PERMISSIVENESS of the host cell to productive infection by onco-retroviruses is cell-cycle dependent¹, and nuclear localization of viral nucleoprotein preintegration complexes will occur only after cells have passed through mitosis². In contrast, establishment of an integrated provirus after infection by the lentivirus HIV-1 is independent of host cell proliferation^3–5. The ability of HIV-1 to replicate in non-dividing cells is partly accounted for by the kary-ophilic properties of the viral preintegration complex which, after virus infection, is actively transported to the host cell nucleus. Here we report that the gag matrix protein of HIV-1 contains a nuclear localization sequence which, when conjugated to a heterologous protein, directs its nuclear import. In addition, HIV-1 mutants containing amino-acid substitutions in this nuclear localization signal integrate and replicate within dividing but not growth-arrested cells, and thus display a phenotype more representative of an onco-retrovirus.