• Robert W Johnson, Gunnar Wasner, Patricia Saddier, and Ralf Baron.
• Bristol Royal Infirmary and University of Bristol, Bristol, United Kingdom. r.w.johnson@bris.ac.uk
• Drug Aging. 2008 Jan 1;25(12):991-1006.

AbstractHerpes zoster (HZ) results from reactivation of varicella-zoster virus (VZV) that has been persistent and clinically dormant in spinal ganglia or cranial sensory nerves since primary infection with VZV. The most common reason for reactivation is a decline in zoster-specific cell mediated immunity as a result of aging (immunosenescence). More than two-thirds of HZ cases occur in people >or=60 years of age. HZ incidence is higher in persons who are immunocompromised as a result of disease (e.g. malignancies such as lymphoma, HIV/AIDS, diabetes mellitus) or treatments such as chemotherapy and radiotherapy. HZ incidence is also increased by therapeutic immune suppression following organ transplantation and in patients taking high-dose corticosteroids. However, HZ may occur in otherwise healthy young people. Although serious and life-threatening complications sometimes occur, the most common complication is postherpetic neuralgia (PHN), which may persist for months or years and is significantly resistant to treatment despite substantial advances in the understanding of its pathological mechanisms. The medical and social costs of HZ and PHN are high, particularly in older patients. Prevention of PHN in patients with HZ is unsatisfactory although antiviral drugs reduce the duration of pain after HZ. A live attenuated vaccine has been shown to reduce the incidence of HZ and PHN as well as the burden of illness in subjects aged >or=60 years. In view of the increasing numbers of elderly persons in the population and the poor outcomes of PHN treatment, vaccination against HZ at approximately 60 years of age appears to be an appropriate strategy.

17 keywords...

hide…