Herpes simplex virus type 1 (HSV-1) is a highly successful pathogen that can result in significant human morbidity. Within the cornea, it was thought the initial recognition of the pathogen was through Toll-like receptors expressed on/in resident cells that then elicit pro-inflammatory cytokine production, activation of anti-viral pathways, and recruitment of leukocytes. However, our lab has uncovered a novel, TLR-independent innate sensor that supersedes TLR induction of anti-viral pathways following HSV-1 infection. In addition, we have also found HSV-1 induces the genesis of lymphatic vessels into the cornea proper by a mechanism independent of TLRs and unique in the field of neovascularization. This review will focus on these two innate immune events during acute HSV-1 infection of the cornea.