2002 • JID 2005:191 (15 June) • Jumaan et al.
M A J O R A R T I C L E
Incidence of Herpes Zoster, Before
and After Varicella-Vaccination–Associated
Decreases in the Incidence of Varicella, 1992–2002
Aisha O. Jumaan,1Onchee Yu,2Lisa A. Jackson,2Kari Bohlke,2Karin Galil,3and Jane F. Seward1
1Centers for Disease Control and Prevention, Atlanta, Georgia;
2Group Health Cooperative, Seattle, Washington;
(See the editorial commentary by Whitley, on pages 1999–2001.)
Varicella zoster virus (VZV) causes varicella and, later in the life of the host, may reactivate to
cause herpes zoster (HZ). Because it is hypothesized that exposure to varicella may boost immunity to latent VZV,
the vaccination-associated decrease in varicella disease has led some to suggest that the incidence of HZ might
increase. We assessed the impact that varicella vaccination has on the incidence of varicella and of HZ.
Codes for cases of varicella and of HZ in an HMO were determined in automated databases of
inpatients and outpatients, on the basis of the Ninth Revision of the International Classification of Diseases. We
calculated the incidence, during 1992–2002, of varicella and of HZ.
The incidence of HZ remained stable as the incidence of varicella decreased. Age-adjusted and -specific
annual incidence rates of varicella decreased steadily, starting with 1999. The age-adjusted rates decreased from
2.63 cases/1000 person-years during 1995 to 0.92 cases/1000 person-years during 2002; among children 1–4 years
old, there was a 75% decrease between 1992–1996 and 2002. Age-adjusted and -specific annual incidence rates of
HZ fluctuated slightly over time; the age-adjusted rate was highest, at 4.05 cases/1000 person-years, in 1992, and
was 3.71 cases/1000 person-years in 2002.
Our findings revealed that the vaccination-associated decrease in varicella disease did not result
in an increase in the incidence of HZ. These early findings will have to be confirmed as the incidence of varicella
disease continues to decrease.
After causing varicella, the varicella zoster virus (VZV)
remains dormant in the sensory ganglia and reactivates
later in life to cause herpes zoster (HZ). Both varicella
and HZ are characterized by a vesicular skin rash that
is commonly generalized in the case of varicella and
localized in the case of HZ . Before the introduction
of varicella vaccine in the United States during 1995,
almost everyone contracted varicella by the age of 30
years [2, 3]; however, only ∼10%–30% of persons in-
fected with VZV develop HZ [4, 5]. A decrease in cell-
Received 28 October 2004; accepted 5 January 2005; electronically published
12 May 2005.
Presented in part: 43rd Annual Interscience Conference on Antimicrobial Agents
and Chemotherapy, Chicago, 14–17 September 2003 (abstract G-1084).
Financial support: Group Health Cooperative (Centers for Disease Control and
Prevention, under cooperative agreement for surveillance of varicella and herpes
zoster [grant UR6/CCU017728]).
Reprints or correspondence: Dr. Aisha O. Jumaan, CDC/ATSDR, Century Center,
2400 Century Pkwy., Rm. 3202, Atlanta, GA 30345 (email@example.com).
The Journal of Infectious Diseases
? 2005 by the Infectious Diseases Society of America. All rights reserved.
mediated immunity is thought to play a critical role in
the reactivation of the virus in healthy individuals .
Widespread childhood vaccination in the United
States has led to a 75%–80% decrease in the incidence
of varicella [7, 8], raising concern that the incidence of
HZ might increase because of decreased circulation of
the wild-type virus . In 1965, Hope-Simpson hy-
pothesized that external exposure to VZV may boost
immunity, thereby reducing the likelihood that the vi-
rus would reactivate as HZ . Subsequent studies
have reported that the risk of HZ is lower inindividuals
exposed to varicella or to children than it is in indi-
viduals without such exposures [11–14]. Finally, mod-
eling predicts that the vaccination-associated decrease
in varicella disease would lead to an increase in the
incidence of HZ, an increase that may last for as long
as 50 years [15, 16]. Since 1998, the Centers for Disease
Control and Prevention (CDC) has collaborated with
Group Health Cooperative (GHC), an HMO in Wash-
ington State, to monitor the incidence rates of varicel-
la and of HZ. The objectives of this project were to
Surveillance of Varicella and Zoster—1992–2002 • JID 2005:191 (15 June) • 2007
constant during the study period, the study may have been con-
cluded too early to detect an increase attributable to a decrease
in exposure to varicella. In the population considered by the
present study, the uptake of varicella vaccine was slightly lower
than the national average, and the study covered only the first
7 years after varicella vaccine was introduced . Finally, the
population in the present study may not be representative of
those who do not have health insurance, although this should
not affect the trends observed.
We will continue to monitor the incidence of HZ as the rate
of varicella disease continues to decrease. Other studies have
reported the results of boosting VZV-specific cell-mediated
immunity by administering another dose of VZV vaccine ?5
years after the first dose [31–33]. Future public-health inter-
ventions focusing on VZV may include a vaccine to prevent
or modify HZ.
We thank Mary McCauley for editorial assistance and John Zhang for
help with the analysis.
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