Herpes zoster in HIV infection with osteonecrosis of the jaw and tooth exfoliation.

BACKGROUND: Herpes zoster (HZ) infection of the trigeminal nerve is associated with complications such as postherpetic neuralgia, facial scarring, loss of hearing ability and conjunctivitis. Until 2005, postherpetic alveolar necrosis and spontaneous tooth exfoliation have been described in 20 cases unrelated to HIV infection. OBJECTIVE: The aim of this study was to describe HIV infection in patients (two women, two men, average age 30 years) who suffered from HZ attacks to their trigeminal nerves. MAIN OUTCOME MEASURES: None of the patients had received antiherpetic medications or antiretroviral therapy. HIV infection was only diagnosed after the development of HZ. Facial scarring with depigmentation and hyperesthesia (postherpetic neuralgia) was diagnosed in all four patients. Oral findings consisted of spontaneous loss of both maxillary or mandibular teeth. Osteonecrosis of varying extent was also found. Treatment consisted of extractions of teeth and administration of antibiotics and analgesics. Healing of alveolar wounds was unremarkable. CONCLUSION: Complications affecting the alveolar bone and teeth seem to be rare in HIV-infected patients.

Chronic varicella-zoster virus ganglionitis--a possible cause of postherpetic neuralgia.

Postherpetic neuralgia (PHN) is dermatomal distribution pain that persists for months to years after the resolution of herpes zoster rash. The cause of PHN is unknown. Herein, we report clinical, molecular virological, and immunological findings over an 11-year period in an immunocompetent elderly woman with PHN. Initially, blood mononuclear cells (MNCs) contained varicella-zoster virus (VZV) DNA on two consecutive occasions. Random testing after treatment with famciclovir to relieve pain did not detect VZV DNA. However, the patient was reluctant to continue famciclovir indefinitely and voluntarily stopped drug treatment five times. Pain always recurred within 1 week, and blood MNCs contained many, but not all, regions of the VZV genome on all five occasions. Immunological analysis revealed increased cell-mediated immunity to VZV. Chronic VZV ganglionitis-induced PHN best explains the recurrence of VZV DNA in MNCs whenever famciclovir was discontinued; the detection of only some regions of the viral genome in MNCs, compared to the detection of all regions of the VZV genome in latently infected ganglia; the increased cell-mediated immunity to VZV; and a gratifying clinical response to famciclovir. The presence of fragments of VZV DNA in MNCs likely represents partial degradation of viral DNA in MNCs that trafficked through ganglia during productive infection.