Institutional members access full text with Ovid®

Share this article on:

HLA-B27-mediated protection in HIV and hepatitis C virus infection and pathogenesis in spondyloarthritis: two sides of the same coin?

Neumann-Haefelin, Christoph

Current Opinion in Rheumatology: July 2013 - Volume 25 - Issue 4 - p 426–433
doi: 10.1097/BOR.0b013e328362018f

Purpose of review HLA-B27 is associated with low viral load and long-term nonprogression in HIV infection as well as spontaneous clearance of hepatitis C virus (HCV) infection. This review summarizes mechanisms that have been suggested to be involved in this protective effect of HLA-B27, and highlights possible lessons for the role of HLA-B27 in spondyloarthritis.

Recent findings Recent studies linked protection by HLA-B27 in HIV and HCV infection to virological mechanisms such as a complicated pathways of viral escape from immunodominant HLA-B27-restricted virus-specific CD8+ T-cell epitopes. In addition, several immunological mechanisms have been proposed, including CD8+ T-cell polyfunctionality and functional avidity, thymic selection of CD8+ T-cell precursors, specific T-cell receptor repertoires and clonotypes, efficient antigen processing, and evasion from regulatory T-cell-mediated suppression.

Summary Multiple virological and immunological mechanisms have been suggested to contribute to HLA-B27-mediated protection in HIV and HCV infection. Some of these mechanisms may also be involved in HLA-B27-associated pathogenesis in spondyloarthritis.

Department of Medicine II, Freiburg University Medical Center, University of Freiburg, Freiburg, Germany

Correspondence to Christoph Neumann-Haefelin, MD, Department of Medicine II, Freiburg University Medical Center, Hugstetter Strasse 55, 79106 Freiburg, Germany. Tel: +49 761 270 33530; e-mail:

© 2013 Lippincott Williams & Wilkins, Inc.