Skip to main content
. Author manuscript; available in PMC: 2020 Apr 21.
Published in final edited form as: Nat Microbiol. 2019 Oct 21;4(12):2044–2051. doi: 10.1038/s41564-019-0592-5

Fig. 1. Disruption of the CA-CypA interaction in primary human blood cells renders HIV-1 susceptible to restriction by TRIM5.

Fig. 1.

a, Macrophages, b, dendritic cells, or c and d, CD4+ T cells, were selected after transduction with a lentivirus expressing shRNA targeting TRIM5 or Luc control, and challenged with single-cycle, VSV G-pseudotyped, HIV-1NL4–3GFP (a-c) or HIV-1ZM249MGFP (d), bearing WT CA or CA-P90A (mean ± SEM, n = 3 donors for each). e, TRIM5 knockdown or Luc knockdown macrophages were challenged with HIV-1NL4–3GFP in the presence of 8 μM CsA or DMSO solvent (mean ± SEM, n = 4 donors). f, TRIM5 knockdown or Luc knockdown CD4+ T cells were challenged with HIV-1ZM249MGFP in the presence of 2.5 μM GS-CypAi3 or DMSO solvent (mean ± SEM, n = 3 donors). g, Macrophages were transduced simultaneously with two vectors expressing shRNAs, as indicated, and selected with puromycin and blasticidin. Cells were then challenged with HIV-1NL4–3GFP (mean ± SEM, n = 3 donors). The percentage of GFP+ cells was assessed by flow cytometry and normalized to WT in Luc control knockdown cells in all cases. Significance was determined by two-tailed, paired t-test.