Varicella zoster virus (VZV) is one of eight herpes viruses known to cause childhood chicken pox. After primary infection of the host immune system, the virus becomes latent in the dorsal root ganglia and reactivates later to cause shingles and other neurologic complications (Arvin, 1996). The virus is transmitted by airborne viral particles or through contact of vesicular fluid from an infected contact (Arvin, 1996). VZV enters the respiratory tract and infects the mucous membrane while spreading to regional lymph nodes where viral proliferation occurs in T-cells of the blood (Moffat, 2003).
Primary viremia carries the virus to the liver or other cells of the mononuclear phayocyte system (Arvin, 1996). During this 2 to 3 week incubation period, a fever develops and within a few days a second round of VZV viremia infects the epidermis, producing the typical vesicular lesions of chicken pox (Hambleton, 2005). The itchy rash appears and eventually turns into fluid-filled blisters that dry and form scabs. VZV can then travel from the skin to sensory nerves, characterizing the early stage of latent neuronal infection (Hambleton, 2005).
Varicella-Zoster Virus Virology and Genome Sequence VZV is the smallest of human alphaherpesviruses, consisting of an envelope encasing a nucelocapsid surrounding the single double stranded DNA molecule (Hambleton, 2005). VZV encodes at least 70 genes that are classified into immediate early (IE), early (E) and late (L) genes. IE and E code for nonstructural proteins that regulate viral transcription and replication. L genes code for structural proteins such as nucleocapsids, and several glycoproteins allowing VZV to spread without its viral envelope (Hambleton, 2005).
These proteins code for VZV entry into host cells, bondage to a cellular receptor, and transport of the virus to the cell surface allowing it to fuse into adjacent cells (Arvin, 1996). During lytic infection, VZV enters cells by fusion of the viron envelope with the host plasma membrane, or by endocytosis where capsids localize to the nucleus (Reichelt, 2009). VZV induces cellular DNA machinery to favor virus replication, and with cell-associated viremia the virus has the ability to travel and spread to epidermal cells (Arvin, 1996).
Here, the virus recreates it’s envelope to release into the extracellular space creating the typical vesicular lesions of the chicken pox rash (Hambleton, 2005). Prevention of Varicella and Herd Immunity The Oka vaccine is a live attenuation of the variella virus and remains the only vaccination to be used against herpesviruses (Hambleton, 2005). The wild type VZV is passaged in sub-physiological temperatures through human and nohuman tissue, which is then sonicated and centrifuged to produce a live cell-free virus (Hambleton, 2005).
This vaccine strain replicates less efficiently and is less transmissible than the wild type due to multiple mutations, disabling growth and synthesis of the virus (Cohen, 2010). Two doses of the vaccine are administered 3 months apart, accounting for 85% of complete protection in children (Hambleton, 2005). Those who developed breakthrough infection developed mild disease and required no antiviral therapy (Hambleton, 2005). The vaccine is extremely safe in susceptible children and adults where irratation at the injection site were minor and transient.
Ultimately there were no reports of fatal VZV infection by the Oka vaccine (Hambleton, 2005). Herd immunity is a form of immunity that occurs when the majority of a population is vaccinated, providing an indirect form of protection for susceptible individuals who have not been immunized (Fine, 1993). The goal is to reach herd immunity threshold by immunizing a large percentage of the population to prevent further transmission of the disease. This value is determined by many factors.
In terms of chicken pox, the virulence of the disease is fairly high, with a clinical attack rate of 65 to 86% (Hambleton, 2005). As the virus is highly contagious, depending on the frequency of person-to-person contact in a population, and vaccine efficacy, the magnitude of herd immunity threshold varies. In 2000, Texas, California, and Pennsylvania were subject to active surveillance of varicella where vaccination coverage ranged from 73. 6% to 83. % among children 19 to 35 months old (Hambleton, 2005).. Of this population, varicella cases decreased by 71 and 84% (Hambleton, 2005). Varicella incidence had also declined in nonvaccinated groups such as adults and infants who were too young to be immunized, suggesting that herd immunity had occurred (Hambleton, 2005). Conclusion Occurrences of breakthrough varicella have been reported, suggesting a loss of protection from the vaccine when there is no immune response after vaccination (Hambleton, 2005).
This has been observed in children who have been vaccinated before 15 months, and in patients who were given doses 1 month apart. (Hambleton, 2005) The Oka vaccine also brings complications to those who are pregnant, have compromised immune systems, and who are allergic to the vaccine (Hambleton, 2005). Although the vaccine for chicken pox is effective, continued investigations are necessary to fully understand how to optimally use the Oka vaccine to effectively and completely protect a population from chicken pox by preventing breakthrough chickenpox.