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English: Figure 1. Schematic diagram and model showing important host proteins and their roles in pathophysiology of ocular herpes infection. HSV-1 entry into a corneal cell starts with the binding of viral glycoproteins gB and/or gC to cell surface heparan sulfate. Next, HSV-1 gD binds to one of its cognate receptors (Nectin-1, HVEM, and 3-OS HS) to start viral capsid penetration into the cytoplasm. Toll-like receptors sense viral invasion and activate intrinsic immune responses to control infection. A newly identified restriction factor, optineurin, reduces incoming or outgoing viral load by selective degradation of viral capsid and essential proteins via autophagy. In parallel, mTORC2 complex acts to reduce viral replication in the nucleus. In a pro-viral role, heparanase, a host enzyme is upregulated to facilitate HSV-1 release from the corneal cell by removal of cell surface HS. While the events summarized here do not describe the complete picture of viral invasion, they do highlight many new findings and interventional targets in context with HSV-1 infection of the cornea. A cartoon describing the essential structural components of a matured HSV-1 virion is shown (bottom right).