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Figure 6 | Retrovirology

Figure 6

From: GCN5-dependent acetylation of HIV-1 integrase enhances viral integration

Figure 6

Mutations at IN acetylation sites cause a replication defect at the step of integration. (A) HEK 293T cells infected with NL4.3-Luc/IN WT, NL4.3-Luc/IN K264,266,273R, or NL4.3-Luc/IN K258,264,266,273R were analyzed for luciferase activity 48 hours after infection. (B-D) Total DNA extracted from HEK 293T cells infected with the same viral clones as in (A) was analyzed by RT-Q-PCR for total HIV-1 DNA at 24 hours after infection (B), integrated HIV-1 DNA at 48 hours after infection (C) and two-LTR circles at 24 hours after infection (D). In (A-D), results are presented as percentages relative to cells infected with NL4.3-Luc/IN WT virus. Reported values are means ± SEM from three independent experiments. Statistical significance values shown in (A-D) were calculated by using the Student's two-sided t test. Asterisks directly above bars indicate differences between cells infected with mutant viruses and cells infected with wild type virus. ***, P < 0,001; **, P < 0,01. Conversely, where asterisks are not present, values obtained did not significantly differ (P > 0,05) from those obtained with cells infected with wild type virus. (E) RT activity detected in the culture supernatants of CEM cells at different time points after infection with NL4.3/IN WT, NL4.3/IN K264,266,273R, or NL4.3/IN K258,264,266,273R. (F) Infections performed as in (E), using 10-fold lower viral loads.

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