The ability to infect non-dividing cells sets aside lentiviruses such as HIV-1 from the animal onco-retroviruses which are only able to infect actively dividing cells. This difference in lentivirus and oncovirus biology can be attributed to the relative ability of the reverse transcription complex (preintegration complex) of the virus to enter the nucleus. For lentiviruses such as HIV, active transport processes facilitate this translocation. By contrast, nuclear membrane breakdown at mitosis is required before the reverse transcription complex of onco-retroviruses can enter the nucleus. Several components of the HIV reverse transcription complex that facilitate its nuclear transport have now been identified and an analysis of these import factors is yielding insight into how opposing targeting functions of viral proteins are regulated.