Serological studies estimate approximately 67% and 16% of the global population are living with Herpes Simplex Virus (HSV)-1 and -2, respectively. (6, 7). Both HSV-1 and -2 are typically acquired in childhood or early adulthood, primarily through vertical or sexual transmission, and are never cleared. (8) In the immunocompetent population, HSV infection is typically latent and asymptomatic, although asymptomatic viral shedding (particularly for HSV-1) means ongoing sexual transmission is common. Multiple population studies have observed a bimodal association between HSV and HIV infection, resulting from a combination of behavioural risk factors and viral synergy. (9-12) 

Clinical presentation 

Herpes simplex virus (HSV) types 1 and 2 can result in highly varied mucocutaneous manifestations. Most commonly, oral (herpes labialis) and genital sites (herpes genitalis)  present with characteristic vesicular or pustular lesions with an erythematous base. (13) . Primary infection may also be associated with systemic symptoms such as fever and malaise. Other, less common presentations may include crops of vesicles on non-mucosal skin (herpes gladiatorum or herpes folliculitis), digits (herpetic whitlow), or disseminated superinfection in the context of underlying eczematous conditions (eczema herpeticum). Extracutaneous involvement may also occur including  herpetic keratoconjunctivitis and herpes encephalitis.  

In PLWHIV, mucocutaneous flares of HSV may be more extensive, recurrent or slower to resolve spontaneously compared to immunocompetent individuals. (4) Furthermore, atypical HSV lesions may develop including larger, more widespread and deeper cutaneous involvement, resulting in necrotising ulcers or verrucous lesions. (13, 14) The presence of herpes ulcers for 1 month or more in PLWHIV is associated with advanced stages of infection with CD4+ T-cell counts below 200 cells/μL, and is therefore considered an AIDS-defining illness. (15-17)