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. Author manuscript; available in PMC: 2019 May 28.
Published in final edited form as: Nat Microbiol. 2018 Mar 27;3(4):503–513. doi: 10.1038/s41564-018-0131-9

Fig. 4 |. Cellular iNOS/NO induced by STAT3 activity play a critical role in suppressing HCMV IE1 expression and viral replication in HPCs.

Fig. 4 |

a,b, Levels of iNOS (a) and NO (b) in HPCs transfected with iNOS siRNA or scramble oligonucleotide. c, Increase of HCMV IE1 expression and genome replication in NR-1-infected HPCs after iNOS siRNA transfection. d, Depletion of cellular NO by NG-M-L-Arg. e, Increase of HCMV IE1 expression and genome replication in NR-1-infected HPCs after direct depletion of cellular NO by NG-M-L-Arg. f, Lentivirus-mediated iNOS overexpression in HL-60 cells increased intracellular NO level. g, Increase of NO level in HL-60 cells suppressed viral IE1 activity and genome replication. h,i, Inhibition of cellular NO on the activity of HCMV IE1 promoter. A luciferase reporter consisting of IE1/2 promoter region was constructed in pMIR-REPORT plasmid (h) and then transfected into HL-60 and THP-1 cells, respectively. HL-60 and THP-1 cells were treated with LV-iNOS or LV-iNOS siRNA to overexpress or knock down iNOS, respectively, prior to NR-1 infection at MOI of 2. Cellular luciferase activity (i) was assayed. Data are presented as the mean ± s.e.m. of three independent experiments. *P < 0.05, **P < 0.01 as determined by the two-tailed t-test (the P values are detailed in Supplementary Table 1). LV, lentivirus vector.