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J. Exp. Med.,
Volume 189, Number 9, May 3, 1999 1391-1398
By
From the * Regional Primate Research Center and the We previously found that activation of primary CD4+ T cells via both the T cell antigen receptor (TCR) and CD28 is required for HIV-1 DNA to be translocated from the cytoplasm to
the nucleus. Here we report that expression of c-Myc protein in CD4+ T cells is induced only
after such costimulation. In addition, cyclosporin A not only inhibits nuclear import of HIV-1
DNA but also inhibits expression of c-Myc protein. Because of these correlations, we tested
whether c-Myc is necessary for nuclear import of HIV-1 DNA. Specific c-myc antisense, but
not sense or non-sense, phosphorothioate oligodeoxynucleotides selectively induced the accumulation of two NH2-terminally truncated c-Myc proteins and abolished HIV-1 genome entry
into host nuclei. Consequently, both virus replication and HIV-1-induced apoptotic cell death
were inhibited. Synthesis of viral full-length DNA was not affected. Specific c-myc antisense oligonucleotide inhibited HIV-1 infection under conditions that did not affect cell cycle entry or
proliferation. Thus, c-Myc appears to regulate HIV-1 DNA nuclear import via a mechanism
distinct from those controlling entry into the cell cycle.
Department of Microbiology, University of
Washington, Seattle, Washington 98195
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