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New research establishes genetic associations in hepatitis C

April 9, 2003 (San Diego, CA) -- Hepatitis C Virus (HCV), as a major agent of non-A, non-B hepatitis (NANBH), has been described as an insidious disease and a silent epidemic, mainly because the infection is often sub-clinical. Acute infection is recognized in a minority of patients and in most cases the virus results in chronic infections taking 10-20 years before the emergence of liver disease. In the US, almost four million individuals are infected and up to 170 million worldwide.

Background

An imbalance in helper T-cell type-1 (Th1) and type-2 (Th2) cytokines has been suggested as playing an important role in the cause of chronic viral infections, but this issue is not resolved in patients with hepatitis C virus (HCV) infection. Inflammation of the portal and portal areas is a common feature of chronic hepatitis C. Antigen presenting dendritic, or "tree-like," cells are located in the portal area, and infiltrating T-cells are initially exposed to infected hepatocytes in the peripheral area. Thus, these areas could be sites of the initial processes of the immune response in chronic hepatitis C.

The pathogenesis of hepatitis C virus associated liver injury involves many genes from multiple pathogenic pathways. Blockade of CC-chemokine receptor 5 (CCR5) has been proposed as therapy for HIV-1. Therefore, an examination was conducted to determine if the CCR5-delta32 homozygous genotype has phenotypic expression other than those related to HIV-1. Other genes associated with viral infection (RANTES, CD4), and in inflammation (Interleukin1B) were also reviewed for their possible association.

Hepatitis C virus (HCV) is commonly seen in the Coachella Valley of Southern California. Genetic Research institute of the Desert (GRID), a nonprofit research center was established in the Coachella valley with a goal to investigate genetic aspects of cancer, as well as infectious and some neurological diseases. This research effort fo
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Contact: Donna Krupa
djkrupa1@aol.com
703-967-2751
American Physiological Society
9-Apr-2003


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