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Fig. 3 | Retrovirology

Fig. 3

From: Natural APOBEC3C variants can elicit differential HIV-1 restriction activity

Fig. 3

HIV-1 replication phenotypes following A3C disruption and variant complementation in non-permissive CEM2n cells. a Immunoblots of endogenous A3C in SupT11, H9, and CEM2n cells. Tubulin was used as a loading control. b Immunoblots of endogenous A3C in CEM2n clones following targeted disruption of A3C exon 3 by Cas9/gRNA complexes. Tubulin was used as a loading control. c A3C exon 3 sequences from parental CEM2n and an A3C-disrupted clone (CEM2n ∆A3C). d Flow cytometry plots for CEM2n ΔA3C cell pools 72 h post-transduction with GFP-reporter complementation vectors. The percentage of GFP+ cells is indicated for each population. e Immunoblots of A3C in the parental CEM2n line, CEM2n ΔA3C, and complemented CEM2n ΔA3C derivatives. Tubulin was used as a loading control. f, g Spreading infection kinetics of Vif-proficient and Vif-deficient HIV-1 (initial MOI = 0.02) in CEM2n, CEM2n ΔA3C, and the indicated complemented conditions. SupT11 cells are included as a control permissive cell type. Virus infectivity was determined by infection of CEM-GFP with culture supernatants followed 48 h later by quantification with flow cytometry. Each spreading infection experiment was performed 3 times and representative data are shown

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