Human immunodeficiency virus infection of cells arrested in the cell cycle

EMBO J. 1992 Aug;11(8):3053-8.

Abstract

Cell proliferation is necessary for proviral integration and productive infection of most retroviruses. Nevertheless, the human immunodeficiency virus (HIV) can infect non-dividing macrophages. This ability to grow in non-dividing cells is not specific to macrophages because, as we show here, CD4+ HeLa cells arrested at stage G2 of the cell cycle can be infected by HIV-1. Proliferation is necessary for these same cells to be infected by a murine retrovirus, MuLV. HIV-1 integrates into the arrested cell DNA and produces viral RNA and protein in a pattern similar to that in normal cells. In addition, our data suggest that the ability to infect non-dividing cells is due to one of the HIV-1 core virion proteins. HIV infection of non-dividing cells distinguishes lentiviruses from other retroviruses and is likely to be important in the natural history of HIV infection.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Base Sequence
  • CD4 Antigens / physiology
  • Cell Cycle / physiology*
  • Cell Cycle / radiation effects
  • Cell Division / physiology
  • Chromosome Deletion
  • G2 Phase
  • Genes, Viral*
  • Genes, tat
  • HIV-1 / genetics
  • HIV-1 / physiology*
  • HeLa Cells
  • Humans
  • Leukemia Virus, Murine / genetics
  • Leukemia Virus, Murine / physiology
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides
  • Plasmids
  • Polymerase Chain Reaction / methods
  • Virus Replication* / radiation effects
  • beta-Galactosidase / biosynthesis
  • beta-Galactosidase / genetics

Substances

  • CD4 Antigens
  • Oligodeoxyribonucleotides
  • beta-Galactosidase