The heme oxygenase 1 product biliverdin interferes with hepatitis C virus replication by increasing antiviral interferon response.
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The heme oxygenase 1 product biliverdin interferes with hepatitis C virus replication by increasing antiviral interferon response. / Lehmann, Elisabeth; El-Tantawy, Walid Hamdy; Ocker, Matthias; Bartenschlager, Ralf; Lohmann, Volker; Hashemolhosseini, Said; Tiegs, Gisa; Sass, Gabriele.
in: HEPATOLOGY, Jahrgang 51, Nr. 2, 2, 2009, S. 398-404.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - The heme oxygenase 1 product biliverdin interferes with hepatitis C virus replication by increasing antiviral interferon response.
AU - Lehmann, Elisabeth
AU - El-Tantawy, Walid Hamdy
AU - Ocker, Matthias
AU - Bartenschlager, Ralf
AU - Lohmann, Volker
AU - Hashemolhosseini, Said
AU - Tiegs, Gisa
AU - Sass, Gabriele
PY - 2009
Y1 - 2009
N2 - The anti-inflammatory and antiapoptotic heme degrading enzyme heme oxygenase-1 (HO-1) has been shown recently to interfere with replication of hepatitis C virus (HCV). We investigated the effect of HO-1 products carbon monoxide (CO), iron and biliverdin on HCV replication using the replicon cell lines Huh-5-15 and LucUbiNeo-ET, stably expressing HCV proteins NS3 through NS5B. Incubation of these cell lines in the presence of the CO donor methylene chloride transiently reduced HCV replication, whereas an increase of iron in cell culture by administration of FeCl(3) or iron-saturated lactoferrin did not interfere with HCV replication. Likewise, depletion of iron by deferoxamine during induction of HO-1 by cobalt-protoporphyrin IX did not restore HCV replication. The most prominent effect was observed after incubation of replicon cell lines in the presence of biliverdin. Biliverdin seems to interfere with HCV replication-mediated oxidative stress by inducing expression of antiviral interferons, such as interferon alpha2 and alpha17. Conclusion: The antioxidant biliverdin reduces HCV replication in vitro by triggering the antiviral interferon response and might improve HCV therapy in the future. (HEPATOLOGY 2009.).
AB - The anti-inflammatory and antiapoptotic heme degrading enzyme heme oxygenase-1 (HO-1) has been shown recently to interfere with replication of hepatitis C virus (HCV). We investigated the effect of HO-1 products carbon monoxide (CO), iron and biliverdin on HCV replication using the replicon cell lines Huh-5-15 and LucUbiNeo-ET, stably expressing HCV proteins NS3 through NS5B. Incubation of these cell lines in the presence of the CO donor methylene chloride transiently reduced HCV replication, whereas an increase of iron in cell culture by administration of FeCl(3) or iron-saturated lactoferrin did not interfere with HCV replication. Likewise, depletion of iron by deferoxamine during induction of HO-1 by cobalt-protoporphyrin IX did not restore HCV replication. The most prominent effect was observed after incubation of replicon cell lines in the presence of biliverdin. Biliverdin seems to interfere with HCV replication-mediated oxidative stress by inducing expression of antiviral interferons, such as interferon alpha2 and alpha17. Conclusion: The antioxidant biliverdin reduces HCV replication in vitro by triggering the antiviral interferon response and might improve HCV therapy in the future. (HEPATOLOGY 2009.).
M3 - SCORING: Zeitschriftenaufsatz
VL - 51
SP - 398
EP - 404
JO - HEPATOLOGY
JF - HEPATOLOGY
SN - 0270-9139
IS - 2
M1 - 2
ER -
