Fig. 1: Vpr counteracts LAPTM5 to promote HIV-1 infection in macrophages.
From: Vpr counteracts the restriction of LAPTM5 to promote HIV-1 infection in macrophages
a Lentiviral shRNA-transduced MDMs were infected with 10 or 100 ng of wild-type or Vpr-defective HIV-1AD8 for 18 days. Before infection, the aliquoted MDMs were lysed for western blotting to assess LAPTM5 and GAPDH expression (Supplementary Fig. 1e). Viral production was measured by p24 ELISA at the indicated time points, and the data were derived from single measurement. b, c Lentiviral shRNA-transduced MDMs were infected with 100 ng of wild-type or Vpr-defective HIV-1 for 18 days. Before infection, aliquoted cells were lysed for western blotting to assess LAPTM5 and GAPDH expression (Supplementary Fig. 1f). Viral production was measured using p24 ELISA at the indicated time points, and the data were derived from single measurement. d, e MDMs were transduced with lentiviral shRNA targeting the 3’-UTR of LAPTM5 transcripts or control, and the shLAPTM5-depleted MDMs were further transduced with or without a lentiviral expression vector of non-tagged LAPTM5. MDMs were further infected with 100 ng of wild-type or Vpr-defective HIV-1AD8 for 18 days and viral production was measured by p24 ELISA at the indicated time points. Data presented are means ± SD of three independent measurements (d). Before HIV-1 infection, the aliquoted shRNA-transduced MDMs were lysed for western blotting to assess LAPTM5 and GAPDH expression (e). All western blot data are representative of three independent experiments; their full-size images are presented in the Source Data.
