Absence of exposure to varicella does not increase the risk of zoster.

The remarkable new hypothesis put forth by R. Edgar Hope-Simpson, a general practitioner in Cirencester, England, in 1965 on the nature of herpes zoster was based on the observation of every case of herpes zoster by Hope-Simpson and his partner over 16 years in their practice of 3500 persons [1]. They recorded 192 cases of zoster during the 16-year period of 1947–1962, for an annual rate of 3.4 cases per 1000 persons. Because zoster presents such a dramatic and clean-cut clinical picture, he stated that they had no evidence for missing a single case. HopeSimpson also pointed out the age-specific incidence of zoster, with the number of cases increasing after the age of 50 to 6.79 cases per 1000 population per year for the age group 60–69 years and to 10.10 cases per 1000 population per year for the age group 80–89 years. He also predicted that if a cohort of 1000 people lived to be 85 years old, 50% would have an attack of zoster and only 10 individuals (1%) would have a second attack of zoster. The link between varicella virus and zoster was noticed in 1888 by von Bokay [2], and Hope-Simpson in 1954 found evidence by means of an epidemiologic approach in the Shetland Islands of Scotland that varicella and zoster had identity [3]. The ability of Weller and Stoddard in 1952 [4] to grow the varicella virus in tissue culture led to the proof in 1954 by Weller and Coons [5] that the virus from a patient with varicella and that obtained from a zoster patient were the identical varicella-zoster virus (VZV). In his hypothesis of 1965, HopeSimpson suggested that outbreaks of zoster were prevented by levels of neutralizing antibody to VZV and that 2 mechanisms stimulated antibody production and delayed outbreaks of zoster until after the age of 50: (1) subclinical reactivation of endogenous virus from the sensory ganglia and (2) exogenous exposure to the virus from a case of varicella or zoster provides a ‘‘boost’’ to the neutralizing antibody titer. This concept of exogenous boosting has been supported by results of 4 recent epidemiological studies showing that repeated family and occupational exposure is associated with a reduced risk of zoster [6–9]. An unproven assumption of the exogenous boosting hypothesis that ‘‘repeated contact with varicella reduces the risk of zoster’’ is the converse idea that ‘‘the absence of contact with varicella causes an increased risk of zoster.’’ To test this assumption, the team of investigators led by Gaillat et al [10] report in this issue of Clinical Infectious Diseases on an imaginative study designed to compare the frequency and age of onset of zoster in monks and nuns not exposed to children with those of the general population in France. The primary objective of the study was to compare the frequency of zoster in a population not exposed to children, such as members of contemplative monastic orders (CMOs) of the Roman Catholic Church, with that of the general population. Secondary objectives were to compare the reported age of onset of zoster in members of the CMO with that in the general population and to describe the frequency and age of onset of zoster in monks compared with nuns. A national, multicenter, observational comparative epidemiological study in an ‘‘exposed/nonexposed’’ design was conducted by using questionnaires. The authors applied vigorous standards to the questionnaires, and those who were members of monastic orders for ,2 years or had zoster before entering the monastery were excluded. In France, varicella vaccine is not given to children, and by age 10 years, 90% of French children have acquired VZV antibodies by means of natural infection with VSV. To ensure that members of the CMO had not been exposed to VZV, all those who had regular contact with children aged ,10 years were Received 16 May 2011; accepted 24 May 2011. Correspondence: Clyde S. Crumpacker II, MD, Division of Infectious Diseases, Beth Israel Deaconess Medical Center, 330 Brookline Ave, DA 617, Boston, MA 02215 (ccrumpac@ bidmc.harvard.edu). Clinical Infectious Diseases 2011;53(5):411–412 The Author 2011. 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]. 1058-4838/2011/535-0002$14.00 DOI: 10.1093/cid/cir439