(RxWiki News) Natalizumab is often used to fight the symptoms and progression of multiple sclerosis, but the drug comes with a significant risk of a rare and potentially fatal viral infection.
Multiple sclerosis patients who take natalizumab (brand name Tysabri) have about three times the rate of progressive multifocal leukoencephalopathy (PML) — a rare and usually fatal disease of the brain. While it is known that PML is caused by the JC virus, it isn’t clear why more MS patients taking natalizumab get PML.
A recent study found that the JC virus may live and grow in certain cells of the immune system and that natalizumab may enhance this process.
"Ask your doctor about your MS treatment options."
Elliot M. Frohman, MD, PhD from the Department of Neurology at the University of Texas Medical Center in Dallas, TX led the research team.
The study involved three groups of people. Twenty-six multiple sclerosis (MS) patients had their blood drawn before starting natalizumab and regularly over the next 10 monthly treatments. Another group of 23 patients had their blood drawn once after they had completed at least 24 treatments with natalizumab. Blood was also collected for a third group of 18 people without MS who served as the control group for the study.
The research team measured the amount of JC virus in the blood of the study participants. They looked at different types of white cells in the patients, called CD34 and CD19 cells, to see which cells the virus was found in.
JC virus was found in either the CD34 or CD19 white cells of people in all three groups. The virus was found in cells of 50 percent of the patients starting natalizumab treatment, 44 percent of the patients who had more than 24 treatments, and in 17 percent of the normal control group.
Results of the research showed that the percentages of CD34 and CD19 cells were higher in the blood of MS patients treated with natalizumab, compared to people in the healthy control group. This increase started after three months of treatment.
The authors theorized that the JC virus might have lived in CD34 cells in the bone marrow and that natalizumab moved these cells into the bloodstream. They also suggested that the cells infected with JC virus might become CD19 cells where the virus could then grow.
“Continued studies are needed to further investigate natalizumab treatments as the mechanism of PML,” the authors concluded.
The research was published in the March issue of JAMA Neurology.
Funding for the study was provided by the National Institute of Neurological and Communicative Diseases and the National Institute of Allergy and Infectious Disease, as well as a grant from the National Multiple Sclerosis Society.
Dr. Frohman disclosed receiving fees for speaking and consulting from Biogen Idec, makers of natalizumab.
