An additive effect was seen with inhibition of HDAC-6 as well. These findings support data regarding the selectivity of class I HDAC-1, −2 and −3 for induction of HIV-1 gene expression. However, preserving the deacetylated status of HDAC-6 prevents HIV-1 infected CD4+ T cells from Env-mediated syncytia formation (49). Therefore, analogs that have inhibitory properties targeting HDAC-6 may not be optimal.