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Figure 7 | Retrovirology

Figure 7

From: The phosphorylation of HIV-1 Gag by atypical protein kinase C facilitates viral infectivity by promoting Vpr incorporation into virions

Figure 7

The inhibition of aPKC significantly reduces replication competent HIV-1 infection. (A) Schema of the experimental system using HIV-1 replication competent HIV-189.6 and HIV-1NLAD-8. Monocytes were isolated from buffy coat from healthy blood donors by positive selection on Monocyte Enrichment Cocktail and density gradient centrifugation as described in Methods. MDMs were generated by culturing monocytes with 100 ng/ml granulocyte-macrophage colony-stimulation factor for 5 days before HIV-1 infection. MDMs were infected with 5 ng of p24 from (B) HIV-189.6 or (C) HIV-1NLAD-8 virus and the levels of p24 capsid released into media during viral replication were assayed over a period of 12 days post infection. Data are the mean ± s.e.m. of three independent experiments: **P < 0.01, Student’s t-test. (D) Effects of aPKC inhibitor on viability of MDMs. MDMs cells were treated with aPKC inhibitor (2 or 5 μM) or 1 μM Staurosporine (STS) and analysed for cell viability using trypan blue exclusion at 96 hours. (E) Schematic model of our current study. aPKC phosphorylate HIV-1 Gag at Ser487. This phosphorylation promotes the interaction between Gag and Vpr, thereby facilitating viral infectivity in macrophages.

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