HSV-2 uses envelope glycoprotein D (gD) to recognize nectin-1 and initiate host-cell entry, making receptor binding a core biological function for infection models
[1]. Mechanistically, HSV-2 alters mucosal innate immunity by blocking type I interferon production, which helps the virus cross genital mucosal defenses
[2]. In disease research, genital HSV-2 shedding explains transmission risk because symptomatic infection sheds more frequently than asymptomatic infection
[3]. Compared with HSV-1, HSV-2 keeps a conserved nectin-1 recognition mode but generates greater genetic diversity during controlled cell-culture evolution
[1][4]. For experimental applications, soluble nectin-1 can block vaginal HSV-1 and HSV-2 infection, while valacyclovir reduces genital HSV-2 transmission in discordant couples
[5][6].