Clinical presentation
HSV types 1 and 2 are the causative agents of herpes labialis, herpes genitalis, herpes gladiatorum, herpetic whitlow, herpetic keratoconjunctivitis, eczema herpeticum, herpes folliculitis (herpes sycosis), lumbosacral herpes, disseminated herpes, neonatal herpes and herpes encephalitis. They have also been linked to some cases of erythema multiforme.[33]
The onset of clinical illness is usually sudden, with the appearance of multiple characteristic vesicular lesions superimposed upon an inflammatory, erythematous base. Primary infection may also be associated with systemic symptoms such as fever and malaise. In the setting of HIV infection, HSV lesions may be chronic, larger, atypical, more widespread in distribution, and extend into deeper cutaneous layers resulting in necrotising ulcers. The presence of herpes ulcers for 1 month or more in patients with HIV infection is considered an AIDS-defining illness. Recurrent episodes are common in HIV. Mucocutaneous herpes can present as an IRIS- like phenomenon in patients initiated on ART.[34]
Most people with sexually-acquired HIV have HSV-2 co-infection. Recently studies have shown an association between HSV-2 infection and HIV acquisition. HIV-1 is shed from genital ulcers caused by HSV-2.[35] In this setting, ART has little influence on frequency or level of mucosal HSV-2 shedding, with 85% of episodes being subclinical. Frequent subclinical episodes of HSV-2 reactivation are associated with both a higher frequency and a higher amount of HIV-1 in genital secretions. In addition, valaciclovir has activity against HIV replication.[36] In spite of this proven interaction between HSV-2 and HIV, there is no strong evidence that supports the acceleration of the HIV disease progression, either clinically or regarding the decrease of CD4 cells count, with the HSV-2 co-infection.[37],[38] However, acyclovir appears to have both some direct anti-HIV activity as well as some indirect immunologic changes.[39]