Immunotherapy for Chronic Hepatitis B Virus Infection.

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hepatitis B 21 infectiousdiseases
hepatitis C 2 infectiousdiseases
hepatitis D 1 infectiousdiseases

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hepatitis B 466 chronic hepatitis C virus infection have delivered remarkable cure rates, curative therapies for chronic hepatitis B virus (HBV) infection remain a distant goal. Although current direct antiviral therapies are very efficient
hepatitis B 1263 potential toxicities in different groups of chronically infected HBV patients. We also discuss the chronic hepatitis B patient populations that best benefit from therapeutic immune interventions.INTRODUCTIONIn contrast
hepatitis B 1462 interventions.INTRODUCTIONIn contrast to most communicable diseases, morbidity and mortality rates related to infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) have increased over the last 20 years.[1] The two different
hepatitis B 2689 providing functional cure,[4] a virological and clinical situation defined by undetectable levels of hepatitis B surface antigen (HBsAg) and HBV DNA in the serum, normality of alanine aminotransferase (ALT) and development
hepatitis B 2814 antigen (HBsAg) and HBV DNA in the serum, normality of alanine aminotransferase (ALT) and development of hepatitis B surface antibody (anti-HBs). The term “functional cure” is thus used to define a virological situation
hepatitis B 2979 cure” is thus used to define a virological situation in which, like in patients who resolved acute hepatitis B infection, HBV is not fully eliminated and few hepatocytes harbor covalently closed circular DNA (cccDNA)
hepatitis B 7429 CHB patients.[30] On the other hand, immunosuppressive treatments targeting cellular immunity in anti- hepatitis B core (anti-HBc) positive subjects often trigger rapid reactivation of HBV.[31] These data therefore
hepatitis B 8594 and liver.[37] The drug administered to HBV-infected chimpanzees and woodchucks infected by woodchuck hepatitis B virus (WHBV) have shown a robust even though transient anti-HBV activity.[37],[38]The compound has been
hepatitis B 14158 boosting the existent HBV-specific T cells, particularly in the category of CHB that is more in need, hepatitis B e antigen positive (HBeAg+) patients with high levels of HBsAg and viral replication.Therefore the development
hepatitis B 24216 of HBV (Myrcludex-B).[91]HBV IMMUNOTHERAPY - WHICH PATIENTS SHOULD BE TREATED?Current guidelines for hepatitis B indicate that antiviral therapy should be reserved until the appearance of clinically active liver disease
hepatitis B 27674 tolerant” phase of the disease, now redefined as HBeAg+ infection, than older subjects with chronic active hepatitis B (now better defined as HBeAg+ hepatitis, EASL guidelines[98]) (Fig. 3). Our argument centers around
hepatitis B 28458 boost. TNFα, released by inflammatory monocytes that are increased in the advanced phase of chronic hepatitis B ,[89] can directly inhibit virus-specific T cells.[99] Furthermore, the intrahepatic environment of patients
hepatitis B 31100 new immunotherapeutic approaches.Fig. 1Immune therapeutic approaches to achieve a functional cure of hepatitis B virus (HBV). (A) Schematic representation of immune responses and viral load in chronic and resolved
hepatitis B 31858 killer T; TCR, T cell receptor; APC, antigen-presenting cell; PD-1, programmed cell death-1; HBsAg, hepatitis B surface antigen.Fig. 2Therapeutic strategies designed to restore hepatitis B virus (HBV)-specific T
hepatitis B 31935 programmed cell death-1; HBsAg, hepatitis B surface antigen.Fig. 2Therapeutic strategies designed to restore hepatitis B virus (HBV)-specific T cell responses in chronic hepatitis B patients. Vaccine therapy aims to induce
hepatitis B 31996 2Therapeutic strategies designed to restore hepatitis B virus (HBV)-specific T cell responses in chronic hepatitis B patients. Vaccine therapy aims to induce and boost new HBV-specific T cells and check point inhibitors
hepatitis B 32540 TCR, T cell receptor; CAR, chimeric antigen receptor.Fig. 3Pathogenesis of liver damage during chronic hepatitis B virus (HBV) infection. Increased levels of alanine aminotransferase (ALT) are not proportional to the
hepatitis B 34709 HCC[69]–[73]TLR, Toll-like receptor; NK, natural killer; MAIT, mucosal associated invariant T; CHB, chronic hepatitis B ; IL, interleukin; RIG-I, retinoic acid-inducible gene-I; TCR, T cell receptor; HBV, hepatitis B virus;
hepatitis B 34805 chronic hepatitis B; IL, interleukin; RIG-I, retinoic acid-inducible gene-I; TCR, T cell receptor; HBV, hepatitis B virus; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; ADCC, antibody-dependent cellular
hepatitis B 34831 interleukin; RIG-I, retinoic acid-inducible gene-I; TCR, T cell receptor; HBV, hepatitis B virus; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; ADCC, antibody-dependent cellular cytotoxicity; PD-1,
hepatitis B 34861 acid-inducible gene-I; TCR, T cell receptor; HBV, hepatitis B virus; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; ADCC, antibody-dependent cellular cytotoxicity; PD-1, programmed cell death-1; HCC,
hepatitis C 369 SingaporePublication date (ppub): 9/2018Publication date (epub): 1/2018AbstractWhile new therapies for chronic hepatitis C virus infection have delivered remarkable cure rates, curative therapies for chronic hepatitis B virus
hepatitis C 1490 communicable diseases, morbidity and mortality rates related to infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) have increased over the last 20 years.[1] The two different viruses (HCV is an RNA virus
hepatitis D 5522 observation that co-infection with hepatotropic viruses able to activate innate immunity like HCV and hepatitis D virus, causes a drop of HBV replication.[15],[16] Thus, strategies aiming to activate these different

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