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10.3389/fimmu.2017.00436

http://scihub22266oqcxt.onion/10.3389/fimmu.2017.00436
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C5390110!5390110!28450868
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suck abstract from ncbi


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pmid28450868      Front+Immunol 2017 ; 8 (ä): ä
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  • Hepatitis B Virus Immunopathology, Model Systems, and Current Therapies #MMPMID28450868
  • Sandhu P; Haque M; Humphries-Bickley T; Ravi S; Song J
  • Front Immunol 2017[]; 8 (ä): ä PMID28450868show ga
  • 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-?, 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.
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