Immune Response in Hepatitis B Virus Infection

Tan, Anthony T.; Koh, Sarene; Bertoletti, Antonio

doi:10.1101/cshperspect.a021428

Cited by 102 publications

(111 citation statements)

References 160 publications

Supporting

Mentioning

104

Contrasting

Order By: Relevance

“…As discussed by Tan et al 2015, the likelihood of progression to chronicity, following infection with HBV, is predominantly determined by age at infection. Infants infected at birth develop chronic infection in 90% of cases, whereas for children aged between 1 and 5 years, this falls to 25% -30%, and, for immunocompetent adults, the likelihood of progression to chronicity is 5% (Edmunds et al 1993).…”

Section: Natural History Infection and Immunitymentioning

confidence: 99%

“…These phases, described in more detail in Tan et al (2015), are: † immune tolerance-high infectivity, little ongoing liver damage; † immune clearance-variable infectivity, active inflammation of the liver; † immune control-low infectivity, little ongoing liver damage; and † immune escape-variable infectivity, recurrent liver inflammation.…”

Section: Natural History Infection and Immunitymentioning

confidence: 99%

See 1 more Smart Citation

Hepatitis B Virus Epidemiology

MacLachlan

Cowie

2015

Cold Spring Harbor Perspectives in Medicine

253

163

View full text Add to dashboard Cite

The epidemiology of hepatitis B virus (HBV) infection is geographically diverse, with population prevalence, age and mode of acquisition, and likelihood of progression to chronic infection mutually interdependent. The burden of chronic HBV infection is increasingly being recognized, with cirrhosis and liver cancer attributable to HBV continuing to increase. The outcomes of chronic HBV infection are affected by a range of factors, including viral genotype, the presence of coinfections with other blood-borne viruses, and the impact of other causes of liver disease. The increased recognition of HBV infection as a leading cause of death globally has resulted in the development of new structures and policies at the international level; immediate attention to implementing these strategies is now required.

show abstract

Section: Natural History Infection and Immunitymentioning

confidence: 99%

Section: Natural History Infection and Immunitymentioning

confidence: 99%

Hepatitis B Virus Epidemiology

MacLachlan

Cowie

2015

Cold Spring Harbor Perspectives in Medicine

253

163

View full text Add to dashboard Cite

show abstract

“…It depends on the intensity of immune response (function f ( v )), the initial virus load (initial condition) and the growth rate of the virus in accordance with the existing view of the regulation of virus infections [1, 2, 4, 11, 29, 33, 34, 38]. We assume that the maximal intensity of the immune response is sufficiently high to overcome virus growth and spread in a low-dose infection.…”

Section: Discussionmentioning

confidence: 99%

“…Hence prey is not only consumed by predators but it can also hunt predators [2, 29, 30]. Straightforward examples are provided by HIV, HBV and HCV infections in humans [31–33] and experimental LCMV infection in mice [34–37]. In this paper we propose a model of spatiotemporal virus infection dynamics which considers a non-linear bell-shaped regulation of the cytotoxic T cells response with a time lag needed for their clonal expansion.…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal Dynamics of Virus Infection Spreading in Tissues

et al. 2016

View full text Add to dashboard Cite

Virus spreading in tissues is determined by virus transport, virus multiplication in host cells and the virus-induced immune response. Cytotoxic T cells remove infected cells with a rate determined by the infection level. The intensity of the immune response has a bell-shaped dependence on the concentration of virus, i.e., it increases at low and decays at high infection levels. A combination of these effects and a time delay in the immune response determine the development of virus infection in tissues like spleen or lymph nodes. The mathematical model described in this work consists of reaction-diffusion equations with a delay. It shows that the different regimes of infection spreading like the establishment of a low level infection, a high level infection or a transition between both are determined by the initial virus load and by the intensity of the immune response. The dynamics of the model solutions include simple and composed waves, and periodic and aperiodic oscillations. The results of analytical and numerical studies of the model provide a systematic basis for a quantitative understanding and interpretation of the determinants of the infection process in target organs and tissues from the image-derived data as well as of the spatiotemporal mechanisms of viral disease pathogenesis, and have direct implications for a biopsy-based medical testing of the chronic infection processes caused by viruses, e.g. HIV, HCV and HBV.

show abstract

“…Both frequencies and magnitudes of response were significantly lower in these patients compared to HBsAg loss subjects. We also showed that both CD4 + and CD8 + T cells contributed to the anti‐HBV immune responses by secreting IFN‐γ CD4 + T cells are robust producers of cytokines and required for the efficient development of effector CD8 + CTLs . Our IFN‐γ ICS analysis revealed that especially HBV Core IFN‐γ‐secreting CD4 + subsets were significantly lower in CHB patients compared with HBsAg loss subjects.…”

Section: Discussionmentioning

confidence: 99%

Recognition of Core‐ and Polymerase‐derived immunogenic peptides included in novel therapeutic vaccine by T cells from Chinese chronic hepatitis B patients

Huang

Sansas

Jiang

et al. 2017

Journal of Viral Hepatitis

View full text Add to dashboard Cite

SummaryChronic hepatitis B (CHB) is one of the major public health challenges in the world.Due to a strong interplay between specific T-cell immunity and elimination of hepatitis B virus (HBV), efforts to develop novel immunotherapeutics are gaining attention. TG1050, a novel immunotherapy, has shown efficacy in an animal study. To support the clinical development of TG1050 in China, specific immunity to the fusion antigens of TG1050 was assessed in Chinese patients. One hundred and thirty subjects were divided into three groups as CHB patients, HBV spontaneous resolvers, and CHB patients with HBsAg loss after antiviral treatment. HBV-specific T-cell responses to pools of HBV Core or Polymerase genotype D peptides included in TG1050 were evaluated. HBV Core-or Polymerase-specific cells were detected in peripheral blood mononuclear cells (PBMCs) from the different cohorts. The frequencies and intensities of HBV Core-specific immune responses were significantly lower in CHB patients than in HBsAg loss subjects. In CHB patients, a dominant pool derived from Polymerase (Pol1) was the most immunogenic. CHB patients with low viral loads (<10 6 IU/mL) were more likely to have a positive response specific to the Core peptide pool. Overall, genotype D-derived peptides included in TG1050 could raise broad and functional T-cell responses in PBMCs from Chinese CHB patients infected with genotype B/C isolates. Core-specific immunogenic domains appeared as "hot spots" with the capacity to differentiate between CHB vs HBsAg loss subjects. These observations support the extended application and associated immune monitoring of TG1050 in China. K E Y W O R D SCore and Polymerase, HBV, HBV genotype, immune response, TG1050This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

show abstract

Immune Response in Hepatitis B Virus Infection

Cited by 102 publications

References 160 publications

Hepatitis B Virus Epidemiology

Hepatitis B Virus Epidemiology

Spatiotemporal Dynamics of Virus Infection Spreading in Tissues

Recognition of Core‐ and Polymerase‐derived immunogenic peptides included in novel therapeutic vaccine by T cells from Chinese chronic hepatitis B patients

Contact Info

Product

Resources

About