Here, we develop a mathematical framework that defines how manipulating CD4 T cell trafficking could influence HIV-1 control. By boosting the traffic of CD4 T cells harboring virus out of drug sanctuaries to regions where antiretroviral drugs effectively penetrate, the virus cannot continue to replenish the persistent viral reservoir. Our analyses show that if the rate of trafficking of infected CD4 T cells exceeds a certain critical threshold, ongoing cycles of viral replication in drug sanctuaries become unsustainable. This strategy points towards a novel adjunct strategy to the treatment of HIV-1 infection and a promising new approach to a functional cure.