CD4 and HIV-1 infection: The inability of these ECs’ HIV-1 Envs to bind to CD4 and trigger cell signals to reorganize and modify the cytoskeleton, to generate a pseudopod where cytoskeleton and cell-surface receptors for HIV-1 infection concentrate [121,123,125] (Figure 3), accounts for the defect of the HIV-1 Envs for the promotion of pore fusion formation and transfer of viral material to primary non-infected CD4+ T cells [121] (Figure 2c,d and Figure 3).