DOI
https://doi.org/10.25772/K54R-GD16
Defense Date
2010
Document Type
Thesis
Degree Name
Master of Science
Department
Physiology
First Advisor
Valeria Mas
Abstract
The leading causes of liver disease are Hepatitis C virus infection and chronic alcohol abuse. Alcohol accelerates liver disease in HCV but the mechanisms are poorly understood. The identification of molecular gene expression profiles on human liver tissue was performed using microarrays. Samples were obtained from alcoholic-cirrhotic, HCV-cirrhotic, HCV/alcohol-cirrhotic and control non-cirrhotic liver tissue. Probe set expression summaries were calculated using RMA. Probe set level linear models were fit where probe set expression was modeled by HCV status, alcohol status, and the interaction between HCV and Alcohol. HCV cirrhosis was associated with up-regulation of genes related to viral and immune response, apoptosis and inflammation. There were down-regulation of genes in the ubiquititin-proteasome system in alcoholic cirrhosis. The interaction of HCV and alcohol revealed negative interaction for genes involved in apoptosis and immune response. There was a negative estimate for genes involved in class II restricted antigen presentation.
Rights
© The Author
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
August 2010