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Editorial commentary: Boosting Japanese encephalitis vaccine.

Japanese encephalitis (JE), caused by a zoonotic flavivirus and transmitted by mosquitos during twilight and at night, is the most common vaccine-preventable viral encephalitis in rural areas from Eastern Pakistan to Northern Queensland in Australia and to Japan. Among the 3 billion people at theoretical risk of infection, an estimated 220 million people live in rice-irrigated areas where the risk may be considerably increased [1]. The impact of pig farming (amplifying host) on the epidemiology of JE infections is a matter of debate, particularly in periurban areas, but no conclusive evidence can be drawn from the existing literature [2]. Every year, up to 50 000 often severe JE clinical cases occur among the resident populations, in contrast with 1–2 cases among tourists, expatriates, and visiting friends or relatives in endemic areas [3]. The inactivated, mouse brain–derived wild-type Nakayama strain (JE-MB) vaccine, shown to be protective in endemic areas [4] but causing rare severe drug reactions, has widely been replaced by a new, purified, formalin-inactivated Vero cell culture–derived (IC51, JE-VC; attenuated SA14-14-2) strain. Erra and colleagues provide a timely answer on how to boost JE–vaccinated subjects in a nonendemic population, filling a relevant gap of knowledge in travel medicine practice and beyond. A diligently chosen study design clearly shows that boosting the immune response following vaccination with 2–3 doses of the previously used JE-MB with a single dose of the JE-VC vaccine results in noninferior immunogenicity to boosting with a JE-MB vaccine. In addition, it confirms the validity of the known vaccination schedules with JE-MB and JE-VC. The decision to assess the immunogenicity of heterologous JE vaccines is scientifically sound. It shows that it is essential to rule out a potential bias that may result in favoring one vaccine over the other. The interaction of concomitantly administered vaccines, including those against other flaviviruses, does not appear to negatively influence the immune response to JE-VC on the basis of the researchers’ data. A randomized controlled trial would be preferred. The small group size and the lack of ruling out the possibility of natural boosting are further limitations of the study. However, such complex studies are hardly feasible without substantial industry support. The study of Erra et al [5] also shows that investigator-driven studies are increasingly necessary to address practical questions that the user of medicinal products need to know, in order to provide the best and most costeffective service to the client or patient. Thus, a single dose of JE-VC will suffice to successfully boost previous priming with 2–3 doses of JE-MB vaccination. Two doses of JE-VC are not required in correctly prevaccinated travelers if the assumed correlate of a 50% plaque reduction neutralization test titer of ≥10 [6] is protective. The question remains how long the assumed protective level of antibodies will last in persons exposed to the wild-type virus and whether it is boosted by the respective exposure. The true risk for travelers of suffering from the severe consequences of JE is under debate. The slight increase of reported JE cases among travelers over the past 36 years reflects the higher number of tourists rather than an increased risk for the individual traveler. The JE risk for 2 destinations with the highest risk for short-term travelers, Bali (Indonesia) and Thailand, is estimated to be 1 case in 1 million and 3.3 million travelers, respectively [3]. The respective risk estimates for Swedish (1 case per 400 000) and Finnish (1 case per 257 000) travelers to Thailand are higher [7, 8]. Even an assumed doubling of the number of cases will result in a low risk. The fact that a new, apparently safe vaccine is now available is not necessarily a reason to boost its use in a population that may be at very limited risk. Thus, a careful assessment of the points in favor Received 30 May 2012; accepted 1 June 2012; electronically published 13 June 2012. Correspondence: Prof Dr Christoph Hatz, Medical Department, Swiss Tropical Institute, Socinstrasse 57, Basel CH4002, Switzerland (Christoph.Hatz@unibas.ch). Clinical Infectious Diseases 2012;55(6):835–6 © The Author 2012. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. DOI: 10.1093/cid/cis548