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Tumor Necrosis Factor-Alpha In Hepatitis C Virus Infection: A Correlation With Viral Activity and Serum Aminotransferases

1Ghada F. Helaly and 2Lobna A. Abou Shamaa

Departments of 1Microbiology and 2Immunology Medical Research Institute, Alexandria University, Alexandria, Egypt.

Tumor necrosis factor-alpha (TNF-a) is an immunoregulatory cytokine with a wide range of biological effects. It is secreted mainly by activated monocytes/macrophages and lymphocytes in a variety of pathological conditions including viral hepatitis. The objectives of the study were to measure serum TNF-α levels in patients infected with hepatitis C virus (HCV) and estimate the relation between serum TNF-α levels and the presence or absence of HCV viraemia as well as serum alanine and aspartate aminotransferases’ (ALT and AST) activities, which are considered as parameters of liver injury. Twenty HCV infected patients along with ten healthy control subjects were enrolled in this study. HCV infected patients were tested for the presence of HCV viraemia through carrying out nested reverse transcription-polymerase chain reaction assay. Serum levels of TNF-α were assayed using an enzyme immunoassay and Liver biochemistry in the form of determination of serum ALT and AST activities were done for all cases. TNF-a levels were dramatically elevated in HCV infected patients, in spite of their normal serum aminotransferases’ activities as compared with healthy control subjects [27.31 ± 10.75 vs. 7.13 ± 1.85 pg/ml (p=0.0001), respectively]. Although, serum levels of TNF-α were slightly elevated in viraemic than non-viraemic HCV infected patients, yet this difference did not reach the statistically significant level [28.59 ± 13.99 vs. 26.03 ± 6.70 pg/ml (p= 0.3)], also Serum TNF-a levels were not significantly correlated with serum ALT and AST activities in HCV infected patients.  It is concluded that measurement of TNF-a levels in HCV infected patients could reflect liver injury despite normal levels of liver enzymes and its serum level is not affected by viral activity.