In a recent study of more than 1,200 patients with multiple sclerosis (MS), a research team reported that treatment with the drug natalizumab (Tysabri) could lead to a tenfold increase in the levels of blood antibodies associated with a virus causing a rare but severe brain disease known as progressive multifocal leukoencephalopathy (PML). 
The study, “Therapy with natalizumab is associated with high JCV seroconversion and rising JCV index values,” was published in the journal Neurology: Neuroimmunology and Neuroinflammation and recently discussed in a Multiple Sclerosis News Today article.
The John Cunningham virus (JCV) is responsible for PML development, especially in individuals who have a weakened immune system or are undergoing immunosuppressive treatments. PML leads to the destruction of white matter in the brain.
However, increasing levels of JCV-antibodies do not necessary translate into a higher risk for patients to develop PML, as neurologists Adil Javed, MD, PhD, and Anthony Reder, MD, from the University of Chicago, said in a corresponding editorial.
Following the study publication, Dr. Javed highlighted the benefits of natalizumab as therapy for MS a
nd explained its mechanism of action in a University of Chicago news release. “MS is an autoimmune disease, meaning that it’s a disease of mistaken self identity. The body’s own immune system attacks myelin, an essential layer of insulation around nerve fibers. Without this protective layer, neurons in the central nervous system misfire or fail to fire at all, causing muscle weakness, balance and coordination problems, i.e. disability” he said. “Natalizumab blocks migration of immune cells into the brain and thereby leads to an immunosuppressive state in the central nervous system. It’s by this mechanism that it prevents immune cells from destroying the body’s own myelin. Due to its potent effects on the immune system and the demonstrated high efficacy of the drug inclinical trials in comparison to the older agents, natalizumab was a game changer when it came out in 2004. MS neurologists all thought, ‘why shouldn’t every MS patient be on this drug?’”
nd explained its mechanism of action in a University of Chicago news release. “MS is an autoimmune disease, meaning that it’s a disease of mistaken self identity. The body’s own immune system attacks myelin, an essential layer of insulation around nerve fibers. Without this protective layer, neurons in the central nervous system misfire or fail to fire at all, causing muscle weakness, balance and coordination problems, i.e. disability” he said. “Natalizumab blocks migration of immune cells into the brain and thereby leads to an immunosuppressive state in the central nervous system. It’s by this mechanism that it prevents immune cells from destroying the body’s own myelin. Due to its potent effects on the immune system and the demonstrated high efficacy of the drug inclinical trials in comparison to the older agents, natalizumab was a game changer when it came out in 2004. MS neurologists all thought, ‘why shouldn’t every MS patient be on this drug?’”
When asked if the increase in JCV antibodies in MS patients meant that they were 10 times more likely to develop PML, Dr. Javed said: “Absolutely not. When we see rising antibody levels, or titer, we assume that there must be more replication of the virus. The higher the replication rate of the virus, the higher the chance that the virus could infect brain cells. But this is all based on assumptions and circumstantial evidence. There has never been a good study that shows that rising antibody titers are proportionally correlated with higher viral replication or load. The fact remains that even though JC virus-antibody levels rise over time while on natalizumab therapy, the risk of PML over time continues to remain relatively low.”
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