Hence, our data indicate that cell
signals that promote HDAC6 transcription and its subsequent
cytoplasmic export should induce a more protective
phenotype to host cells against HIV-1 infection. Accordingly,
the different cellular levels of HDAC6 could account
for the differential susceptibility shown by some cell types to
HIV-1 viral infection in vitro. However, it is also feasible that
under certain conditions, HDAC6 could be located in the
nucleus and participate in the control of HIV-1 replication
by repressing LTR activation.