图1:CSDE1水疱性口炎病毒的一个积极的调制器复制。Hep3B细胞转染没有siRNA -控制核,或[s15373小干扰rna) + 15374 (2 CSDE1-specific siRNA) 46和CSDE1水平由西方墨点法24或48 h后化验。(代表三个独立的实验)。罪犯与核转染后48小时,Hep3B细胞感染VSV-GFP (MOI 0.1)。48小时(B)或96 h (C)后,病毒滴度测定空斑实验和D存活细胞的数量在96 h后感染病例数。代表两个不同的实验。E B16转椅、B16-CSDE1C-T或B16-CSDE1WT-overexpressing细胞感染VSV-IFN-β莫伊的0.1。24、48和72 h后,病毒滴度测定博鸿泰细胞通过空斑实验。代表三个独立的实验。F父母Hep3B Hep3B-overexpressing野生型CSDE1WT细胞或人口集中,或突变CSDE1C-T,感染了VSV-IFN-β(MOI 0.1)(3井/组)。 Forty-eight hours later (Passage 1), supernatants were assayed for infectious titers on the same cells on which the virus was passaged. Virus was recovered every 48 h (P2–5) and similarly titered. Representative of three separate experiments. G Stock VSV-IFN-β virus or VSV-IFN-β, which had been passaged five times through Hep3B parental or Hep3B-CSDE1C-T cells as in F, was titered on either Hep3B parental cells or on Hep3B-CSDE1C-T cells. Representative of two separate experiments. Means ± SD of three technical replicates are shown. P-values were determined using a one-way (B–D) or two-way (E–G) ANOVA with a Tukey’s multiple comparisons post test on log-transformed data. Statistical significance was set at p < 0.05, ns > 0.05. Source data are provided as a Source Data file. Credit: DOI: 10.1038/s41467-021-22115-1
