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1996-01-30
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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).