       Document 0073
 DOCN  M9610073
 TI    Molecular basis of cell cycle dependent HIV-1 replication. Implications
       for control of virus burden.
 DT    9601
 AU    Stevenson M; Brichacek B; Heinzinger N; Swindells S; Pirruccello S;
       Janoff E; Emerman M; Department of Pathology and Microbiology,
       University of Nebraska; Medical Center, Omaha 68198-5120, USA.
 SO    Adv Exp Med Biol. 1995;374:33-45. Unique Identifier : AIDSLINE
       MED/96047236
 AB    Research is beginning to yield insight into determinants which govern
       cell cycle dependence of provirus establishment by the
       onco-retroviruses. In the case of HIV-1, nucleophilic components
       associated with the viral preintegration complex facilitate mitosis
       independent nuclear localization of viral DNA and provirus
       establishment. Differences in the metabolic activity between G0 T cells
       and macrophages, the two primary targets for HIV-1 infection, lead to
       significantly different outcomes with regards to provirus establishment
       following infection of these cells. Thus, macrophages appear fully
       permissive to productive HIV-1 replication while non-dividing (G0 T
       cells) restrict virus replication at a step which proceeds nuclear
       import of viral DNA. The requirement for T cell activation in productive
       HIV-1 replication has important implications for the relationship
       between immune activation and virus burden. It remains to be determined
       whether modulating the immune activation status of the infected
       individual may provide an opportunity for modulating virus burden and
       influencing disease course.
 DE    Acquired Immunodeficiency Syndrome/IMMUNOLOGY/*PHYSIOPATHOLOGY  Animal
       Cell Nucleus/METABOLISM  Human  HIV-1/*PHYSIOLOGY  Lymphocyte
       Transformation  Mitosis/IMMUNOLOGY  Nucleic Acids/METABOLISM
       T-Lymphocytes/IMMUNOLOGY  *Virus Replication  JOURNAL ARTICLE  REVIEW
       REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

