Varicella-zoster virus (VZV) establishes lifelong latency following primary infection and can reactivate later in life to cause herpes zoster (HZ) and its debilitating complication postherpetic neuralgia (PHN). The implementation of varicella vaccinations has profoundly altered the epidemiological landscape of VZV. This narrative review examines the current literature to evaluate the impact of these vaccination programs on the incidence of HZ and PHN. Early mathematical models based on the “exogenous boosting” hypothesis predicted a substantial surge in adult HZ due to reduced exposure to circulating wild-type virus. However, long-term epidemiological data demonstrate that the incidence of adult HZ was already increasing prior to the introduction of vaccination programs and did not accelerate post-implementation, suggesting other primary drivers, such as an aging population. This review highlights the significant decline in HZ incidence among vaccinated pediatric populations, as the attenuated vOka vaccine strain is substantially less prone to reactivation than the wild-type virus. Furthermore, HZ that does occur in vaccinated individuals tends to be milder, resulting in a reduced risk of progression to PHN. To address the persistent risk in older adults, a recombinant zoster vaccine is recommended as a highly effective secondary prevention strategy. Despite challenges, such as breakthrough infections and the need for long-term monitoring of vaccine-induced immunity, varicella vaccination remains a cornerstone of public health, offering broad protection across different ages. Further research is needed to fully understand the long-term impact of varicella vaccinations on the incidence of HZ and PHN and to identify additional risk factors for these conditions.
Valaciclovir is metabolized to acyclovir after ingestion and thereafter exerts its antiviral activity. Because of its superior pharmacokinetic profile, it has quickly replaced acyclovir in the treatment of herpesvirus infection. Neurotoxicity caused by valaciclovir has been reported, however, among patients with pre-existing impaired renal function. This paper reports a case of neurotoxicity of valaciclovir in a patient with end-stage renal disease who was undergoing continuous ambulatory peritoneal dialysis (CAPD). A 67-year-old female on CAPD took 500 mg of valaciclovir twice for herpes zoster. After she took her second dose orally, she developed confusion and disorientation, along with involuntary movements. Her mental confusion progressed to a coma. Discontinuation of valaciclovir showed no rapid improvement. There- fore, hemodialysis was started. After two sessions of hemodialysis, the patient became alert; and after four sessions of hemodialysis, her neurological abnormalities were completely reversed. In conclusion, valaciclovir can induce life-threatening neurotoxicity, especially in CAPD patients, even with appropriate dose reduction, which can be effectively managed by hemodialysis.
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Comparison of Renal Function Indicators According to Hydration Volume in Patients Receiving Intravenous Acyclovir With CNS Infection Sanghee Kim, Youngsoon Byun Biological Research For Nursing.2015; 17(1): 55. CrossRef
Valacyclovir-Induced Neurotoxicity in a Maintenance Hemodialysis Patient June Seong Hwang, Hyo Yoep Song, Hoon Gil Jo, Song I Lee, Byung Hun Lim, Jung Sub Song, Seon Ho Ahn Journal of the Korean Geriatrics Society.2014; 18(2): 85. CrossRef
The two distinctive clinical features of varicella-zoster virus (VZV) are varicella (chickenpox) by primary infection and zoster (singles) by the reactivation of latent infection. In addition to the two typical clinical symptoms mentioned above, diverse clinical manifestations have been reported as a result of VZV reactivation, including chronic radicular pain without rash, visual loss, facial palsy, dysphagia, sore throat, odynophagia, otalgia, hearing loss, dizziness, headache, hemiplegia, etc. Most of these symptoms are derived from neuropathy and vasculopathy of affected nerves and arteries. Diagnosis of VZV disease can be difficult if there is no appearance of a skin rash during development of atypical symptoms. In addition to natural infection, vaccination and anti-viral agent treatment have influenced the changes of epidemics and clinical presentations of varicella and zoster. In this article, diverse clinical manifestations caused by VZV reactivation, particular without skin rash, are reviewed.