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. 2018 Feb 15;14(2):e1006884. doi: 10.1371/journal.ppat.1006884

Fig 1. mSAMD9L is a poxvirus restriction factor that needs to be overcome for poxvirus replication.

Fig 1

(A). The restriction of K1L and C7L deletion vaccinia virus (vK1L-C7L-) in 3T3 cells was abolished by knocking out mSAMD9L with CRISPR-Cas9. A validated mSAMD9L knockout cell clone (ΔmSAMD9L #1) and the parental 3T3 cells were left untreated (-) or treated (+) with 200 U/ml of murine IFN-β for 24 h, before they were infected with vK1L-C7L- at an MOI of 1 PFU/cell. Viral growth was determined by measuring viral titers at 0 and 24 hour-post-infection (hpi). (B). The restriction of vK1L-C7L- in mouse embryo fibroblasts (MEF) was abolished by knocking out mSAMD9L. MEFs isolated from SAMD9L+/+ or SAMD9L-/- mice were infected with vK1L-C7L- or wild-type (WT) VACV strain WR.