLE are better grasped, clinical studies of anti–T-cell therapies directed at those mechanisms will be appropriate.

“I expect most of the biologics will be evaluated in SLE before too long,” the physician added.

“If you accept the idea that the virus is a necessary condition in order to develop lupus—just hypothetically—then if a way was developed to rid the body of the virus and the virus’ presence was needed to sustain the disease, then that would be a new therapeutic approach. The virus has been adapted to human beings for something like 20 million years. So it has found a wonderful niche in our peculiar environment, and it has many presumably unknown ways of sustaining that infection. Nevertheless, a focused effort on trying to understand how the virus works would be a therapeutic approach that hasn’t been explored yet,” he said.

In terms of genetic predisposition, Dr. Harley and colleagues have identified 13 new genes associated with SLE.

Dr. Harley disclosed that he is on the board of directors of IVAX Diagnostics Inc., and JK Autoimmunity Inc. He is also a consultant to UCB and Bio-Rad Laboratories Inc.