Targeting a host-cell entry factor barricades antiviral-resistant HCV variants from on-therapy breakthrough in human-liver mice.
- Vercauteren, Koen
- Brown, Richard J P
- Mesalam, Ahmed Atef
- Doerrbecker, Juliane
- Bhuju, Sabin
- Geffers, Robert
- van den Eede, Naomi
- Mcclure, C Patrick
- Troise, Fulvia
- Verhoye, Lieven
- Baumert, Thomas
- Farhoudi, Ali
- Cortese, Riccardo
- Ball, Jonathan K
- Leroux-Roels, Geert
- Pietschmann, Thomas
- Nicosia, Alfredo
- Meuleman, Philip
DOIAbstract
Direct-acting antivirals (DAAs) inhibit hepatitis C virus (HCV) infection by targeting viral proteins that play essential roles in the replication process. However, selection of resistance-associated variants (RAVs) during DAA therapy has been a cause of therapeutic failure. In this study, we wished to address whether such RAVs could be controlled by the co-administration of host-targeting entry inhibitors that prevent intrahepatic viral spread
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