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. 2019 Aug 20;10(4):e01344-19. doi: 10.1128/mBio.01344-19

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Copyright © 2019 Wang and Su.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

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FIG 6 — The Vpr-TET2 axis independently enhances HIV-1 replication through reduced IFITM3 and sustained IL-6 expression. (A) Vpr-enhanced Env processing is independent of IL-6 signaling. MDMs were infected with HIV-1 or HIV-1 ΔVpr viruses for 4 days, with NVP added at 2 dpi, and treated with the isotype control or anti-IL-6 neutralizing antibody. Western blots were performed with cell lysates. Env proteins gp160 and gp120 were detected with anti-gp120 antibody, gp41 was detected by anti-gp41 antibody, and p24 was detected by anti-p24 antibody. gp120/p24 and gp120/gp160 ratios are shown. (B) MDMs transduced with control shRNA, shTET2, and shIFITM3 were infected with HIV-1 or HIV-1 ΔVpr and treated with the isotype control or anti-IL-6 neutralizing antibody. p24 levels in the supernatant were measured at 6 dpi. (C) Relative ability of Vpr to enhance HIV-1 replication in cells treated with the isotype control and anti-IL-6 neutralizing antibody at day 6. Data from two different donors are summarized by setting Vpr-enhanced replication in isotype control MDMs transduced with control shRNA at 1.0. * indicates P < 0.05. (D) The Vpr-TET2 axis enhances HIV-1 replication in macrophages independently by modulating expression of IFITM3 and IL-6 during HIV-1 infection.