Figures & data
Figure 1. Reversal of HIV latency (graphics: Ken Kragsfeldt. Modified from Richman DD. et al. Science 2009 [Citation4] with permission from Richman DD.). Latency reversing agents (LRAs) can disrupt HIV-1 latency through different mechanisms: Protein kinase C (PKC) activators stimulates via kinase signaling and the PKC pathway. Second mitochondria-derived activator of caspases mimetics (SMACm) stimulates the NF-κB pathway. DNA methyltransferase inhibitors (DNMTi) decrease methylation of the HIV-1 promoter in the long terminal repeat (LTR). Histone deacetylase (HDACi) and methyltransferase inhibitors (HMTi) prevent removal of acetyl groups and attachment of methyl groups to the histone, respectively. Bromodomain inhibitors (BRDi) might favor competitive binding of the viral transactivation protein (Tat) to the positive transcription elongation factor b (p-TEFb) complex and/or affect transcription factors. Hexamethylbisacetamide (HMBA) stimulates p-TEFb in the absence of Tat. Hydroxybenzotrialzole and interleukin-7 (IL-7) stimulates the JAK/STAT pathway. Toll-like receptor (TLR) 7/9 agonists stimulate the plasmacytoid dendritic cells (pDC) to produce cytokines that activates the T cell and thus HIV-1 transcription.
![Figure 1. Reversal of HIV latency (graphics: Ken Kragsfeldt. Modified from Richman DD. et al. Science 2009 [Citation4] with permission from Richman DD.). Latency reversing agents (LRAs) can disrupt HIV-1 latency through different mechanisms: Protein kinase C (PKC) activators stimulates via kinase signaling and the PKC pathway. Second mitochondria-derived activator of caspases mimetics (SMACm) stimulates the NF-κB pathway. DNA methyltransferase inhibitors (DNMTi) decrease methylation of the HIV-1 promoter in the long terminal repeat (LTR). Histone deacetylase (HDACi) and methyltransferase inhibitors (HMTi) prevent removal of acetyl groups and attachment of methyl groups to the histone, respectively. Bromodomain inhibitors (BRDi) might favor competitive binding of the viral transactivation protein (Tat) to the positive transcription elongation factor b (p-TEFb) complex and/or affect transcription factors. Hexamethylbisacetamide (HMBA) stimulates p-TEFb in the absence of Tat. Hydroxybenzotrialzole and interleukin-7 (IL-7) stimulates the JAK/STAT pathway. Toll-like receptor (TLR) 7/9 agonists stimulate the plasmacytoid dendritic cells (pDC) to produce cytokines that activates the T cell and thus HIV-1 transcription.](/cms/asset/3cc7dbfa-cd78-42d2-b07b-550b3829c04b/ierz_a_1164031_f0001_oc.jpg)