RT Journal Article SR Electronic(1) A1 Prechtel, Alexander T. A1 Turza, Nadine M. A1 Kobelt, Dieter J. A1 Eisemann, Jutta I. A1 Coffin, Robert S. A1 McGrath, Yvonne A1 Hacker, Christine A1 Ju, Xinsheng A1 Zenke, Martin A1 Steinkasserer, AlexanderYR 2005 T1 Infection of mature dendritic cells with herpes simplex virus type 1 dramatically reduces lymphoid chemokine-mediated migration JF Journal of General Virology, VO 86 IS 6 SP 1645 OP 1657 DO https://doi.org/10.1099/vir.0.80852-0 PB Microbiology Society, SN 1465-2099, AB Herpes simplex virus type 1 (HSV-1) is able to establish latency in infected individuals. In order to characterize potential new immune-escape mechanisms, mature dendritic cells (DCs) were infected with HSV-1 and total cellular RNA was isolated from infected and mock-infected populations at different time points. RNA profiling on Affymetrix Human Genome U133A arrays demonstrated a dramatic downregulation of the migration-mediating surface molecules CCR7 and CXCR4, an observation that was further confirmed by RT-PCR and fluorescence-activated cell sorting analyses. Furthermore, migration assays revealed that, upon infection of mature DCs, CCR7- and CXCR4-mediated migration towards the corresponding CCL19 and CXCL12 chemokine gradients was strongly reduced. It is noteworthy that the infection of immature DCs with HSV-1 prior to maturation led to a failure of CCR7 and CXCR4 upregulation during DC maturation and, as a consequence, also induced a block in their migratory capacity. Additional migration assays with a Δvhs mutant virus lacking the virion host shutoff (vhs) gene, which is known to degrade cellular mRNAs, suggested a vhs-independent mechanism. These results indicate that HSV-1-infected mature DCs are limited in their capacity to migrate to secondary lymphoid organs, the areas of antigen presentation and T-cell stimulation, thus inhibiting an antiviral immune response. This represents a novel, previously unrecognized mechanism for HSV-1 to escape the human immune system., UL https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.80852-0