Protein link to arthritis opens new chance of drug development

Groundbreaking research linking an immune protein to the debilitating condition of
virus-induced arthritis and viral exacerbation of rheumatoid arthritis, is set to have
important implications for drug development.

Groundbreaking research linking an immune protein to the debilitating condition of

virus-induced arthritis and viral exacerbation of rheumatoid arthritis, is set to have

important implications for drug development.

Conducted by Griffith University’s Institute for Glycomics and published in the

prestigious science journal Proceedings of the National Academy of Science USA, the research has resulted in the first scientific paper to specifically link a protein called MIF (macrophage migration inhibitory factor) with the disease following viral infection.

MIF is normally found in low levels in the joints, with the protein’s link to rheumatoid arthritis being well documented.

“This research has shown that in cases where a virus has induced arthritis, the prevalence of MIF within the joints is increased,” said Professor Suresh Mahalingam, lead researcher on the study.

“MIF is responsible for causing the inflammation and tissue damage.

“Our studies have shown that viral infections can trigger this protein which may explain why patients diagnosed with rheumatoid arthritis suffer from flare-ups when they have an infection.”

Professor Mahalingam said the findings opened up opportunities to develop anti-inflammatory

drugs which will target the receptors bound by MIF.

“MIF is known to bind to receptors which cause inflammation in the joints. New drugs can now be developed to target MIF in order to neutralise it and prevent it binding to a receptor. The best part is that blocking MIF does not compromise antiviral immunity.”

He added that the research was also applicable to other viral infections which result in tissue inflammation such as Dengue Fever and pneumonia.

“Pharmaceutical companies are already targeting MIF but we are now seeking to engage with them about extending the application of those drugs with regards to viral induced inflammation.”