The oral commensal, Streptococcus gordonii, synergizes with Tat protein to induce HIV-1 promoter activation in monocytes/macrophages

Trans-activator of transcription (Tat) is an HIV-1 protein essential for viral replication. Oral periodontopathogens (e.g. Fusobacterium nucleatum) enhance HIV-1LTR promoter activation in monocytes/macrophages in absence of Tat; however, some oral commensals fail to trigger this response. We sought to determine the effect of Tat on HIV-1LTR promoter activation induced by the representative oral commensal Streptococcus gordonii in monocytes/macrophages. S. gordonii enhanced HIV-1LTR reactivation in THP89GFP (Tat(+)), but not in BF24 (Tat(-)) cells. Interestingly, S. gordonii, but not Streptococcus sanguinis enhanced HIV-1LTR activation in the presence of recombinant Tat in BF24 cells. This response correlated with IL-8 but not TNF alpha or IL-6 production, and was abrogated by the NF kappa B inhibitor BAY 11-7082. Kinetics of NF kappa B-RelA activation did not explain the S. gordonii-induced HIV-1LTR activation in presence of Tat. These results suggest that S. gordonii-induced HIV-1 reactivation in monocytes/macrophages is Tat-dependent and appears to involve NF kappa B activation. (C) 2011 Elsevier Inc. All rights reserved.