By Katie Campbell
Chikungunya virus, the mosquito-transmitted virus responsible for over 1 million cases and almost 200 deaths since 2015, has long been known to cause debilitating joint pain and arthritis. This pain and inflammation can persist for months or years after infection. The current treatment for this long-lasting symptom is anti-inflammatory drugs, but the current treatment standards are not particularly effective.
Researchers Jane Wilson and Natalie Prow at QIMR Berghofer Medical Research Institute, Australia have developed a mouse model to study the inflammatory response to the chikungunya pathogen. They recently validated their model, by showing how the activated inflammatory genes mirror the process in infected humans. As a result, the scientists we able to show how certain granzymes, proteinases secreted by immune cells, actually promote inflammation despite previous thought that all granzymes assist in apoptosis, or the killing of infected cells.
Upon infection of granzyme A deficient mice with chikungunya virus, the researchers saw significantly less foot swelling and arthritis. Additionally, when mice were treated with a granzyme A inhibitor, the mice showed reduced swelling and arthritis. Elevated granzyme A levels have been found in non-human primates infected with chikungunya, therefore granzyme A could be a potential drug target for anti-inflammatory drugs that treat chikungunya and other inflammatory diseases.
PLOS. (2017, February 16). Mouse study reveals potential drug target for arthritis caused by chikungunya virus: A specific immune system proteinase may promote arthritic inflammation after viral infection. ScienceDaily. Retrieved February 20, 2017 from www.sciencedaily.com/releases/2017/02/170216144008.htm