The ability to infect non-dividing cells sets aside lentiviruses such
as HIV-1 from the animal onco-retroviruses which are only able to infe
ct actively dividing cells. This difference in lentivirus and oncoviru
s biology can be attributed to the relative ability of the reverse tra
nscription complex (preintegration complex) of the virus to enter the
nucleus. For lentiviruses such as HIV, active transport processes faci
litate this translocation. By contrast, nuclear membrane breakdown at
mitosis is required before the reverse transcription complex of onco-r
etroviruses can enter the nucleus. Several components of the HIV rever
se transcription complex that facilitate its nuclear transport have no
w been identified and an analysis of these import factors is yielding
insight into how opposing targeting functions of viral proteins are re
gulated.