HIV-1 viral protein Vpr is involved in viral replication, nuclear transport of the viral preintegration comples, induction of cell cycle G2 arrest and ultimately cell death. Rhesus monkeys infected with vpr and vpr/vpx defective SIV showed either attenuated or no disease respectively. Defective vpr genes have also been found in long-term survivors, suggesting an important role of Vpr. One of the Vpr-binding proteins identified (VIP4D1) appears to be a protein kinase known to be involved in cell signalling. By testing interaction of VIP4D1 with a panel of point mutants and deletions of vpr (known to affect various Vpr functions) we observed that VIP4D1 failed to interact with G2 arrest-defective mutants. This preliminary observation implicates a potential role of Vpr-VIP4D1 interaction in Vpr-induced cell cycle G2 arrest.