A mouse version of Epstein-Barr seems to prevent, not trigger, symptoms of autoimmune disease
A viral infection may help combat lupus. The mouse version of a virus thought to be a prime suspect in the disease, the Epstein-Barr virus, actually prevents certain features of the autoimmune disease, a study in mice shows.
“It might be that this virus has positive effects,” says study author Roberta Pelanda of the National Jewish Health hospital and the University of Colorado Denver School of Medicine. “We really don’t know what these chronic viruses do to the immune system.” Pelanda and her colleagues describe the findings online April 2 in the Proceedings of the National Academy of Sciences.
In people with lupus, the immune system makes antibodies called autoantibodies that attack the body, including the kidneys, heart, skin and blood. While the cause of lupus remains poorly understood, some studies have suggested that the Epstein-Barr virus may trigger the disease in susceptible individuals. The virus, a member of the herpesvirus family, is best known as the cause of mononucleosis. Infection with Epstein-Barr is extremely common, and in most people the virus remains dormant for much of a person’s lifetime.
In the new work, scientists set out to examine the link between Epstein-Barr and the production of autoantibodies in mice. Because Epstein-Barr virus doesn’t actually infect mice, Pelanda and her team used a similar rodent virus, the murine gammaherpesvirus 68, as a stand-in. Analyzing blood samples and the kidneys from lupus-susceptible mice infected with the mouse virus, the team found something unexpected: These animals tended to have healthier, higher-functioning kidneys compared with mice that had not been infected with the virus.
Though levels of autoantibodies rose initially after infection, over the course of a year, lupus-prone female mice tended to make lower levels of autoantibodies compared with noninfected females.
What’s more, healthy mice that were not susceptible to lupus also tended to make low levels of self-attacking antibodies following infection with this virus. These findings suggest that the mouse virus does not trigger autoimmunity.
“The most exciting aspect of this paper is that an infection by a very common virus might be protective from systemic autoimmunity, such as lupus,” says Laurence Morel, a lupus researcher the University of Florida in Gainesville. Though these results are intriguing, she cautions that what’s seen in lab mice might not represent what goes on in humans.
J. Larson et al. Murine gammaherpesvirus 68 infection protects lupusprone
mice from the development of autoimmunity. Proceedings of the National Academy of Sciences. Published online April 2, 2012. Abstract available: [Go to]