Journal
VIROLOGY
Volume 361, Issue 2, Pages 325-334Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2006.11.014
Keywords
HIV-1; reservoir; cell-cell contact; latency; co-culture
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Reservoir cells latently infected with HIV-1 pose one of the major obstacles that hamper ultimate eradication of HIV-1 from infected patients. In this report, we showed that direct contact with MOLT-4 T cells induced HIV-1 replication ill J(22)-HL-60 latently infected cells without any additional stimulus. Neutralization experiments revealed that pro-inflammatory cytokines, whose production was increased following cell-cell contact, were unlikely to be primarily involved in the induced HIV-1 replication. Cell-cell contact, but not soluble components in the culture supernatant, caused a rapid phosphorylation and degradation of I kappa B alpha, which led to elevated NF-kappa B DNA binding activity in J(22)-HL-60 cells. Furthermore, forced expression of a super-repressor form Of I kappa B alpha or pretreatment with ritonavir efficiently blocked the activation of NF-kappa B and HIV-1 replication in J(22)-HL-60 cells co-cultured with MOLT-4 T cells. Moreover, either resting or PHA stimulated primary CD4(+) T cells induced HIV-1 replication ill J(22)-HL-60 cells in a similar way with that of MOLT-4 cells. These results indicated that direct contact with CD4(+) T cells induced HIV-1 replication in latently infected cells and provide insight into the molecular mechanism of virus release from myeloid progenitor cells latently infected with HIV-1. (c) 2006 Elsevier Inc All rights reserved.
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