Recently both Van't Wout et al. (69) and Krishnan and Zeichner (70) have provided evidence that the expression of several cellular RNA helicases including DDX24, DDX21, DDX18, DDX11 and DDX9 is modulated during HIV-1 infection; however, the precise cellular role and significance of these helicases for HIV-1 pathogenesis have not be characterized. Interestingly, Krishnan and Zeichner reported microarray data which examined the transition of HIV-1 infection from latency to productive replication, and found that several cellular RNA helicases were upregulated (71) . For future understanding of functions, it will be important to design experiments which can segregate helicases which serve direct, although perhaps overlapping and redundant, roles on HIV-1 from those that might participate indirectly in the viral life cycle. Nevertheless, the convergence of evidence would support that several discrete cellular RNA helicases contribute importantly to the efficient execution of several steps in the HIV-1 replicative cycle.