الفهرس 
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Abstract
Hepatitis C virus is a hepatotropic and lymphotropic virus that has been found to be associated with various diseases and syndromes. Infection with HCV tends to become chronic in most infected individuals, reflecting an inability of the immune system to mount an effective antiviral response.
Autoimmune hepatitis is a chronic disease of unknown cause, characterized by continuing hepatocellular inflammation and necrosis and tending to progress to cirrhosis. Immune serum markers frequently are present, autoantibodies against liver-specific and non-liver-specific antigens and increased immunoglobulin G (IgG) levels.
In August 2012, the Centers for Disease Control and Prevention (CDC) expanded their existing, risk-based testing guidelines to recommend a one-time blood test for hepatitis C virus (HCV) infection in baby boomers - the generation born between 1945 and 1965, who account for approximately three fourths of all chronic HCV infections in the United States - without prior ascertainment of HCV risk.
The proposed pathogenesis of autoimmune hepatitis involves the combination of genetic predisposition and environmental triggers. The genetic predisposition may relate to several defects in immunologic control of autoreactivity. An environmental agent triggers the autoimmune response against liver antigens, causing necroinflammatory liver damage, fibrosis, and, eventually, cirrhosis, if left untreated.
Genetic susceptibility to developing autoimmune hepatitis has been associated with the HLA haplotypes gene deletions and are associated with the development of autoimmune hepatitis in younger patients.
HLA-DR3–positive patients are more likely than other patients to have aggressive disease, which is less responsive to medical therapy and more often results in liver transplantation; in addition, these patients are younger than other patients at the time of their initial presentation. HLA-DR4 - positive patients are more likely to develop extrahepatic manifestations of their disease.
Among the several viruses implicated as triggering agents are rubella, Epstein-Barr, and hepatitis A, B, and C. Some authors have shown a high amino acid sequence homology between hepatitis C virus (HCV) polyprotein and cytochrome P450IID6 (CYP2D6), the molecular target of liver-kidney microsomal type 1 (LKM 1) antibody, which suggests that molecular mimicry may trigger production of LKM_1 antibody in HCV infection.
Current evidence suggests that liver injury in a patient with autoimmune hepatitis is the result of a cell-mediated immunologic attack. Aberrant display of human leukocyte antigen (HLA) class II on the surface of hepatocytes facilitates the exposure of normal liver cell membrane constituents to antigen-presenting cells (APCs).
The reasons for the aberrant HLA display are unclear. It may be initiated or triggered by genetic factors, viral infections (e.g., acute hepatitis A or B, Epstein-Barr virus infection), and chemical agents (e.g., interferon, melatonin, alpha methyldopa, oxyphenisatin, nitrofurantoin, tienilic acid).
As the etiology of autoimmune hepatitis is unknown, several factors (eg, viral infection, drugs, environmental agents, genetic factors) may trigger an autoimmune response and autoimmune disease.
The aim of the our study was to illustrate the genetic association between different (HLA class II alleles: DRB1*01* - DRB1*15*) and HCV hepatitis as well as AIH.
Eighty subjects were included in the study, divided into three groups; group I: 30 chronic HCV, group II: 30 autoimmune hepatitis free of HBV and HCV infection, group III: 20 healthy controls.
In the present study HLA DRB1∗07, DRB1∗11 were highly associated with chronic HCV cases.