Herpes simplex virus 1 and 2 ( HSV-1 and HSV-2 ), also known as human herpesvirus 1 and 2 ( HHV-1 and HHV-2 ), are two members of the herpesvirus family, Herpesviridae , that infect humans . [1] Both HSV-1 (which produces most cold sores ) and HSV-2 (which produces most genital herpes) are ubiquitous and contagious . They can be spread when an infected person is producing and shedding the virus .

The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex. Condom use decreases the risk somewhat. Daily antiviral medication taken by someone who has the infection can also reduce spread. There is no available vaccine and once infected, there is no cure. [1] Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms. [2] Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes. [1] [2]


In the case of a herpes virus, initial interactions occur when two viral envelope glycoprotein called glycoprotein C (gC) and glycoprotein B (gB) bind to a cell surface particle called heparan sulfate. Next, the major receptor binding protein, glycoprotein D (gD), binds specifically to at least one of three known entry receptors. These cell receptors include herpesvirus entry mediator (HVEM), nectin-1 and 3-O sulfated heparan sulfate. The nectin receptors usually produce cell-cell adhesion, to provide a strong point of attachment for the virus to the host cell. These interactions bring the membrane surfaces into mutual proximity and allow for other glycoproteins embedded in the viral envelope to interact with other cell surface molecules. Once bound to the HVEM, gD changes its conformation and interacts with viral glycoproteins H (gH) and L (gL), which form a complex. The interaction of these membrane proteins may result in a hemifusion state. gB interaction with the gH/gL complex creates an entry pore for the viral capsid. gB interacts with glycosaminoglycans on the surface of the host cell.

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