Fig. 6 |. US28-KO cannot establish latency in human CD34⁺ HPCs because it fails to activate the STAT3–iNOS–NO axis and reprogramme HPCs to an immunosuppressive monocyte subset.

a–c, US28-KO or Mock infection in human HPCs failed to activate STAT3 (a), or increase cellular levels of iNOS (b) and NO (c). d,e, US28-KO infection failed to reprogramme HPCs to the B7-H4⁺CD16⁺ immunosuppressive monocyte subset, as indicated by negative or low expression of B7-H4 and CD16 (d), as well as no suppression of CD4 T-cell proliferation (e). f, US28-KO infection failed to achieve latency in HPCs. g, Levels of viral genome and IE1 expression in HPCs infected with US28-KO or NR-1. h, NOS overexpression suppressed viral IE1 and genome expression in the HPCs infected with US28-KO. i, iNOS overexpression decreased the apoptotic rate of US28-KO-infected HPCs. j,k, Depleting cellular NO by NG-M-L-Arg abolished the effect of iNOS overexpression on facilitating US28-KO latency. NG-M-L-Arg depleted NO in US28-KO-infected HPCs that were overexpressed with iNOS (j), leading to significant increase of HCMV IE1 and genome levels (k). Data are presented as the mean ± s.e.m. of three independent experiments. **P < 0.01, ***P < 0.001 as determined by the two-tailed t-test (the P values are detailed in Supplementary Table 1).