Figure 1.

Mechanism of CNS–HIV infection along with the relative therapeutic targets. 1. Selective killing of migrant macrophages (MGBM); 2. neutralization of Vif on microvascular endothelial cells (IFNα and IFNγ) and subsequent inhibition of viral entry into the CNS; 3. inhibition of HIV replication in macrophages and viral spread into the CNS (NK-1-agonists); 4. inhibition of cytoprotective effect exerted by Tat proteins over microglial cells which act as CNS viral reservoirs (PI3K and Akt inhibitors); 5. protection of neural integrity and plasticity along with prevention of neurotoxicity and neuronal death (glutamate receptors-, GSK3β-, JNK-, and p38-inhibitors).