Among several common human viruses, the neurotropic HSV-1 was suggested a target of host cell dioxin receptor transcriptional (AhR-Arnt) complex. The latter was proven to up-regulate the expression of mammalian and viral genes containing multiple dioxin-responsive elements (DRE). Here, 7 to 8 potentially active DRE in the regulatory regions of five HSV-1 genes, including critical immediate-early (IE) ones, were revealed by SITECON, a tool for transcription factor binding sites recognition. With regard to the possession of abundant promoter DRE, HSV-1 resembles another herpes virus, CMV, and as well as with CMV, it was experimentally demonstrated that the HSV-1 might be trans-activated in host cells by concentrations of 2,3,7,8-TCDD corresponding to current body burden of dioxin in general population. The above approach was applied also to chemokines and cytokines the recruitment of those involves in the first line of defense against HSV-1 infections together with production of IFN-α/β. Thus in cilico studies revealed that genes encoding "antiviral" IFN-γ, IL-1β, IL-6, IL-18, NF-kB1 (p50), TNF-α each contain just one or two promoter DRE, whereas genes encoding "pro-viral" RANTES/CCL5, NF-kB3/p65/RelA and STAT3 possess seven to nine active 5'-upstream DRE. As virus-host interactions are crucial for the outcome of infections, our findings of multiple potentially active DRE in promoter region of HSV-1 genes, as well as in genes encoding major host cell "pro-viral" cytokines, this suggests that a subnanomolar dioxin in host cell is able to promote HSV-1 infection. From a clinical standpoint, an inhibition of dioxin can cause augmentation of HSV-1 infections which can be achieved with inhibitors of dioxin binding to host cell Ah receptor, or blockage of activated AhR-Arnt transcriptional complex binding to the viral promoter DRE.