Varicella zoster virus vaccines: potential complications and possible improvements
- 527 Downloads
Varicella zoster virus (VZV) is the causative agent of varicella (chicken pox) and herpes zoster (shingles). After primary infection, the virus remains latent in sensory ganglia, and reactivates upon weakening of the cellular immune system due to various conditions, erupting from sensory neurons and infecting the corresponding skin tissue. The current varicella vaccine (v-Oka) is highly attenuated in the skin, yet retains its neurovirulence and may reactivate and damage sensory neurons. The reactivation is sometimes associated with postherpetic neuralgia (PHN), a severe pain along the affected sensory nerves that can linger for years, even after the herpetic rash resolves. In addition to the older population that develops a secondary infection resulting in herpes zoster, childhood breakthrough herpes zoster affects a small population of vaccinated children. There is a great need for a neuro-attenuated vaccine that would prevent not only the varicella manifestation, but, more importantly, any establishment of latency, and therefore herpes zoster. The development of a genetically-defined live-attenuated VZV vaccine that prevents neuronal and latent infection, in addition to primary varicella, is imperative for eventual eradication of VZV, and, if fully understood, has vast implications for many related herpesviruses and other viruses with similar pathogenic mechanisms.
Keywordsvaricella zoster virus herpesvirus vaccine neurovirulence neuro-attenuation latency latent infection herpes zoster shingles chicken pox ORF7
Unable to display preview. Download preview PDF.
- Drolet M, Brisson M, Schmader K E, Levin M J, Johnson R, Oxman M N, Patrick D, Blanchette C, Mansi J A. 2010. The impact of herpes zoster and postherpetic neuralgia on healthrelated quality of life: a prospective study. CMAJ: Canadian Medical Association journal = journal de l’Association medicale canadienne, 182: 1731–1736.CrossRefGoogle Scholar
- Dulal K, Silver B, Zhu H. 2012. Use of Recombination-Mediated Genetic Engineering for Construction of Rescue Human Cytomegalovirus Bacterial Artificial Chromosome Clones. Biomed and Biotechnol.Google Scholar
- Klassen T P, Hartling L, Wiebe N, Belseck E M. 2005. Acyclovir for treating varicella in otherwise healthy children and adolescents. Cochrane Database Syst Rev: CD002980.Google Scholar
- Niizuma T, Zerboni L, Sommer M H, Ito H, Hinchliffe S, Arvin A M. 2003. Construction of varicella-zoster virus recombinants from parent Oka cosmids and demonstration that ORF65 protein is dispensable for infection of human skin and T cells in the SCID-hu mouse model. J Virol, 77: 6062–6065.PubMedCrossRefPubMedCentralGoogle Scholar
- Yih W K, Brooks D R, Lett S M, Jumaan A O, Zhang Z, Clements K M, Seward J F. 2005. The incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage, 1998–2003. BMC Public Health, 5: 68.PubMedCrossRefPubMedCentralGoogle Scholar