Molecular basis of cell cycle dependent HIV-1 replication: Implications for control of virus burden

M. Stevenson, B. Brichacek, N. Heinzinger, S. Swindells, S. Pirruccello, E. Janoff, M. Emerman

Research output: Contribution to journalReview articlepeer-review

26 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)33-45
Number of pages13
JournalAdvances in experimental medicine and biology
StatePublished - 1995

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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