title: HIV-1 Vpr: G2 cell cycle arrest, macrophages and nuclear transport.
abstract: HIV-1 possesses six open reading frames in addition to the gag, pol, and env shared by all retroviruses. One of these accessory genes, vpr, is required for maximal viral replication in macrophages. The molecular mechanism underlying this effect may be related to one of the unusual properties of the encoded protein: some believe Vpr promotes nuclear translocation of preintegration complexes in non-dividing cells; also, Vpr arrests the cell cycle in G2 by inhibiting an upstream activator of p34cdc2-cyclin B. Elucidation of Vpr-cell cycle interactions may provide insight into both HIV-1 and basic cell biology.
authors.affiliation: Department of Microbiology, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.
authors.forename: F
authors.initials: F
authors.lastname: Re
authors.forename: J
authors.initials: J
authors.lastname: Luban
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology; D002467:Cell Nucleus / Q000821:virology; D016195:G2 Phase / Q000502:physiology*; D016336:Gene Products, vpr / Q000502:physiology*; D016334:Genes, vpr; D015497:HIV-1 / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D008264:Macrophages / Q000821:virology; D014779:Virus Replication / Q000235:genetics / Q000502:physiology; D054325:vpr Gene Products, Human Immunodeficiency Virus
chemical_list: D016336:Gene Products, vpr; D054325:vpr Gene Products, Human Immunodeficiency Virus