| Abstract: |
SUMMARVlnterferons are a multifunctional proteins first observed to have antiviral activity and IS produced by both CD4 and CD8 T - Iymphocytes and natural killer cells.Interferon y known to have antiviral actions as well as immunomodulatory action. IFN y is affecting humoral immunity indirectly by regulating the development of specific T helper cell subsets and by direct effects on B cell by regulating development and Ig heavy chain switching IFN a1~ enhance the cytotoxicity ofNK cells via induction of IL-15 from monocytes/macrophages.During acute viral infection multiple arms of immune system were activated and probably must act in concert in order to achieve viral clearance. A defect in the production of IFN a contributes to continued viral replication in many case of viral infection.Immunological impairment in HCY, HBY and schistosomal infection patients and development of chronicity due to decreased levels of IFN y secoundry to decrease number of Thl secreting cells, moreover IFN a production by peripheral blood mononuclear cells is impaired in chronic HeV and HBY infections.Differences in the immunological host responses are thollght to be important factor that determine course of viral hepatitis is alteration of the cell mediated immune response which is insufficient to clear the virus.In acute HCV infection individuals whom have a more vIgorous proliferative response to HCV antigens are able to clear HCV infection after interferon therapy. The vigorous antiviral CD4 T cell response intbe early phase of acute hepatitis C is not only required for virus elimination leading to self limited course of the disease, but also that antiviral CD4 T cell response in the late phase is a prerequisite for achieving long-term viral control.The magnitude of IFN y production specific for HE V antigen has been noted to depend on the helper activity of CD4+ T cells, activated CDf HLA-DR+ helper cells infiltrating liver should spontaneously produce larger amounts of IFN y. Increased CD8+ cells regulate HBV antigen specific IFN y production in the liver. During acute HEV infection multiple arms of immune systemare activated and probably must act in concrete in order to achieve viral clearance. Coincident with the development of increased transaminases during acute HE V infection and antibodies specific for HBV proteins develop the most critical of which is anti HEc.During schistosomal infection IFNy production was found to be generally suppressed which plays a role in regulation of fibroblast activity and inhibition of collagen deposition in murine schistosomiasis, lower levels of this cytokines related to the increased scar tissue and fibrosis in schistosomal patients.Patients suffering from chronic schistosomal infection showed high prevalence of anti-HCV antibodies, several studies reported tIaschistosomiasis plays an important role in maintaining HCV Vlremla among patients exposed to HCV infection. Moreover the clinical morbidity associated with uncomplicated chronic schistosomisis may be caused by a concomitant occult HBV infection.To define the role ofIFNy and IFNa in the progression or limitation of the course of viral hepatitis Band C with or without schistosomal infection, we measured the level of endogenous IFNy and IFNa levels in viral hepatitis B (acute and chronic), hepatitis C infection (early and late), and schistososmal infection active and chronic comparing between its level in different subgroups and to find the role of associated schistosomal infection in the progression of viral replication.70 patients were included in this study divided into three groups:Group I : 20 patients hepatitis B (11 acute, 9 chronic). Group II : 30 patients hepatitis C (7 early, 23 late).Group III : 20 patients schistosomal infection ( 10 active, 1 0 chronic). Group IV : 12 normal healthy control.Interferon serum level alpha and gamma were estimated III different groups.All groups were subjected to routine laboratory investigationr including CBC, liver function tests, abdominal ultrasonography examination, liver biopsy to selected cases, detection of associated schistosomal infection by stool analysis, rectal snip examination, indirect haemagglutination test, circulating immuncomplex, viral hepatitis serology (Hev Ab, HBsAg, HBcAb), PCR examination, IFN a and IFNy assay.The results showed that:In group 1: The mean level of IFN Cl in acute HEV infection was presei and detectable while was not detectable in late cases, the mean level of IFNy was significantly higher in acute HEV infection than in chronic HBV infection moreover IFN Cl and IFNy level were significantly higher in PUle HEV infection than in mixed infection with schistosoma!’In group 11: The mean level of IFN Cl in early infection is significantly higher than in chronic cases, while patients on IFN therapy showed higher mean level of IFN Cl than chronic cases on conventional therapy simill results were detected as regards mean serum IFNy. Pure HeV infectiOll showed higher level of IFN Cl and IFNy than mixed infection with schistosomal infection.In group Ill: There was no detectable in schistosomal infection.There was positive correlation between mean serum IFN Cl and IFNy and serum bilirubin level and also prothrombin level was denoted.Correlation between mean serum IFN Cl and IFNy and histopathological diagnosis of HCV infection and HEV infection our study showed higher serum level of IFN Cl and IFNy in chronic persistent hepatitis and chronic active hepatitis than in cases ofliver cirrhosis and mixed liver cirrhosis and periportal fibrosis.These findings suggests that the influence of IFNy protection ofliver cell against HCY infection and its role of eliminating HCY before affecting other liver cells. Mixed schistosomal infection with HCY and HBC down¬modulate interferon production which enhances progression to liver cirrhosis.The decreased level of IFNy may be attributed to the decreased number of Th 1 cell types or due to elevated antinterferon antibody titers or ~ue to consumption of IFNy intrahepatic ally by IFNy receptors in these cells before reaching the serum.The development of chronic infection is linked to weak or absent Tb] responses to HCY and HBY infection and to the presence of Th2 cytokines IL-4 and IL-l 0 after stimulation of peripheral blood mononuclear cells with recombinant HCY antigens in particular the core protein.Schistosomisis coinfection with HCY and HBY infection enhance progression of chronic infection, due to immunological alteration and decreased interferon level.
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