Despite the clinical importance of Highly Active Antiretroviral Therapy (HAART), the Human Immunodeficiency Virus-1 (HIV-1) remains latently infecting various immune cell reservoirs (e.g. T cells, macrophages, dendritic cells). Several bacterial and host products have the capacity to regulate HIV-1 recrudescence. OBJECTIVE: To determine the ability of oral keratinocytes (OKF4) and gingival fibroblasts (HGF) to activate the HIV-1 LTR promoter in BF24 macrophages (mf) using a co-culture model, following challenge with P.gingivalis (Pg) or T.denticola (Td). METHODS: Three different co-culture systems were used: (1) Bacterial challenge of HGF/OKF4 prior to co-culture with BF24 mf (2) HGF/OKF4 priming of BF24 mf prior to bacterial challenge in co-culture, (3) Challenge of BF24 mf with bacteria following priming of BF24 mf with HGF/OKF4. HIV-1 reactivation was measured using a CAT colorimetric assay. RESULTS: HIV-1 reactivation in BF24 mf was significantly increased in all three co-culture systems by Pg challenge in the presence of OKF4 host cells, whereas Td addition to this system down-regulated the promoter activation. OKF4 also induced HIV-1 reactivation in absence of bacteria. HIV-1 reactivation induced by both Pg and Td was significantly reduced in presence of HGF in the co-cultures. CONCLUSIONS: Interactions of oral nonimmune cells (epithelial, fibroblasts), oral pathogens, and HIV-1 latently infected mf can differentially regulate the reactivation of HIV-1. These interactions appear to be microorganism and cell type-dependent. Furthermore, these results suggest that host factors from resident cells of the periodontium can interact with periodontopathogens resulting in stimulation or inhibition of HIV-1 reactivation in latently-infected mf. Supported by NIH grant P20RR020145

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