Ini1/hSNF5 is dispensable for retrovirus-induced cytoplasmic accumulation of PML and does not interfere with integration

Retroviral infection triggers the cytoplasmic translocation of two Crm1-dependent shuttle factors, namely the Inil (integrase interactor 1, hSNF5) and the promyelocytic leukemia (PML) protein. Blocking nuclear export of shuttle factors by leptomycin B increases the efficiency of retroviral integration, suggesting that some may mediate antiviral activity. While PML was shown to counteract proviral establishment, it remained unclear whether Inil, a protein implicated in various processes during human immunodeficiency virus replication, has the same potential. Employing RNA interference-mediated knockdown of Ini1, we show here that the simultaneous accumulation of both proteins in the cytoplasm likely reflects two non-interdependent phenomena. Furthermore, Inil does not interfere with retroviral integration, as cells lacking Inil show no increased infection susceptibility. (C) 2004 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.