Herpes zoster may occur at any stage of HIV infection, and may be the first clinical evidence of previously undiagnosed HIV infection. Herpes zoster has also been recognized as a manifestation of immune reconstitution disease.
Varicella zoster virus (VZV) is a human neurotropic alphaherpes DNA virus that is usually transmitted by the respiratory route. It is the causative agent of both varicella (chickenpox) and zoster (shingles). Varicella results from primary infection of VZV and is a common childhood illness, usually presenting as a benign self-limiting illness with fever and generalized pruritic vesicular rash. Following primary infection, VZV establishes lifelong latency in the cells of the dorsal root ganglia. Reactivation results in herpes zoster disease. In HIV-seropositive patients, reactivation is more common, and in those with advanced immune deficiency may result in severe and disseminated clinical disease.
In the general population, the incidence of herpes zoster (shingles) is 1.5–3 per 1000 persons per year. It is seen more frequently in patients aged 60 years and older and in those who are immunocompromised. Individuals with HIV infection have significantly higher rates of herpes zoster than the general population with an estimated relative risk of 15 or greater compared to age-matched HIV-seronegative controls. Herpes zoster occurs more frequently in HIV-seropositive persons with a CD4 count <200–250 cells/μL and, unlike the non-immunocompromised individual, recurrences are common (up to 20–30% of cases) which may be more severe with increasing immune deficiency.
In patients with advanced HIV disease, prolonged lesion formation, and dissemination of virus can occur. Cutaneous dissemination may be widespread, making it indistinguishable from primary varicella infection. Despite an impaired immune system, the majority of HIV-seropositive patients with zoster do not develop life-threatening complications, and most have an uncomplicated clinical course.
Treatment of zoster in HIV-seropositive patients should begin as soon as possible (preferably within 72 h of onset of the skin rash) and be continued for 2 days after all lesions have dried and crusted. Intravenous foscarnet is the agent of choice for aciclovir-resistant VZV infection.
Lesions evolve over 1–2 days to form vesicles.
patients, zoster may be particularly haemorrhagic. |
Treatment should be continued for 2 days after all lesions have dried and crusted.
This page was last updated in February 2015.