Given the opposite effects of CXCR4 and CD2 prestimulation on HIV-1 latent infection as demonstrated above (Figure 1) (Wang et al., 2012; Yoder et al., 2008), we speculated that CD2-initiated cofilin and actin polymerization may spatially compete with the HIV-1/CXCR4-initiated cofilin and actin activity that is needed for viral entry and nuclear migration. The gene discussed is CXCR4; the disease is disease arising from reactivation of latent virus.