Figure 4.

HIV post-entry process and replication in Th17 cells. Th17 cells and HIV have different interactions (activating in black arrows and inhibiting in red arrows) to promote HIV replication in these cells. (A) In the mTOR pathway: at an early stage of the infection, HIV stops the autophagy mechanism directed by mTORc1 to block the elimination of invading viruses. At a later stage, HIV interacts with mTORc1 to hijack the autophagy mechanism to help form new viruses. By interacting with HIV or its proteins (Env, Tat, or Nef), mTORc1 also increases Th17 proliferation, HIV protein production, HIV replication, and latency. (B) by interaction with NF-κB: increased production of TNFα and TLR2 ligation increase in Th17 cells NF-κB translocation and activity, leading to increased HIV replication. Increased NF-κB activity also increases the activity of the mTORc1 pathway and the activation and survival of T cells. (C) Th17 cells exhibit Vif-mediated degradation of the HIV restriction factor, APOBEC3G. (D) SAMHD1 and Grb2 are downregulated in Th17 cells, allowing increased HIV transactivation and replication. (E) RNase2, RNAse3, and RNAse6 genes known to inhibit viral replication are downregulated in Th17 cells.