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Archive - Sep 2, 2019

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Scientists Locate RNA of Persistent Arthritis-Causing Chikungunya Virus Hidden in Dermal and Muscle Fibroblasts and Skeletal Myofibers

Since chikungunya virus emerged in the Americas in 2013, it has infected millions of people, causing fever, headache, rash, and muscle and joint pain. For some people, painful, debilitating arthritis lasts long after the other symptoms have resolved. Researchers have suspected that the virus or its genetic material - in this case, RNA - persist in the body undetected, but they have been unable to find its hiding places. Now, researchers at Washington University School of Medicine in St. Louis have figured out a way to detect cells infected with chikungunya virus that survive the infection. The scientists genetically modified the virus such that it activated a fluorescent tag within cells during infection. Months after the initial infection, the researchers could detect glowing red cells still harboring viral RNA. The study, in mice, opens up new ways to understand the cause of - and find therapies for - chronic viral arthritis. The findings were published August 29, 2019 in PLOS Pathogens. The open-access article is titled “Dermal and Muscle Fibroblasts and Skeletal Myofibers Survive Chikungunya Virus Infection and Harbor Persistent RNA.” Senior author Deborah Lenschow, MD, PhD, an Associate Professor of Medicine and of Pathology and Immunology, and co-first author and graduate student Marissa Locke answered questions about the research, which was conducted in collaboration with co-first author Alissa Young, PhD, co-author Michael S. Diamond, MD, PhD, the Herbert S. Gasser Professor of Medicine, and others. How common is chronic arthritis caused by chikungunya infection? Dr. Lenschow: Between 30% and 60% of people infected with chikungunya virus go on to develop chronic arthritis that can last up to three or four years after infection.

Promising Gene Replacement Therapy for Niemann-Pick Type A Disease Moves Forward at Ohio State

Research led by Krystof Bankiewicz (photo), MD, PhD, who recently joined The Ohio State University College of Medicine, shows that gene replacement therapy for Niemann-Pick type A disease is safe for use in nonhuman primates and has therapeutic effects in mice. These research findings were published online on August 21, 2019, in the journal Science Translational Medicine. The article is titled “Adeno-Associated Viral Vector Serotype 9–Based Gene Therapy for Niemann-Pick Disease Type A.” Prior to joining Ohio State as a Professor of Neurosurgery, Dr. Bankiewicz conducted this translational gene therapy research at the University of California at San Francisco, in conjunction with researchers in New York, Massachusetts, and Spain. Niemann-Pick disease type A (NPD-A) is a lysosomal storage disorder characterized by neurodegeneration and early death. It is caused by loss-of-function mutations in the gene coding for the enzyme acid sphingomyelinase (ASM), which hydrolyzes sphingomyelin into ceramide. With this disease, the body's ability to metabolize fat within cells is affected, causing these cells to malfunction and, eventually, die. This inherited disease can affect the brain, nerves, liver, spleen, bone marrow, and lungs. The three main types of Niemann-Pick disease are types A, B and C. The signs and symptoms experienced depend on the type and severity of the condition. Some infants with type A will show signs and symptoms within the first few months of life. Those with type B may not show signs for years and have a better chance of surviving to adulthood. People with type C may not experience any symptoms until adulthood. Dr.