• Título:  ANÁLISIS MOLECULAR DEL EFECTO REGULADOR INDUCIDO POR EL VIRUS DE LA HEPATITIS C
• Autor:  Fernández Ponce, Cecilia Matilde
• Universidad:  Universidad de Cádiz
• Departamento:  BIOMEDICINA, BIOTECNOLOGÍA Y SALUD PÚBLICA
• Fecha de Lectura:  31/07/2013
• Mención Europeo / Mención Internacional: concedido
• Programa de doctorado:  Bases Celulares y Moleculares de la Patología Humana
• Dirección: 
  • García Cózar, Francisco Jose (DIRECTOR)
• Tribunal: 
  • AGUADO VIDAL, ENRIQUE (PRESIDENTE)
  • ESPINAZO ROMEU, MARÍA LUISA (SECRETARIO)
  • Saffarzadeh, Mona (VOCAL)
• Descriptores: 
  • INMUNOLOGIA
• Resumen:
  Hepatitis C virus (HCV), identified as the major etiological agent responsible for post-transfusion, originally called, non-A and non-B hepatitis 1, infects an estimated 170 million persons worldwide and thus represents a viral pandemic 2. HCV is currently the most important cause of chronic viral hepatitis in the world and one of the commonest indications for liver transplantation 3; 4. One of the puzzling features of HCV infection is that, even among healthy and fully immunocompetent individuals, up to 80% of individuals with HCV infection develop persistent viremia; approximately 3% of the world¿s population. HCV evades clearance mechanisms and establishes persistent infection, leading to progressive hepatic fibrosis, cirrhosis, death from liver failure, as well as the advent of hepatocellular carcinoma 1; 5. The HCV infection immune response is variable. During the acute infection is induced an immunological response specific for the virus, mediated by CD4+ and CD8+ T cell. The CD4 T-cell response to HCV is polyclonal, easy to detect, and maintained indefinitely in most patients who recover, while it is narrowly focused and infrequently detected in chronically infected patients 6. The way in which the virus inflicts its long-term damage is not well understood. Regarding virus mediated T-cell dysfunction; we and others have reported the effect of HCV Core expression in CD4+ T cells, showing that this protein induces a state of unresponsiveness similar to clonal anergy 7; 8; 9. There are several additional mechanisms that have been suggested to contribute to CD4+ T cell unresponsiveness during chronic HCV infection, among which suppression of T cell function by CD4+ CD25+ Treg-cells (regulatory T-cells) is emerging as one of the most important 9; 10; 11; 12; 13; 14. The high percentage of chronicity in HCV infected patients, as well as the limited benefits of the current therapy makes necessary the development of new antiviral strategies able to control and/or eradicate HCV infection. To achieve this goal, it is desirable to know the mechanisms employed by the virus to evade the immune response and persist in the host. In this context, it is important to be familiar with the effects of the various viral proteins in the immune cells to understand the molecular mechanisms of viral persistence. Our results shed light on the development of adaptive regulatory-like CD4+ T cells in the periphery by the expression of a viral protein.