Clinical and Vaccine Immunology, August 2006, p. 972-974, Vol. 13, No. 8
1071-412X/06/$08.00+0 doi:10.1128/CVI.00396-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Gastrointestinal and Liver Unit, Prince of Wales Hospital and University of New South Wales, Sydney, Australia,1 Department of Infectious Diseases, Monash Medical Centre and Department of Medicine, Monash University, Melbourne, Australia,2 Victorian Infectious Diseases Reference Laboratory and University of Melbourne, Melbourne, Australia3
Received 18 November 2005/ Returned for modification 5 February 2006/ Accepted 24 May 2006
Persistent infection with hepatitis B virus (HBV) likely depends on viral inhibition of host defenses. We report that chronic hepatitis B e antigen-positive HBV infection is associated with a significant reduction in peripheral blood monocyte expression of Toll-like receptor 2, a key component of innate immunity, thereby providing a mechanism by which wild-type HBV may establish persistent infection.
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