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Curr Opin Rheumatol. 2013 Jul;25(4):426-33. doi: 10.1097/BOR.0b013e328362018f.

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

Author information

  • Department of Medicine II, Freiburg University Medical Center, University of Freiburg, Freiburg, Germany. christoph.neumann-haefelin@uniklinik-freiburg.de

Abstract

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.

PMID:
23656712
[PubMed - indexed for MEDLINE]
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