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The Toll-like receptor (TLR) 7 is highly expressed by immune cells including macrophages. Agonists to TLR7 are attractive therapeutic agents as they have the potential of activating both innate and acquired immunity against viral infections. Imiquimod, a specific TLR7 agonist, has been successfully used for the topical treatment of genital/perianal warts in immunocompetent individuals. Here we examined the anti-HIV effect of imiquimod in primary human macrophages and demonstrated that TLR7 activation by imiquimod could effectively inhibit infection of the cells by different strains of HIV. Further mechanistic studies revealed that while imiquimod had little effect on interferons expression, its treatment of macrophages resulted in the increased production of the CC chemokines, the natural ligands of the HIV entry co-receptor CCR5, and decreased expression of CD4 and CCR5. These findings are clinically important and indicate that activating the intracellular antiviral immunity by imiquimod has the potential for developing TLR7 agonist-based therapy for HIV infection.

The Toll-like receptor (TLR) 7 is a viral sensor for detecting single-stranded ribonucleic acid (ssRNA), the activation of which can induce intracellular innate immunity against viral infections. Imiquimod, a synthetic ligand for TLR7, has been successfully used for the topical treatment of genital/perianal warts in immunocompetent individuals. We studied the effect of imiquimod on the human immunodeficiency virus (HIV) infection of primary human macrophages and demonstrated that the treatment of cells with imiquimod …