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Title: Cell cycle regulation of human immunodeficiency virus type 1 integration in T cells: antagonistic effects of nuclear envelope breakdown and chromatin condensation

Journal Article · · Virology
 [1];  [2];  [3]
  1. EMI-0013 Institut National de la Sante et de la Recherche Medicale-Universite Paris 7, 75010 Paris (France) and Laboratoire d'Immunologie Cellulaire et Immunopathologie de l'Ecole Pratique des Hautes Etudes, Institut Universitaire d'Hematologie, hopital Saint-Louis, 75010 Paris (France) and Laboratoire de Biochimie and JFR 3012 Associee a l'Agence Universitaire Francophone (AUPELF-UREF), Faculte des Sciences, Rabat (Morocco)
  2. EMI-0013 Institut National de la Sante et de la Recherche Medicale-Universite Paris 7, 75010 Paris (France) and Laboratoire d'Immunologie Cellulaire et Immunopathologie de l'Ecole Pratique des Hautes Etudes, Institut Universitaire d'Hematologie, hopital Saint-Louis, 75010 Paris (France)
  3. EMI-0013 Institut National de la Sante et de la Recherche Medicale-Universite Paris 7, 75010 Paris (France) and Laboratoire d'Immunologie Cellulaire et Immunopathologie de l'Ecole Pratique des Hautes Etudes, Institut Universitaire d'Hematologie, hopital Saint-Louis, 75010 Paris (France); and others

We examined the influence of mitosis on the kinetics of human immunodeficiency virus type 1 integration in T cells. Single-round infection of cells arrested in G1b or allowed to synchronously proceed through division showed that mitosis delays virus integration until 18-24 h postinfection, whereas integration reaches maximum levels by 15 h in G1b-arrested cells. Subcellular fractionation of metaphase-arrested cells indicated that, while nuclear envelope disassembly facilitates docking of viral DNA to chromatin, chromosome condensation directly antagonizes and therefore delays integration. As a result of the balance between the two effects, virus integration efficiency is eventually up to threefold greater in dividing cells. At the single-cell level, using a green fluorescent protein-expressing reporter virus, we found that passage through mitosis leads to prominent asymmetric segregation of the viral genome in daughter cells without interfering with provirus expression.

OSTI ID:
20637175
Journal Information:
Virology, Vol. 329, Issue 1; Other Information: DOI: 10.1016/j.virol.2004.08.022; PII: S0042-6822(04)00515-X; Copyright (c) 2004 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0042-6822
Country of Publication:
United States
Language:
English