Abstract
We report that the antimalarial drug artemisinin inhibits hepatitis C virus (HCV) replicon replication in a dose-dependent manner in two replicon constructs at concentrations that have no effect on the proliferation of the exponentially growing host cells. The 50% effective concentration (EC{sub 5}) for inhibition of HCV subgenomic replicon replication in Huh 5-2 cells (luciferase assay) by artemisinin was 78 {+-} 21 {mu}M. Hemin, an iron donor, was recently reported to inhibit HCV replicon replication [mediated by inhibition of the viral polymerase (C. Fillebeen, A.M. Rivas-Estilla, M. Bisaillon, P. Ponka, M. Muckenthaler, M.W. Hentze, A.E. Koromilas, K. Pantopoulos, Iron inactivates the RNA polymerase NS5B and suppresses subgenomic replication of hepatitis C virus, J. Biol. Chem. 280 (2005) 9049-9057.)] at a concentration that had no adverse effect on the host cells. When combined, artemisinin and hemin resulted, over a broad concentration range, in a pronounced synergistic antiviral activity. Also at a concentration (2 {mu}M) that alone had no effect on HCV replication, hemin still potentiated the anti-HCV activity of artemisinin.
Paeshuyse, Jan;
[1]
Coelmont, Lotte;
[1]
Vliegen, Inge;
[1]
Hemel, Johan van;
[2]
Vandenkerckhove, Jan;
[2]
Peys, Eric;
[2]
Sas, Benedikt;
[2]
Clercq, Erik De;
[1]
Neyts, Johan
[1]
- Rega Institute for Medical Research, Minderbroedersstraat 10, KULeuven, B-3000 Leuven (Belgium)
- Kemin Pharma, Atealaan 4H, B-2200 Herentals (Belgium)
Citation Formats
Paeshuyse, Jan, Coelmont, Lotte, Vliegen, Inge, Hemel, Johan van, Vandenkerckhove, Jan, Peys, Eric, Sas, Benedikt, Clercq, Erik De, and Neyts, Johan.
Hemin potentiates the anti-hepatitis C virus activity of the antimalarial drug artemisinin.
United States: N. p.,
2006.
Web.
doi:10.1016/j.bbrc.2006.07.014.
Paeshuyse, Jan, Coelmont, Lotte, Vliegen, Inge, Hemel, Johan van, Vandenkerckhove, Jan, Peys, Eric, Sas, Benedikt, Clercq, Erik De, & Neyts, Johan.
Hemin potentiates the anti-hepatitis C virus activity of the antimalarial drug artemisinin.
United States.
https://doi.org/10.1016/j.bbrc.2006.07.014
Paeshuyse, Jan, Coelmont, Lotte, Vliegen, Inge, Hemel, Johan van, Vandenkerckhove, Jan, Peys, Eric, Sas, Benedikt, Clercq, Erik De, and Neyts, Johan.
2006.
"Hemin potentiates the anti-hepatitis C virus activity of the antimalarial drug artemisinin."
United States.
https://doi.org/10.1016/j.bbrc.2006.07.014.
@misc{etde_20854457,
title = {Hemin potentiates the anti-hepatitis C virus activity of the antimalarial drug artemisinin}
author = {Paeshuyse, Jan, Coelmont, Lotte, Vliegen, Inge, Hemel, Johan van, Vandenkerckhove, Jan, Peys, Eric, Sas, Benedikt, Clercq, Erik De, and Neyts, Johan}
abstractNote = {We report that the antimalarial drug artemisinin inhibits hepatitis C virus (HCV) replicon replication in a dose-dependent manner in two replicon constructs at concentrations that have no effect on the proliferation of the exponentially growing host cells. The 50% effective concentration (EC{sub 5}) for inhibition of HCV subgenomic replicon replication in Huh 5-2 cells (luciferase assay) by artemisinin was 78 {+-} 21 {mu}M. Hemin, an iron donor, was recently reported to inhibit HCV replicon replication [mediated by inhibition of the viral polymerase (C. Fillebeen, A.M. Rivas-Estilla, M. Bisaillon, P. Ponka, M. Muckenthaler, M.W. Hentze, A.E. Koromilas, K. Pantopoulos, Iron inactivates the RNA polymerase NS5B and suppresses subgenomic replication of hepatitis C virus, J. Biol. Chem. 280 (2005) 9049-9057.)] at a concentration that had no adverse effect on the host cells. When combined, artemisinin and hemin resulted, over a broad concentration range, in a pronounced synergistic antiviral activity. Also at a concentration (2 {mu}M) that alone had no effect on HCV replication, hemin still potentiated the anti-HCV activity of artemisinin.}
doi = {10.1016/j.bbrc.2006.07.014}
journal = []
issue = {1}
volume = {348}
place = {United States}
year = {2006}
month = {Sep}
}
title = {Hemin potentiates the anti-hepatitis C virus activity of the antimalarial drug artemisinin}
author = {Paeshuyse, Jan, Coelmont, Lotte, Vliegen, Inge, Hemel, Johan van, Vandenkerckhove, Jan, Peys, Eric, Sas, Benedikt, Clercq, Erik De, and Neyts, Johan}
abstractNote = {We report that the antimalarial drug artemisinin inhibits hepatitis C virus (HCV) replicon replication in a dose-dependent manner in two replicon constructs at concentrations that have no effect on the proliferation of the exponentially growing host cells. The 50% effective concentration (EC{sub 5}) for inhibition of HCV subgenomic replicon replication in Huh 5-2 cells (luciferase assay) by artemisinin was 78 {+-} 21 {mu}M. Hemin, an iron donor, was recently reported to inhibit HCV replicon replication [mediated by inhibition of the viral polymerase (C. Fillebeen, A.M. Rivas-Estilla, M. Bisaillon, P. Ponka, M. Muckenthaler, M.W. Hentze, A.E. Koromilas, K. Pantopoulos, Iron inactivates the RNA polymerase NS5B and suppresses subgenomic replication of hepatitis C virus, J. Biol. Chem. 280 (2005) 9049-9057.)] at a concentration that had no adverse effect on the host cells. When combined, artemisinin and hemin resulted, over a broad concentration range, in a pronounced synergistic antiviral activity. Also at a concentration (2 {mu}M) that alone had no effect on HCV replication, hemin still potentiated the anti-HCV activity of artemisinin.}
doi = {10.1016/j.bbrc.2006.07.014}
journal = []
issue = {1}
volume = {348}
place = {United States}
year = {2006}
month = {Sep}
}