Biologists at New York University have determined how neurons combat viral infections. Their findings, which appear in the journal Viral Immunology, may offer a path for treating viral encephalitis and related afflictions
Findings May Offer Path for Treating Viral Encephalitis and Related Afflictions
Biologists at New York University have determined how neurons combat viral infections. Their findings, which appear in the journal Viral Immunology, may offer a path for treating viral encephalitis and related afflictions.
Understanding what happens to the body’s neurons-nerve cells that are fundamental to the make-up of the brain and spinal cord-when they become infected has long been a significant area of scientific inquiry. This is because our immune system kills cells when viral infection is seen. However, neurons, unlike other cells, cannot be replaced, and therefore infected neurons are not targeted by killer T cells.
PHOTO CAPTION: The images show the impact of interferons in fighting viral proteins in neurons. The nucleus of each cell is in blue while the viral proteins are in red. In the top image, neurons have not been treated with interferons, thus allowing viral proteins to replicate. The bottom image shows neurons that have been treated with interferons, resulting in a containment of the virus.
In an effort to understand how neurons fight viral infections, the NYU researchers compared and contrasted neurons with non-neuronal cells. To do this, they treated both types of cells with interferons, which are proteins made by the body that are released in response to stimuli-notably infection.
Their results showed significant differences in how interferons function in both types of cells. In non-neuronal cells, interferons work to prevent the expression of viral proteins. Viral proteins are essential to make new viruses and spread the infection. By contrast, in neurons, interferons allow the production of viral proteins, but alter these proteins’ make-up. Under this change-called a post-translational modification-interferon-treated neurons alter the decoration of viral proteins in such a way that they cannot interact with each other and therefore cannot form new, and infectious, progeny.
“This is a paradigm-changing finding because it shows how differently neurons respond to infections,” said Carol Shoshkes Reiss, a professor in NYU’s Department of Biology and the study’s senior author. “Moving forward, it may be possible to develop pharmaceuticals to mimic effect of interferons and thus block the ability of viral proteins to replicate. This would reduce the vulnerability of neurons to viral infection and lead to recovery from encephalitis.”
The study’s other authors were Paul D’Agostino, a doctoral candidate in NYU’s Graduate School of Arts and Science at the time of study and now a post-doctoral fellow at Rockefeller University, and Jessica J. Amenta, a 2007 graduate of NYU’s College of Arts and Science and currently an MD-PhD candidate at the Duke University School of Medicine. Reiss also has appointments at NYU’s Center for Neural Science, the NYU School of Medicine, and the Mount Sinai School of Medicine.