Abstract
Most people develop acute hepatitis B virus (HBV)-related hepatitis that is controlled by both humoral and cellular immune responses following acute infection. However, a number of individuals in HBV-endemic areas fail to resolve the infection and consequently become chronic carriers. While a vaccine is available and new antiviral drugs are being developed, elimination of persistently infected cells is still a major issue. Standard treatment in HBV infection includes IFN-α, nucleoside, or nucleotide analogs, which has direct antiviral activity and immune modulatory capacities. However, immunological control of the virus is often not durable. A robust T-cell response is associated with control of HBV infection and liver damage; however, HBV-specific T cells are deleted, dysfunctional, or become exhausted in chronic hepatitis patients. As a result, efforts to restore virus-specific T-cell immunity in chronic HBV patients using antiviral therapy, immunomodulatory cytokines, or therapeutic vaccination have had little success. Adoptive cell transfer of T cells with specificity for HBV antigen+ cells represents an approach aiming to ultimately eliminate residual hepatocytes carrying HBV covalently closed circular DNA (cccDNA). Here, we discuss recent findings describing HBV immunopathology, model systems, and current therapies.
Highlights
Hepatitis B virus (HBV) belongs to the Orthohepadna genus of the Hepadnaviridae family of virus and has a unique replication strategy wherein it replicates its 3.2 kb DNA genome using an RNA intermediate via reverse transcription [1]
Since T cells are the mediators of hepatitis B virus (HBV) clearance during recovery in an acute infection, it would be an effective strategy to trigger or enhance their response and resolve chronic HBV infection
Several groups have utilized adoptive transfer of memory T cells specific to HBV to generate an immune response as opposed to relying only on the exhausted T cells found in chronic infection
Summary
Hepatitis B virus (HBV) belongs to the Orthohepadna genus of the Hepadnaviridae family of virus and has a unique replication strategy wherein it replicates its 3.2 kb DNA genome using an RNA intermediate via reverse transcription [1]. The cccDNA is transcribed to these four transcripts that are translated in the cytoplasm and assemble the nucleocapsid containing pre-genomic RNA (pgRNA) [18] This pgRNA synthesizes positive and negative strand of the DNA to assemble viral particles containing rcDNA that acquire lipid membranes through the Golgi complex and bud out from the host cell surface [17]. These nucleocapsids can re-enter the nucleus prior to membrane acquisition and enter the HBV replication process as rcDNA [17]. HBV follows this complex lifecycle involving reverse transcription similar to retro-viruses, unlike DNA viruses
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