Fusco, Dahlene NDahlene NFuscoBrisac, CynthiaCynthiaBrisacJohn, Sinu PSinu PJohnYI-WEN HUANGChin, Christopher RChristopher RChinXie, TiaoTiaoXieZhao, HongHongZhaoJilg, NikolausNikolausJilgZhang, LeiliangLeiliangZhangChevaliez, StephaneStephaneChevaliezWambua, DanielDanielWambuaLin, WenyuWenyuLinPeng, LeeLeePengChung, Raymond TRaymond TChungBrass, Abraham LAbraham LBrass2023-01-062023-01-062013-060016-5085https://scholars.lib.ntu.edu.tw/handle/123456789/626953Hepatitis C virus (HCV) infection is a leading cause of end-stage liver disease. Interferon-α (IFNα) is an important component of anti-HCV therapy; it up-regulates transcription of IFN-stimulated genes, many of which have been investigated for their antiviral effects. However, all of the genes required for the antiviral function of IFNα (IFN effector genes [IEGs]) are not known. IEGs include not only IFN-stimulated genes, but other nontranscriptionally induced genes that are required for the antiviral effect of IFNα. In contrast to candidate approaches based on analyses of messenger RNA (mRNA) expression, identification of IEGs requires a broad functional approach.enTreatment; Gene Regulation; Virology; Mechanism; RAT-LIVER; PATHWAYS; PROTEINS; CELLS; EXPRESSION; COFACTOR; GAMMA[SDGs]SDG3A genetic screen identifies interferon-α effector genes required to suppress hepatitis C virus replicationjournal article10.1053/j.gastro.2013.02.026234621802-s2.0-84878279903WOS:000319498500027https://scholars.lib.ntu.edu.tw/handle/123456789/376514