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Maturation of dendritic cells (DC), leading to migration and increased T cell stimulatory capacity, is essential for the initiation of immune responses. This process is triggered by a variety of stimuli, such as inflammatory cytokines, bacterial and viral products. Using a recombinant disabled infectious single cycle herpes simplex virus 1 (HSV-1) encoding green fluorescent protein, we show that the infected DC are defective in up-regulating co-stimulatory molecules, do not produce cytokines, and do not acquire responsiveness to chemokines required for migration to secondary lymphoid organs. These results reveal yet another strategy used by HSV-1 to evade the immune response, namely the inhibition of signaling pathways involved in DC maturation.

Original publication




Journal article


Eur J Immunol

Publication Date





3245 - 3253


Cell Adhesion Molecules, Cell Differentiation, Cells, Cultured, Dendritic Cells, Herpesvirus 1, Human, Humans, Interleukin-10, Interleukin-6, Lymphocyte Activation, Membrane Glycoproteins, Nectins, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Member 14, Receptors, Virus, T-Lymphocytes, Tumor Necrosis Factor-alpha