Model 5 further highlights that any intervention that increases the trafficking rate of free virus, in addition to, or instead of, CD4 T cells, is capable of halting ongoing replication in drug sanctuaries. This is one putative mechanism for how antibodies that bind α4β7 –an integrin involved in gut homing  and demonstrated to integrate into the envelope of HIV-1 –have led to significantly improved control in simian immunodeficiency virus (SIV) infected monkeys  (S6 Text). Furthermore, Model 3 shows that just reducing the inflow of CD4 T cells into, or increasing the outflow of CD4 T cells from drug sanctuaries, can also be sufficient to halt persistent replication. This explicitly highlights a fundamental concept of our study: that any intervention that reduces the average residency time of infected CD4 T cells in the drug sanctuaries can halt persistent replication in these regions.