News JC Virus Carries a Mutation in MS Patients That Amplifies Brain Disease Known as PML JC Virus Carries a Mutation in MS Patients That Amplifies Brain Disease Known as PML by Patricia Silva, PhD | May 24, 2016 Share this article: Share article via email Copy article link A mutation in aĀ mouse modelĀ of the John Cunningham (JC) virus, which causes progressive multifocal leukoencephalopathy (PML), allows the virus to evade the host immune responses in people with multiple sclerosis (MS),Ā according to a study into the mechanisms of PML. Infection with the JC virus most often passes unnoticed in healthy adults. For reasons still eluding scientists, however, MS patients treated with natalizumabĀ (Tysabri), as well asĀ patients withĀ other autoimmune conditions and cancers treated with certain immunosuppressive drugs, are at increased risk of developing the brain disease. “Nobody comes away unscathed from PML ā you either die or you’re left with a lifelong searing neurological defect,” Aron E. Lukacher, chair and professor of microbiology and immunology at Penn State College of Medicine, said in a press release. “Because we don’t know how the drugs cause the JC virus to amplify from a silent infection, we really have no way of controlling it.” Earlier research noted thatĀ JCĀ virus isolated from patients with PMLĀ wasĀ mutated. The mutation, present as a change of a single amino acid, affects the part of the virus shell that allow it to dock into and infect human cells. Scientists demonstratedĀ that the mutation alters the capacity of the virus to infect certain tissues, but until now they did not know whether it also had an impact on immune responses to the virus. The study, āType I Interferons Regulate the Magnitude and Functionality of Mouse Polyomavirus-Specific CD8 T Cells in a Virus Strain-Dependent Manner,āĀ publishedĀ in theĀ Journal of Virology,Ā set out to explore this crucial question. Investigating mice with a mouse variant of the JC virus, the research team indeed found that when the mutation was present, immune T-cell responses were not as pronounced. “We found that mouse polyomaviruses with a single amino acid change in their shell elicit a very different magnitude and quality of the T cell response that is needed to control the infection,” Dr. Lukacher said. Researchers also found that the reduced T-cell activation was a result of altered type 1 interferon responses, immune factors normally activating T-cells. “We need to find ways to improve the T cell responses in patients on these therapies,” concluded Dr. Lukacher. Print This Page About the Author Patricia Silva, PhD PatrĆcia holds a PhD in medical microbiology and infectious diseases from the Leiden University Medical Center, Netherlands, and completed a postdoctoral research fellowship at the Instituto de Medicina Molecular, Lisbon, Portugal. Her work in academia was mainly focused on molecular biology and the genetic traits of infectious agents such as viruses and parasites. PatrĆcia earned several travel awards to present her work at international scientific meetings. She is a published author of several peer-reviewed science articles. Tags John Cunningham virus, progressive multifocal leukoencephalopathy (PML), T-cells
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