N-terminally truncated POM121C inhibits HIV-1 replication

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  • 野田, 岳志
    Department of Molecular Virology, Graduate School of Medicine, Tokyo Medical and Dental University
  • Takeuchi, Hiroaki
    Department of Molecular Virology, Graduate School of Medicine, Tokyo Medical and Dental University
  • Masuda, Takao
    Department of Immunotherapeutics, Tokyo Medical and Dental University
  • Noda, Takeshi
    Division of Ultrastructural Virology, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo･PRESTO, Japan Science and Technology Agency･Laboratory of Ultrastructural Virology, Institute for Frontier Life and Medical Sciences, Kyoto University
  • Yamaoka, Shoji
    Department of Molecular Virology, Graduate School of Medicine, Tokyo Medical and Dental University
  • Yuntao Wu
    editor

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説明

Recent studies have identified host cell factors that regulate early stages of HIV-1 infection including viral cDNA synthesis and orientation of the HIV-1 capsid (CA) core toward the nuclear envelope, but it remains unclear how viral DNA is imported through the nuclear pore and guided to the host chromosomal DNA. Here, we demonstrate that N-terminally truncated POM121C, a component of the nuclear pore complex, blocks HIV-1 infection. This truncated protein is predominantly localized in the cytoplasm, does not bind to CA, does not affect viral cDNA synthesis, reduces the formation of 2-LTR and diminished the amount of integrated proviral DNA. Studies with an HIV-1-murine leukemia virus (MLV) chimeric virus carrying the MLV-derived Gag revealed that Gag is a determinant of this inhibition. Intriguingly, mutational studies have revealed that the blockade by N-terminally-truncated POM121C is closely linked to its binding to importin-β/karyopherin subunit beta 1 (KPNB1). These results indicate that N-terminally-truncated POM121C inhibits HIV-1 infection after completion of reverse transcription and before integration, and suggest an important role for KPNB1 in HIV-1 replication.

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  • PLOS ONE

    PLOS ONE 12 (9), e0182434-, 2017-09-05

    Public Library of Science (PLoS)

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