infections, central nervous system complications including encephalitis, and pneumonia were among the most common causes of hospitalization and death, and these instances occurred most often in healthy individuals who were not severely immunocompromised or undergoing immunocompromis-ing treatments (Meyer et al., 2000).

Since the 1980s, VZV infections in immunocompromised individuals have been treated with acyclovir, a synthetic nucleoside analog that inhibits the replication of human herpes viruses including VZV. In 1992, acyclovir was approved for the treatment of VZV infection in healthy children (CDC, 2007). Used within 24 hours of initial presentation, intravenous acyclovir effectively lessens illness severity and fatality in immunocompromised individuals (Nyerges et al., 1988; Prober et al., 1982). In 1992, oral acyclovir was approved for treatment of varicella in healthy children based on study data indicating favorable clinical outcomes, for example shortening of disease and contagious state, and severity of symptoms, if administered within 24 hours of rash onset (CDC, 2007). However, in 1993, the American Academy of Pediatrics Committee on Infectious Disease issued a statement that the benefit of acyclovir was not sufficient to justify routine administration in healthy children (CDC, 2007). Instead, they recommended that the oral treatment be reserved for otherwise healthy individuals at increased risk for moderate to severe varicella such as individuals 13 years or older and persons with chronic skin or pulmonary disorders (Hall et al., 1993).

The first live attenuated varicella vaccine was developed and tested in Japan by Takahashi and colleagues in the 1970s. The virus, designated Oka strain, was isolated from vesicular fluid of a healthy 3-year-old boy infected with VZV (Takahashi et al., 1975). The virus was attenuated through serial passaging through human embryonic lung cells, guinea-pig cells, and human diploid cells (WI-38 and MRC-5) (Arvin and Gershon, 1996). Takahashi et al. inoculated 51 healthy children who subsequently experienced a 92 percent VZV antibody formation rate (Takahashi et al., 1975). Following this study, Takahashi and his associates studied the impact of the vaccine on the VZV seroconversion in children with underlying diseases such as nephritis, asthma, and hepatitis. This study showed that the VZV vaccine was safe for children receiving low to moderate doses of steroids (Takahashi et al., 1974, 1975).

Reports of varicella vaccination in immunocompromised children showed that with suspended chemotherapy, children with leukemia could be vaccinated successfully against VZV (Arvin and Gershon, 1996). These studies spurred similar studies in the United States and Canada. In 1979, the National Institute of Allergy and Infectious Diseases sponsored the Varicella Vaccine Collaborative Study that looked at the effectiveness of the vaccine on children whose leukemia was in remission. The Collaborative Study showed seroconversion in 88 percent of leukemic children after

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