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. Author manuscript; available in PMC: 2013 May 13.
Published in final edited form as: AIDS. 2010 Jan 2;24(1):155–157. doi: 10.1097/QAD.0b013e32833202f5

Fig. 1. HCP5 alleles did not modulate HIV-1 infectivity.

Fig. 1

(a) The major allele (HCP5 WT) or the minor allele (HCP5 mut) of HCP5 cDNA was transiently transfected into TZM-bl cells and subjected to HIV-1 infection with four different HIV-1 viruses (SF162* is the pseudovirus, SF162 and BG1168 are the primary isolates and MN is the T-cell-line-adapted virus). HIV-1 infectivity was measured for early-stage HIV-1 infection by luciferase activity as expressed relative light unit (RLU). Negative controls were TZM-bl cells with no transfection (No Tx) or with an empty vector (Vector) (Inline graphic, no Tx; Inline graphic, vector; Inline graphic, HCPS WT; Inline graphic, HCPS mut). (b) HIV-1 antigen p24 peptide was measured from culture media in SF162-infected TZM-bl cells stably expressing HCP5 alleles, GFP or TRIM5α (from rhesus monkeys) along with control TZM-bl cells at infection days 3, 6 and 9. (Inline graphic, TZM-bl; Inline graphic, GFP; Inline graphic, HCP5 WT; Inline graphic, HCP5 mut; Inline graphic, TRIM5α) (c) Culture supernatants from the infection day 6 were added to fresh TZM-bl cells for a second round of infectivity for 48 h (Inline graphic, p24; Inline graphic, infectivity). Shown are the results of a representative experiment from three independent experiments.