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. 2020 Jun 19;12(6):665. doi: 10.3390/v12060665

Figure 7.

Figure 7

Proposed model for EV activation of latent HIV-1. Uninfected EVs from healthy cells are taken up by HIV-1 latent infected cells, leading to the phosphorylation and activation of receptor tyrosine kinases (RTK) by c-Src. RTK then activates PI3K, which in turn activates AKT. Following activation, AKT phosphorylates mTOR, resulting in the phosphorylation and activation of the transcription inducer, STAT3. STAT3 then recruits the cofactor SRC-1, before translocating to the nucleus and promoting HIV-1 transcription by recruiting p300 (promotes chromatin remodeling). NF-κB and RNA Pol II increase loading onto the HIV-1 promoter, resulting in the transcription of latent HIV-1.