Overexpression of cyclooxygenase-2 and transforming growth factor-beta 1 is an independent predictor of poor virological response to interferon therapy in chronic HCV genotype 4 patients.
OBJECTIVE
COX-2 and TGF-β1 are overexpressed in hepatitis C virus (HCV) infection and are related to hepatitis pathogenesis and hepatic fibrosis. The current study investigated the relationship between pretreatment COX-2 and TGF-β1 hepatic expression in HCV genotype 4 and the virological response to interferon therapy.


METHODS
Liver biopsies of 55 patients with HCV infection genotype 4 were selected together with 10 liver biopsies as control. The patients' clinicopathological data were collected. Immunohistochemistry was done using anti-COX-2 and anti-TGF-β1 antibodies. Statistical tests were used to determine the association between both COX-2 and TGF-β1 expression in relation to clinicopathological parameters and response to interferon therapy.


RESULTS
COX-2 was upregulated especially in nonresponders and was an independent predictor of poor virological response. However, COX-2 showed no association with other clinicopathological features. TGF-β1 was upregulated and associated with nonresponders, histological activity, and fibrosis stage. There was no association between TGF-β1 and other clinicopathological features. There was an association between COX-2 and TGF-β1 immunoexpression.


CONCLUSIONS
Overexpression of COX-2 and TGF-β1 is an independent predictor for poor outcome of interferon and ribavirin therapy and these might be useful markers for the response to treatment. Both molecules are associated together; however, their role during hepatitis treatment has to be clarified.
Department of Pathology, Faculty of Internal Medicine, Minia University, El-Minia, Egypt; Department of Pathology, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia, .
Wafaey M
WM
Gomaa
Mohammed A
MA
Ibrahim
Mohamed E
ME
Shatat
D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D051546:Cyclooxygenase 2 / Q000096:biosynthesis* / Q000378:metabolism; D004359:Drug Therapy, Combination; D005260:Female; D015967:Gene Expression Regulation, Viral; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000235:genetics* / Q000378:metabolism; D006518:Hepatitis Viruses / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D007372:Interferons / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012254:Ribavirin / Q000627:therapeutic use; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis* / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
D000998:Antiviral Agents; D053773:Transforming Growth Factor beta1; D012254:Ribavirin; D007372:Interferons; D051546:Cyclooxygenase 2