The hepatitis C virus (HCV) nonstructural 5A (NS5A) protein has been implicated in the inherent resistance of HCV to interferon (IFN) antiviral therapy in clinical studies. Biochemical studies have demonstrated that NS5A interacts in vitro with and inhibits the IFN-induced, RNAdependent protein kina
Effects of human γ interferon on cell growth, replication of virus and induction of 2′-5′oligoadenylate synthetase in three human lymphoblastoid cell lines and K562 cells
✍ Scribed by Yoshimi Tomita; Kari Cantell; Tsuguo Kuwata
- Publisher
- John Wiley and Sons
- Year
- 1982
- Tongue
- French
- Weight
- 510 KB
- Volume
- 30
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Human α interferon (IFN‐α) and β interferon (IFN‐β) showed antiviral and anticellular effects on human lymphoblastoid Daudi and P3HR‐1 cells, but up to 1,000 units/ ml of γ interferon (IFN‐γ) showed no such effect. Though a fairly high level of dsRNA‐dependent 2′‐5′‐oligoadenylate synthetase (2–5A synthetase) was found in Daudi cells, treatment of these cells with IFN‐α and β enhanced the enzyme level in cells at least four‐fold, but IFN‐γ did not show any such effect. Lymphoblastoid Raji cells were insensitive to the antiviral and anticellular activities of IFN‐α, β and γ, but 2‐5A synthetase was induced in cells by the treatment with IFN‐α and β, though the enzyme level was lower than that found in interferon‐treated Daudi cells. Human leukemic K562 cells were completely insensitive to IFN‐α, β and at the same time to IFN‐γ with regard to the antiviral, anticellular activities and to the induction of 2‐5A synthetase.
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