Initially, viruses invade the host epithelial tissues found in the oral cavity, respiratory tract, intestinal tract, and the urogenital apparatus ( Figure 1 ). Lamina propria DCs, Langerhans cells, and stromal cells are resident in these tissues. In the connective tissues, fibroblasts resident, and capillary vessel and lymphatic vessel are expanded. Monocytes, macrophages, T cells, B cells, pDC, and mDC circulate within the blood vessels and lymphatic vessels, and patrol the interstitial spaces. All these cells are potential targets for virus infection. Virus-infected epithelial cells and fibroblasts produce IFNs, mainly IFN-β and IFN-λ, which provide surrounding uninfected cells with antiviral state. Furthermore, chemokines and cytokines, such as interleukin-1β (IL-1β), IL-6, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-α (TNF-α) are also produced. These molecules promote chemotaxis of the resident DCs (lamina propria DCs and Langerhans cells) toward virus-infected and dead cells. Neutrophils, monocytes, macrophages, plasma cells, mDCs, and pDCs also migrate from the blood vessels to the site of infection. IFN-γinducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), MIP-3α, and MIP-3β largely contribute to the transmigration of blood DCs. However, these blood-borne immune cells can also be infected by viruses, which can then modulate the production of various cytokines and chemokines.