Abstract
Toll-like receptors (TLR) play a key role in innate immunity. To examine the ability of diverse TLRs to modulate hepatitis B virus (HBV) replication, HBV transgenic mice received a single intravenous injection of ligands specific for TLR2, TLR3, TLR4, TLR5, TLR7, and TLR9. All of the ligands except for TLR2 inhibited HBV replication in the liver noncytopathically within 24 h in a alpha/beta interferon-dependent manner. The ability of these TLR ligands to induce antiviral cytokines at the site of HBV replication suggests that TLR activation could represent a powerful and novel therapeutic strategy for the treatment of chronic HBV infection.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Female
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Hepatitis B e Antigens / genetics
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Hepatitis B virus / genetics
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Hepatitis B virus / immunology*
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Hepatitis B virus / physiology*
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Immunity, Innate
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Interferon-alpha / biosynthesis
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Interferon-beta / biosynthesis
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Ligands
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Liver / immunology
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Liver / virology
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Male
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Membrane Glycoproteins / immunology*
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Membrane Proteins / deficiency
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Membrane Proteins / genetics
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Mice
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Mice, Knockout
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Mice, Transgenic
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Receptor, Interferon alpha-beta
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Receptors, Cell Surface / immunology*
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Receptors, Interferon / deficiency
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Receptors, Interferon / genetics
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Signal Transduction
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Toll-Like Receptor 2
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Toll-Like Receptor 3
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Toll-Like Receptor 4
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Toll-Like Receptor 5
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Toll-Like Receptor 7
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Toll-Like Receptors
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Virus Replication / immunology*
Substances
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Hepatitis B e Antigens
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Interferon-alpha
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Ligands
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Membrane Glycoproteins
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Membrane Proteins
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Receptors, Cell Surface
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Receptors, Interferon
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Toll-Like Receptor 2
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Toll-Like Receptor 3
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Toll-Like Receptor 4
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Toll-Like Receptor 5
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Toll-Like Receptor 7
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Toll-Like Receptors
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Receptor, Interferon alpha-beta
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Interferon-beta