This chapter provides a brief overview of the pathways and mechanisms of cellular nuclear import and relate this to what is currently understood concerning import in three other viral systems: adenovirus, simian virus 40 (SV40), and influenza virus. Following infection-mediated entry into the cytoplasm, retroviral cores form large nucleoprotein complexes (PICs), which undergo reverse transcription and, ultimately, catalyze provirus formation. The ability of these complexes to be specifically imported into the nucleus via nuclear pore complexes (NPCs) explains why nondividing cells can be productively infected with lentiviruses, such as human immunodeficiency virus type 1 (HIV-1), whereas productive infection by the oncoretrovirus murine leukemia virus (MLV) is restricted to proliferating cells. Current evidence suggests that virally encoded protein components of the HIV-1 PIC, particularly integrase (IN) and Vpr, act in concert to target these complexes for nuclear import by recruiting cellular import factors and interacting with the NPCs. The chapter discusses various recent advances made in this complex and fascinating area of HIV-1 biology in relation to models for postentry nuclear import in other retroviral and nonretroviral systems.
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Fouchier et al. (1999) studied this question.
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