[Role of a host in spontaneous recovery from viral hepatitis C: genetic predetermined factors].
The impact of both congenital and specific human immune responses on the invasion of viruses is determined by a broad spectrum of genetically determined parameters. The review attempts to characterize the influence of genetic determinants on the outcome of human hepatitis C viral (HCV) infection. The increased rate of convalescence is associated with female sex and white ethnicity. Hereditary immune disorders/deficiency lead to the reduced probability of spontaneous convalescence and the complicated course of a chronic stage of the disease. The carriage of some HLA haplotypes and gene alleles, which determine the development of an immune response following the Th1 or Th2 type, is essential in predicting both the outcome of acute HCV infection and the course of chronic hepatitis C. Specifically, the higher elaboration of IFN-gamma and IL-12 which specify a Th1 immune response facilitates the good outcome of HCV infection. At the same time, the increased generation of Th2-orienting IL-6 and IL-10 predisposes to the chronic course of the disease. In recent studies, the outcome of the infection is also associated with the polymorphism of genes, encoding for low-density lipoproteins and complement type 1 receptors, with other genes determining the development of a congenital immune response and a specific one. The understanding of genetic predisposition of the outcome of HCV infection and the possibility of its prediction may make a considerable contribution to the definition of treatment policy for viral hepatic C.
Isaguliants
M G
MG
Ozeretskovskaia
N N
NN
D017074:Common Variable Immunodeficiency / Q000235:genetics* / Q000276:immunology; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D020022:Genetic Predisposition to Disease; D005838:Genotype; D016174:Hepacivirus / Q000276:immunology / Q000502:physiology; D006526:Hepatitis C / Q000235:genetics* / Q000276:immunology*; D006649:Histocompatibility Antigens / Q000235:genetics / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D009569:Nitric Oxide / Q000235:genetics / Q000276:immunology; D011110:Polymorphism, Genetic; D055607:Receptors, Natural Killer Cell / Q000235:genetics / Q000276:immunology; D012737:Sex Factors
D016207:Cytokines; D006649:Histocompatibility Antigens; D055607:Receptors, Natural Killer Cell; D009569:Nitric Oxide