Adaptive immune responses during acute uncomplicated and fulminant hepatitis E
Identifieur interne : 002329 ( Main/Exploration ); précédent : 002328; suivant : 002330Adaptive immune responses during acute uncomplicated and fulminant hepatitis E
Auteurs : Ratika Srivastava [Inde] ; Rakesh Aggarwal [Inde] ; Sanjeev Sachdeva [Inde] ; Mohammad Intakhab Alam [Inde] ; Shahid Jameel [Inde] ; Sita Naik [Inde]Source :
- Journal of Gastroenterology and Hepatology [ 0815-9319 ] ; 2011-02.
English descriptors
- Teeft :
- Acute hepatitis, Antiviral, Bioscience, Biosciences pharmingen, Blackwell publishing asia, Cytokine, Disease severity, Fulminant, Fulminant hepatic failure, Fulminant hepatitis, Gastroenterology, Healthy controls, Hepatitis, Hepatology, Hepatology foundation, Immune, Immune responses, Infection, Liver injury, Naik, Natural killer, Open reading frame, Orf2 protein, Pbmc, Peripheral blood, Porf2, Porf3, Pregnant women, Recombinant, Sigma, Sita naik, Srivastava, Tumor necrosis, Uncomplicated, Uncomplicated hepatitis, Viral, Viral clearance, Viral hepatitis, Viral replication, Virus infection.
Abstract
Background and Aim: Hepatitis E virus (HEV) infection is endemic in several developing countries. Clinical manifestations of this infection vary widely from asymptomatic infection to uncomplicated acute viral hepatitis and fulminant hepatic failure. The pathogenesis of this disease and the reason of varying disease severity remain unknown. In viral infections, tissue injury can be caused either by virus itself or by host immune responses directed against infected cells. We therefore studied adaptive immune responses to HEV antigens in patients with hepatitis E of varying disease severity and healthy controls. Methods: Cytokine secreting CD4+ T cells and antibody‐producing B cells specific for HEV were enumerated through intracellular cytokine staining and enzyme‐linked immunosorbent spot assay, respectively. Results: Patients with fulminant hepatitis E had a less marked expansion of HEV‐specific interferon‐γ or tumor necrosis factor‐α secreting CD4+ T cells than patients with uncomplicated hepatitis E and healthy controls. These patients also had fewer CD4+ T cells that produce γ‐interferon or tumor necrosis factor‐α upon in vitro polyclonal stimulation. In addition, patients with fulminant disease had a more marked expansion of B cells that can secrete immunoglobulin G anti‐HEV than patients with uncomplicated infection and control patients. Conclusion: These findings suggest that less‐marked antiviral cellular immune responses and heightened antiviral humoral responses are associated with a more severe disease during HEV infection.
Url:
DOI: 10.1111/j.1440-1746.2010.06356.x
Affiliations:
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Clinical manifestations of this infection vary widely from asymptomatic infection to uncomplicated acute viral hepatitis and fulminant hepatic failure. The pathogenesis of this disease and the reason of varying disease severity remain unknown. In viral infections, tissue injury can be caused either by virus itself or by host immune responses directed against infected cells. We therefore studied adaptive immune responses to HEV antigens in patients with hepatitis E of varying disease severity and healthy controls. Methods: Cytokine secreting CD4+ T cells and antibody‐producing B cells specific for HEV were enumerated through intracellular cytokine staining and enzyme‐linked immunosorbent spot assay, respectively. Results: Patients with fulminant hepatitis E had a less marked expansion of HEV‐specific interferon‐γ or tumor necrosis factor‐α secreting CD4+ T cells than patients with uncomplicated hepatitis E and healthy controls. These patients also had fewer CD4+ T cells that produce γ‐interferon or tumor necrosis factor‐α upon in vitro polyclonal stimulation. In addition, patients with fulminant disease had a more marked expansion of B cells that can secrete immunoglobulin G anti‐HEV than patients with uncomplicated infection and control patients. 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