HERPES ZOSTER: EPIDEMIOLOGY, PATHOPHYSIOLOGY, DIAGNOSIS AND CURRENT THERAPEUTIC APPROACHES

Abstract

Herpes zoster (HZ) is a cutaneous-nervous infection caused by the reactivation of the Varicella-zoster virus (VZV), a beta-herpesvirus that is also the etiological agent of varicella. After the primary varicella infection, the viral agent remains latent in the sensory nerve ganglia and/or the central nervous system; its reactivation occurs when there is a decrease in cellular immunity, being more frequent in individuals aged ≥50 years, carriers of immunocompromising diseases (such as HIV/AIDS, hematological or solid neoplasms) or under immunosuppressive therapies (chemotherapy, long-term corticosteroid therapy, immunomodulatory drugs). Clinically, it is characterized by pre-eruptive neuropathic pain (which may be described as burning, paresthesia, or hyperesthesia) in a single dermatomal territory, followed by the development of an erythematous vesiculobullous eruption, with a unilateral dermatomal distribution, which may evolve into crusts within 2-3 weeks. The main complication is post-herpetic neuralgia (PHN), defined as persistent pain in the affected territory for more than 90 days after the appearance of the eruption. For prevention, live attenuated virus vaccines and recombinant vaccines are available, which significantly reduce the incidence of HZ and PHN. In therapeutic management, the early use of systemic antivirals (acyclovir, valacyclovir, or famciclovir) is indicated to reduce the viral load, the severity of the eruption, and the risk of neurological complications. Pain control involves the use of first-line analgesics (paracetamol, non-steroidal anti-inflammatory drugs) and, in cases of intense pain or postherpetic neuralgia (PHN), agents such as tricyclic antidepressants, anticonvulsants, or opioids may be recommended.