Abstract / Summary
Herpes simplex virus (HSV) is a highly prevalent neurotropic DNA virus that causes orolabial herpes, genital herpes, keratitis, neonatal infection, meningitis and encephalitis. HSV-1 and HSV-2 share epithelial entry, lytic replication, immune evasion, lifelong sensory-ganglion latency and periodic reactivation, yet they differ in typical transmission routes, anatomical recurrence and public-health burden. Rather than mechanically separating both viruses throughout, this review emphasizes shared HSV biology and highlights type-specific differences where they affect clinical interpretation or intervention design. We connect glycoprotein-mediated entry, receptor use, axonal transport, immune evasion and latency with mucocutaneous, ocular, neurologic, neonatal and genital disease. We then synthesize lessons from failed glycoprotein-D vaccine trials, multivalent and mRNA platforms, helicase–primase inhibitors, monoclonal antibodies, RNA-based approaches, genome editing and latency-directed strategies. A mechanism-guided HSV strategy should reduce acquisition, shedding and recurrence, prevent ocular, neurologic and neonatal complications, manage antiviral resistance and ultimately address latent infection.