A nuclear localization signal within HIV-1 matrix protein that governs infection of non-dividing cells

Michael I. Bukrinsky, Sheryl Haggerty, Michael P. Dempsey, Natalia Sharova, Alexei Adzhubei, Lynn Spitz, Paul Lewis, David Goldfarb, Michael Emerman, Mario Stevenson

Research output: Contribution to journalArticlepeer-review

709 Scopus citations

Abstract

PERMISSIVENESS of the host cell to productive infection by onco-retroviruses is cell-cycle dependent1, and nuclear localization of viral nucleoprotein preintegration complexes will occur only after cells have passed through mitosis2. In contrast, establishment of an integrated provirus after infection by the lentivirus HIV-1 is independent of host cell proliferation3-5. The ability of HIV-1 to replicate in non-dividing cells is partly accounted for by the kary-ophilic properties of the viral preintegration complex which, after virus infection, is actively transported to the host cell nucleus. Here we report that the gag matrix protein of HIV-1 contains a nuclear localization sequence which, when conjugated to a heterologous protein, directs its nuclear import. In addition, HIV-1 mutants containing amino-acid substitutions in this nuclear localization signal integrate and replicate within dividing but not growth-arrested cells, and thus display a phenotype more representative of an onco-retrovirus.

Original languageEnglish (US)
Pages (from-to)666-669
Number of pages4
JournalNature
Volume365
Issue number6447
DOIs
StatePublished - Jan 1 1993

ASJC Scopus subject areas

  • General

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