Control of varicella disease, version 2.0.

In this issue of the Journal, Shapiro and colleagues present data from a casecontrolled study of the effectiveness of 2 doses of varicella vaccine during the first several years after implementation of a routine 2-dose recommended schedule. At 98.3%, the effectiveness of the 2-dose schedule is welcome news indeed. These data validate the calculations of experts from the Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) and the American Academy of Pediatrics (AAP) Committee on Infectious Diseases (COID), made in 2006 when both groups approved a recommendation for routine use of 2 doses of varicella vaccine during childhood. Shapiro and colleagues are to be commended for their forethought in establishing a broad surveillance network in Connecticut in the years after licensure of the varicella vaccine in 1995 and for their careful scientific and statistical evaluation of data generated from this important resource. In understanding the context within which these new data should be viewed, it is important to reflect on the overall development and implementation of varicella vaccine. The strain that ultimately became the varicella vaccine in the United States and many other countries was first isolated by Takahashi et al in the early 1970s from a young Japanese boy whose name was Oka (hence the vaccine Oka strain) [1]. Takahashi et al successfully attenuated this isolate through serial passage in the laboratory, followed by 20 years of testing before approval as a monovalent vaccine (Varivax) in the United States in 1995. Its licensure reflected a milestone in vaccinology: as a herpesvirus, the Oka strain establishes latency in the human body, meaning that the vaccine remains in the recipient for the rest of his or her life. Careful scientific assessment then and subsequently has proved that reactivation of the vaccine strain, resulting in zoster or shingles, occurs much less frequently than with wild-type varicellazoster virus [2]. Nevertheless, this was the first vaccine virus that persists even in a latent form. Before licensure of the monovalent varicella vaccine (Varivax; Merck) in March 1995, 4 million cases of varicella, 10,500–13,500 hospitalizations due to complications of varicella, and 100– 150 deaths from varicella occurred annually [3–7]. The initial use of the vaccine was for the prevention of moderate or severe varicella disease, including hospitalization, long-term morbidity, and mortality. To accomplish this objective, the vaccine was recommended to be administered as a single dose given at 12–18 months of age [8, 9]. In the first 10 years after licensure, vaccination coverage increased to 88% among vaccine-eligible children 19–35 months of age [10]. Plummeting hospitalizations and deaths from varicella [7, 11, 12] were unequivocal testaments to the success of these initial goals of the varicella vaccination program. With this success, however, came a new challenge, as breakthrough varicella disease received increasing attention from both public health officials and the general population. Prelicensure efficacy trials of a single dose of the vaccine had documented virtually 100% effectiveness in preventing moderate to severe varicella disease, and 80%–85% efficacy in the prevention of any varicella disease [13–16]. As severe varicella disease became increasingly rare because of the overwhelming success of the 1-dose schedule, and as mild disease decreased as well, those outbreaks of mild Received 7 September 2010; accepted 25 October 2010. Potential conflicts of interest: D.W.K. serves as a member of the American Academy of Pediatrics Committee on Infectious Diseases and is an associate editor of the AAP Red Book: Report of the Committee on Infectious Diseases. Within the past 2 years he has participated as one of dozens of sites for clinical trials conducted by GlaxoSmithKline, Cellex, and Cubist, although none are in the areas of varicella or vaccines. All funds from these trials go to the University of Alabama at Birmingham. Reprints or correspondence: Dr David W. Kimberlin, Professor of Pediatrics, Division of Pediatric Infectious Diseases, University of Alabama at Birmingham, 1600 Seventh Ave S, CHB 303, Birmingham, AL 35233 ([email protected]). The Journal of Infectious Diseases 2011;203:297–298 The Author 2010. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected] 1537-6613/2011/2033-0001$15.00 DOI: 10.1093/infdis/jiq053