Abstract
Chronic hepatitis B and C are the leading causes of liver disease and liver transplantation worldwide. Ability to mount an effective immune response against both HBV and HCV is associated with spontaneous clearance of both infections, while an inability to do so leads to chronicity of both infections. To mount an effective immune response, both innate and adaptive immune responses must work in tandem. Hence, developing protective immunity to hepatitis viruses is an important goal in order to reduce the global burden of these two infections and prevent development of long-term complications. In this regard, the initial interactions between the pathogen and immune system are pivotal in determining the effectiveness of immune response and subsequent elimination of pathogens. Toll-like receptors (TLRs) are important regulators of innate and adaptive immune responses to various pathogens and are often involved in initiating and augmenting effective antiviral immunity. Immune-based therapeutic strategies that specifically induce type I interferon responses are associated with functional cure for both chronic HBV and HCV infections. Precisely, TLR7 stimulation mediates an endogenous type I interferon response, which is critical in development of a broad, effective and protective immunity against hepatitis viruses. This review focuses on anti-viral strategies that involve targeting TLR7 that may lead to development of protective immunity and eradication of hepatitis B.
Highlights
Defense against chronic viral infections is complex and involves both host innate and adaptive immune systems [1]
While the adaptive immune system features specific antigen recognition receptors, the innate immune system utilizes a unique set of pattern recognition receptors (PRRs), such as Toll-like receptors (TLR), which recognize non-specific, but conserved molecular structures on microorganisms [3,4,5]
Myeloid differentiation primary-response protein (MyD88)-deficient Dendritic cells (DCs) treated with antigen did not induce production of CD80, CD86, major histocompatibility complex (MHC) class II or IL-12, which resulted in an inability of DCs to mature and led to inefficient priming of naïve T cells [27]
Summary
Defense against chronic viral infections is complex and involves both host innate and adaptive immune systems [1]. MyD88-deficient DCs treated with antigen did not induce production of CD80, CD86, MHC class II or IL-12, which resulted in an inability of DCs to mature and led to inefficient priming of naïve T cells [27] These results support the theory that innate immune recognition by TLRs is required for induction of accessory signals required for the activation of adaptive immune response and inducing TH1 polarization by expressing IL-12 on APCs [27,36], an event critical for the induction of DC maturation, the generation of TH subsets and the activation of the adaptive immune response against viruses. Chronic infection is usually asymptomatic, it can lead to
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