Inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-6, and IL-8, were highly expressed in IP,18–20 and were up-regulated by CMV infection.21,22 Furthermore, high expression of IL-8 and its receptor in CMV-infected human lung fibroblasts enhanced its function in an autocrine manner and promoted CMV replication in vitro.23 This evidence concerns the gene CXCL8 and cytomegalovirus infection.