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Role of the karyopherin pathway in human immunodeficiency virus type 1 nuclear import

Academic Article
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Overview

authors

  • Gallay, Philippe
  • Stitt, V.
  • Mundy, C.
  • Oettinger, M.
  • Trono, D.

publication date

  • February 1996

journal

  • Journal of Virology  Journal

abstract

  • The interaction of the human immunodeficiency virus type 1 (HIV-1) nucleoprotein complex with the cell nuclear import machinery is necessary for viral replication in macrophages and for the establishment of infection in quiescent T lymphocytes. The karyophilic properties of two viral proteins, matrix (MA) and Vpr, are keys to this process. Here, we show that an early step of HIV-1 nuclear import is the recognition of the MA nuclear localization signal (NLS) by Rch1, a member of the karyopherin-alpha family. Furthermore, we demonstrate that an N-terminally truncated form of Rch1 which binds MA but fails to localize to the nucleus efficiently blocks MA- but not Vpr-mediated HIV-1 nuclear import. Correspondingly, NLS peptide inhibits the nuclear migration of MA but not that of Vpr and prevents the infection of terminally differentiated macrophages by vpr-defective virus but not wild-type virus. These results are consistent with a model in which Rch1 or another member of the karyopherin-alpha family, through the recognition of the MA NLS, participates in docking the HIV-1 nucleoprotein complex at the nuclear pore. In addition, our data suggest that Vpr governs HIV-1 nuclear import through a distinct pathway.

subject areas

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Carrier Proteins
  • Cell Line
  • Cell Nucleus
  • DNA Primers
  • Gene Products, vpr
  • HIV-1
  • Humans
  • Molecular Sequence Data
  • Nucleoproteins
  • Viral Matrix Proteins
  • alpha Karyopherins
  • vpr Gene Products, Human Immunodeficiency Virus
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Identity

PubMed Central ID

  • PMC189908

International Standard Serial Number (ISSN)

  • 0022-538X

PubMed ID

  • 8551560
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Additional Document Info

start page

  • 1027

end page

  • 1032

volume

  • 70

issue

  • 2

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