Immunomodulation frequently occurs during viral infections; the mechanisms of which are continually being defined at the cellular and tissue levels. Recently, a study of the effects of HIV-1 on dendritic cells (DCs) identified inflammatory chemokines as highly upregulated during HIV-1 infection and during viral Tat expression in monocyte-derived DCs. It is becoming increasingly clear that HIV-1 has evolved multiple strategies to ensure the maintenance of a local pool of susceptible cells for additional rounds of virus replication.