Arthritogenic alphaviral infection perturbs osteoblast function and triggers pathologic bone loss

• DOI: 10.1073/pnas.1318859111
• Publication Date: 2014-04-15T03:58:43Z
• Authors: Weiqiang Chen; Suan-Sin Foo; Nestor E. Rulli; Adam Taylor; Kuo-Ching Sheng; Lara J. Herrero; Belinda L. Herring; Brett A. Lidbury; Rachel W. Li; Nicole C. Walsh; Natalie A. Sims; Paul N. Smith; Suresh Mahalingam
• Keywords: Alphavirus infection; Proinflammatory cytokine

Significance Persistent polyarthritis, which occurs in 30–40% of alphavirus-infected patients, has been proposed to be caused by proinflammatory mediators such as IL-6. In the present study we investigated susceptibility and response primary human osteoblasts Ross River virus (RRV) infection determined whether could result bone pathology. RRV resulted increased receptor activator nuclear factor-kappaB ligand (RANKL) but decreased osteoprotegerin (OPG). We are first report that alphavirus results loss an established murine model this is prevented IL-6 inhibition. These findings reveal can disrupt homeostasis play important role alphavirus-induced arthritis regulating contribute disrupting RANKL/OPG balance.