Visvanathan, K.; Skinner, N.; Kurtovic, J.; Nagree, A.; Locarnini, S.; Williams, R.; Riordan, S.M.
April 2003
Gut;Apr2003 Supplement 1, Vol. 52, pA36
Academic Journal
Background: Mechanisms by which hepatitis B virus (HBV) establishes persistent infection remain unclear. In particular, expression of toil-like receptors (TLRs), increasingly recognised as critically involved in the innate immune response to bacterial and viral pathogens, has not been investigated. Methods: Eighteen non-cirrhotic patients with chronic hepatitis B and on-going viral replication (HBV DNA > 200 000 genomes/mL, n = 12 and 200-10 000 genomes/mL, n = 6; Cobas Amplicor HBV MonitorTM Test, USA) and 32 healthy control subjects were studied. TLR2 and TLR4 expression on CD14+ve peripheral blood mononuclear cells (PBMCs) was measured by flow cytometry using anti-CD14 (Becton Dickinson) and anti-TLR2 and anti-TLR4 (eBioscience, USA) monoclonal antibodies. TLR expression was re-assessed in 5 patients in whom HBV DNA fell from > 200 000 to < 200 genomes/mL following treatment with lamivudine. In vitro TLR2 expression by PBMCs was measured in 5 control subjects at baseline and following stimulation for 20 h by partially purified recombinant HBV. Results: TLR2 expression (expressed as a ratio to control results) was significantly reduced in chronic hepatitis B patients with HBV DNA > 200 000 genomes/mL (median: 0.63; range: 0.05-1.52) compared with controls (p = 0.001) and those with HBV DNA 20010 000 genomes/mL (median: 0.98; range: 0.94-1.17, p = 0.04). TLR4 expression did not differ significantly between the 3 groups. TLR2 expression normalised in each of the 5 lamivudine-treated chronic hepatitis B patients in whom HBV DNA became undetectable. In vitro expression of TLR2 fell in a concentration dependent manner following exposure to recombinant HBV. Conclusions: HBV downregulates expression of TLR2 on PBMCs. This virus induced defect in innate immunity may contribute to the development of persistent infection.


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