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Short Communication |
1 Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Hermann-Herder-Str. 11, D-79104 Freiburg, Germany
2 Abteilung Molekulare Virologie, Hygiene Institut, Universität Heidelberg, Otto-Meyerhof-Zentrum, Im Neuenheimer Feld 350, D-69120 Heidelberg, Germany
Correspondence
Michael Frese (at Heidelberg)
michael_frese{at}med.uni-heidelberg.de
It was demonstrated using self-replicating hepatitis C virus (HCV) RNAs that both types of interferons (IFNs) (in particular IFN-
and IFN-
) are potent inhibitors of HCV replication in Huh-7 cells. Because IFN- and tumour necrosis factor (TNF)- trigger a partially overlapping set of antiviral defence mechanisms, it is tempting to speculate that TNF- also inhibits HCV replication. However, this study shows that TNF- does not affect HCV protein and RNA synthesis, nor does it synergistically enhance the inhibitory effect of IFN-. Taken together, these results demonstrate that HCV replication in Huh-7 cells is highly resistant to TNF-. It is, therefore, unlikely that the increased production of TNF-, which is seen in many hepatitis C patients, contributes to HCV clearance by inducing antiviral defence mechanisms in infected hepatocytes.
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