Article

Seroprevalence of Cytomegalovirus (CMV) and Risk Factors for Infection in Adolescent Males

Department of Pediatrics, Division of Infectious Diseases, University of Kentucky, Lexington, KY 40536-0284, USA.
Clinical Infectious Diseases (Impact Factor: 8.89). 10/2010; 51(10):e76-81. DOI: 10.1086/656918
Source: PubMed

ABSTRACT

Congenital cytomegalovirus (CMV) is a leading cause of disability, including sensorineural hearing loss, developmental delay, and mental retardation. Although the seroprevalence of CMV and associated exposure and behavioral risk factors have been reported in adolescent females, few data exist about males.
Serum samples were obtained from males aged 12-17 years from June 2006 through July 2007 in Cincinnati, Ohio; Galveston, Texas; and Nashville, Tennessee. The samples were tested for CMV immunoglobulin G antibody with a commercial assay. Participants completed a computer-assisted screening interview to assess 7 risk categories.
A total of 397 adolescent males were screened, and 165 (47%) were seropositive. African American race, older age, and exposure to children ≤ 3 years of age in the home were significant predictors of CMV infection in the univariate analysis. Hispanic ethnicity, group living situations, saliva-sharing behaviors, and intimate sexual contact were not associated with CMV infection. However, among those with a history of sexual contact, the number of life-time partners was associated with CMV. In the final multivariate model, CMV seroprevalence was significantly higher in African American subjects (odds ratio [OR], 1.93; 95% confidence interval [CI], 1.27-2.95) and subjects ≥ 14 years of age (OR, 1.1; 95% CI, 1.0-1.28). With each additional risk factor, males had a 1.6 times increased risk of CMV.
CMV infections are common in adolescent males and are associated with African American race and increasing age. Further study is needed to understand these risk factors in preparation for a CMV vaccine targeted at both adolescent males and females.

Full-text

Available from: Laura Patricia Stadler, Apr 13, 2015
e76 CID 2010:51 (15 November) Stadler et al
MAJOR ARTICLE
Seroprevalence of Cytomegalovirus (CMV)
and Risk Factors for Infection in Adolescent Males
Laura Patricia Stadler,
1
David I. Bernstein,
2
S. Todd Callahan,
3
Jennifer Ferreira,
5
Gina A. Gorgone Simone,
5
Kathryn M. Edwards,
4
Lawrence R. Stanberry,
6
and Susan L. Rosenthal
6
1
Department of Pediatrics, Division of Infectious Diseases, University of Kentucky, Lexington;
2
Department of Pediatrics, Division of Infectious
Diseases, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio;
3
Department of Adolescent Medicine, Vanderbilt University,
and
4
Department of Pediatrics, Division of Pediatric Infectious Disease, Vanderbilt Vaccine Research Program, Nashville, Tennessee;
5
Emmes
Corporation, Rockville, Maryland; and
6
Department of Pediatrics, Columbia University Medical Center, New York, New York
Background. Congenital cytomegalovirus (CMV) is a leading cause of disability, including sensorineural hearing
loss, developmental delay, and mental retardation. Although the seroprevalence of CMV and associated exposure
and behavioral risk factors have been reported in adolescent females, few data exist about males.
Methods. Serum samples were obtained from males aged 12–17 years from June 2006 through July 2007 in
Cincinnati, Ohio; Galveston, Texas; and Nashville, Tennessee. The samples were tested for CMV immunoglobulin
G antibody with a commercial assay. Participants completed a computer-assisted screening interview to assess 7
risk categories.
Results. A total of 397 adolescent males were screened, and 165 (47%) were seropositive. African American
race, older age, and exposure to children 3 years of age in the home were significant predictors of CMV infection
in the univariate analysis. Hispanic ethnicity, group living situations, saliva-sharing behaviors, and intimate sexual
contact were not associated with CMV infection. However, among those with a history of sexual contact, the
number of life-time partners was associated with CMV. In the final multivariate model, CMV seroprevalence was
significantly higher in African American subjects (odds ratio [OR], 1.93; 95% confidence interval [CI], 1.27–2.95)
and subjects 14 years of age (OR, 1.1; 95% CI, 1.0–1.28). With each additional risk factor, males had a 1.6 times
increased risk of CMV.
Conclusions. CMV infections are common in adolescent males and are associated with African American race
and increasing age. Further study is needed to understand these risk factors in preparation for a CMV vaccine
targeted at both adolescent males and females.
Cytomegalovirus (CMV) is an extremely common in-
fection with estimates of seroprevalence among ado-
lescents ranging from 47% to 89% [1–8]. Studies of
CMV indicate that it may be transmitted from a variety
of sources, including saliva, urine (or handling of di-
apers), blood, cervical secretions, and semen [4, 8–14].
Understanding the prevalence of CMV is important,
because it is one of the leading causes of birth defects
and childhood disability in the United States [15]. Each
year in the United States, an estimated 8,000 infants
Received 7 May 2010; accepted 5 August 2010; electronically published 11 October
2010.
Reprints or correspondence: Dr Laura Patricia Stadler, University of Kentucky,
Kentucky Clinic J414, 740 S Limestone St, Lexington, KY 40536-0284 (laura.stadler@
uky.edu).
Clinical Infectious Diseases 2010;51(10):e76–e81
2010 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2010/5110-00E2$15.00
DOI: 10.1086/656918
develop disabilities, including mental retardation and
sensorineural deafness [16–19], with an estimated an-
nual cost of caring for these children of $1 billion–$2
billion [20]. Although risk factors have been previously
evaluated, primarily in women of childbearing age, few
data exist regarding risk factors associated with CMV
acquisition in adolescent males. Adolescent males en-
gage in personal behaviors (such as saliva-sharing be-
haviors, including sharing drinks and kissing) and have
exposures (such as caring for infants and toddlers and
living in groups) and the onset of sexual activity, all of
which may place adolescents at risk. Given the likeli-
hood of an effective vaccine in the near future [21], it
is critical to understand the prevalence and risk factors
for CMV infection among adolescent males aged 12–
18 years, which may represent a period of increased
CMV acquisition. These are likely to be the target ages
for vaccination and catch-up vaccination. Thus, we
sought to determine the seroprevalence of CMV in ad-
Page 1
CMV Infections in Adolescent Males CID 2010:51 (15 November) e77
Table 1. Cytomegalovirus (CMV) Serostatus of Adolescent Males by Site Location
Site n
Race
Hispanic
ethnicity
Age,
mean,
years CMV+
African
American White Multiracial Other
CCHMC 160 134 (84) 18 (11) 8 (5) 0 (0) 0 (0) 14.7 82 (51)
UTMB 101 29 (29) 48 (48) 24 (24) 0 (0) 34 (34) 14.2 50 (50)
VUMC 136 66 (49) 56 (41) 13 (10) 1 (1) 18 (13) 14.1 54 (40)
Total 397 229 (58) 122 (31) 45 (11) 1 (0) 52 (13) 14.4 186 (47)
NOTE. Data are no. (%) of participants, unless otherwise indicated. Study site was not a statistically sig-
nificant factor (odds ratio, 1.07; confidence interval, 0.65–1.77). CCHMC, Cincinnati Children’s Hospital Medical
Center; UTMB, University of Texas Medical Branch in Galveston; VUMC, Vanderbilt University Medical Center.
olescent males and to examine some of the exposures and be-
haviors associated with infection.
MATERIALS AND METHODS
Study population and design. To determine seroprevalence
of CMV and factors associated with CMV infection in prep-
aration for CMV vaccine trials, males aged 12 through 17 years
were recruited from established patient populations of adoles-
cent health clinics affiliated with Cincinnati Children’s Hospital
Medical Center (CCHMC; Cincinnati, OH), The University of
Texas Medical Branch at Galveston (UTMB), and Vanderbilt
University Medical Center (VUMC; Nashville, TN) from June
2006 through July 2007. A blood specimen was obtained for
each subject for the evaluation of CMV serum immunoglobulin
G antibody using a commercial enzyme-linked immunosorbent
assay (Wampole; Inverness Medical Professional Diagnostics)
in accordance with the manufacturer’s instructions. All CMV
antibody tests were performed at CCHMC laboratories for stan-
dardization. Participants completed a computer-assisted screen-
ing interview (CASI) to assess 7 categories of risk: race, ethnicity,
age, exposure to children 3 years of age in the household, group
living situations, saliva-sharing behaviors (including kissing), and
sexual activity. Race was established by having the participants
list all applicable terms from the following list: African American/
black, American Indian/Alaskan Native, Asian, Hawaiian/Pacific
Islander, and Caucasian/white. In addition, a participant was
asked to describe himself as “Hispanic” or “non-Hispanic,” re-
gardless of race. For participants aged 14 years (legal age of
consent), the CASI included items regarding intimate sexual con-
tact (oral, vaginal, and anal intercourse). The CASI was derived
from questions in a previous study [8] and the experience of the
investigators. The institutional review boards of each site ap-
proved this study before its initiation, and a certificate of con-
fidentiality was obtained.
Statistical analysis. Data analysis was performed with SAS,
version 9.2 (SAS Institute). The overall seroprevalence of CMV
was determined by point prevalence calculations. We performed
x
2
analyses to determine factors associated with CMV infection.
When performing initial analyses, questions qualifying various
exposures as “sometimes,” “often,” or “never or rarely” were
collapsed into “sometimes or often” versus “never or rarely”
categories. For purposes of the analyses, those of African Amer-
ican race were compared with those of “non–African American
race.” Of 45 participants who defined themselves as “multi-
racial” or who listed 1 race, subjects were considered “African
American” if this was listed and “non–African American” if it
was not.
After we performed the univariate analyses of 7 variables
(discussed above), risk factors were entered into a multivariate
logistic regression model with a cut-off value of , usingP
! .10
a forward strategy for adding significant variables and a back-
ward strategy for removing nonsignificant variables. We also
evaluated whether the number of significant factors in the uni-
variate analysis may be additive in determining an adolescent’s
risk for CMV antibody.
RESULTS
Demographics. Of 411 adolescent males initially enrolled, 5
subjects did not have CMV serology results, and another 9
subjects (with serology results) did not fully answer the ques-
tionnaire. The remaining 397 participants had available serol-
ogy results and a completed questionnaire and subsequently
were included in the statistical analysis. Table 1 displays the
characteristics of adolescent males at participating clinics with
regard to race, ethnicity, mean age, and CMV serostatus. There
were no significant differences in CMV serostatus on the basis
of site (odds ratio [OR], 1.07; 95% confidence interval [CI],
0.65–1.77). Therefore, data from all sites were combined for
further analyses. The mean age (SD) of the participants was
14.4 1.67 years. The sample was 58% African American,
31% white, and 11% multiracial. Regardless of race, 13% of
the participants reported Hispanic ethnicity. Overall, 186 (47%)
of the 397 participants were seropositive for CMV.
Table 2 displays the CMV serostatus of adolescent males by
risk factor. Being African American was associated with a 2-
fold increased risk of being CMV seropositive (CI, 1.31–3.03).
Hispanic ethnicity was not associated with CMV antibody
status (OR, 0.97; CI, 0.54–1.74). When age was studied as an
Page 2
e78 CID 2010:51 (15 November) Stadler et al
Table 2. Cytomegalovirus (CMV) Serostatus of Adolescent Males by Risk Factor
Risk factor n CMV+ OR (95% CI) P
African American race
Yes 253 134 (53) 1.99 (1.31–3.03) .001
No 144 52 (36)
Hispanic ethnicity
Yes 52 24 (46) 0.97 (0.54–1.74) .914
No 345 162 (47)
Age 14 years
Yes 261 137 (52) 1.96 (1.28–3.0) .002
No 136 49 (36)
Presence of children 3 years old in home
Yes 165 88 (53) 1.56 (1.04–2.34) .03
No 225 95 (42)
Total 397 186 (47)
NOTE. Data are no. (%) of participants, unless otherwise specified. CI, confidence interval; OR, odds
ratio.
ordinal variable, it was associated with a statistically significant
increase in CMV infection (OR, 1.17; CI , 1.04–1.32). The rate
of CMV infection increased from 36% in 12-year-olds to 57%
in 17-year-olds. When age was categorized as
!14 years and
14 years, males 14 years of age were 2 times more likely
to be CMV positive (OR, 1.96; CI, 1.28–3.0).
Exposure to young children in the home. Overall, 165 sub-
jects (42%) reported exposure to children 3 years of age in
the home (mean number of children, 2.7; range, 0–30). Ex-
posure to a young child in the home was significantly associated
with CMV infection (OR, 1.56; CI, 1.04–2.34); however, in-
dividual activities related to caring for young children in the
home (i.e., changing diapers, feeding children, and watching
young children) were not significantly associated with CMV
infection.
Group living situations. One hundred eighty (45%) of 397
adolescent males had experienced a form of group living, which
was defined as serving as an overnight camp counselor (n p
), attending overnight camp ( ), staying overnight in10 n p 140
juvenile detention and/or jail ( ), or staying overnight inn p 40
a treatment program for drug, alcohol, or mental problems
( ). Participants who had experienced one of these groupn p 11
living situations did not have any significant differences in CMV
serostatus, compared with those who had not (OR, 1.31; CI,
0.88–1.95).
Saliva-sharing behaviors. When evaluated for behaviors
that may transmit saliva (such as sharing drinks, lip balm, or
toothbrushes), 226 (57%) of the adolescents shared 1 item.
Of the 226 participants who shared items, 106 (47%) were CMV
seropositive; there was no difference in serostatus based on
sharing these items (OR, 1.0; 95% CI, 0.68–1.5). Of the 397
adolescent males studied, 294 (74%) reported kissing another
adolescent (male or female). Of these 294 participants, 143
(49%) were CMV seropositive. Kissing was not a statistically
significant risk factor for CMV antibody (OR, 1.27; 95% CI,
0.80–2.0). When sharing items and kissing were grouped to-
gether in a saliva-sharing personal behavior category, 336 (85%)
of the adolescents engaged in this behavior. This also was not
statistically predictive of CMV infection (OR, 1.44; 95% CI,
0.82–2.50).
Sexual activity. Of the 261 participants 14 years of age
and thus eligible to answer the questions regarding sexual ac-
tivity, 132 (51%) reported some form of intimate sexual contact
(defined as anal, oral, or vaginal intercourse). Of those who
had a history of sexual contact, 52% were CMV seropositive,
which was not significantly different from the rate of those who
did not (OR, 1.08; 95% CI, 0.66–1.76). When the 3 individual
sexual intercourse behaviors were examined individually, there
were also no significant associations with CMV infection. The
mean time from first intimate sexual contact to participation
in the study (SD) was 2.46 1.79 years, with no statistically
significant differences in CMV serostatus ( ). However,P p .11
among those with a history of sexual contact, there was a sig-
nificant difference between the mean number of vaginal inter-
course partners for those who were CMV seropositive (5.36
4.53) and the mean number of vaginal intercourse partners for
those who were CMV seronegative (3.79 5.18) ( ).P p .036
Multivariate analysis. Table 3 displays a summary of the
relationship of the 7 factors evaluated with regard to CMV
antibody. Multivariate logistic regression analysis was per-
formed with the 3 significant predictors in the univariate anal-
yses (African American race, age, and exposure to children 3
years of age in the home). In the final model, only African
American race ( ) and age ( ) remained as pre-P p .044 P p .002
dictors of CMV antibody. African American race was associated
with a 2-fold risk of CMV seropositivity (OR, 1.93; CI, 1.27–
Page 3
CMV Infections in Adolescent Males CID 2010:51 (15 November) e79
Table 3. Summary of Risk Factors and Odds Ratios (ORs)
Risk factor n CMV+ OR (95% CI) P
AA race 253 134 (53) 1.99 (1.31–3.03) .001
Hispanic ethnicity 52 24 (46) 0.97 (.054–1.74) .914
Age (continuous variable) 261 137 (52) 1.96 (1.28–3.00) .002
Children 3 years in home 165 88 (53) 1.56 (1.04–2.34) .03
Group living situations 180 91 (51) 1.31 (0.88–1.95) .178
Saliva-sharing behaviors 336 162 (48) 1.44 (0.82–2.50) .203
Sexual activity 132 69 (52) 1.08 (0.66–1.76) .766
NOTE. Data are no. (%) of participants, unless otherwise specified. CI, con-
fidence interval; CMV, cytomegalovirus.
Table 4. Relationship Between Significant Risk
Factors and Presence of Cytomegalovirus (CMV)
Antibody
No. of
risk factors
No. of
participants CMV CMV+
0 40 32 (80) 8 (20)
1 123 75 (61) 48 (39)
2 146 67 (46) 79 (54)
3 88 37 (42) 51 (58)
Total 397 211 (53) 186 (47)
NOTE. Data are no. (%) of participants, unless otherwise
specified. With each additional risk factor, adolescent males
had a 1.66 times increased risk of CMV (confidence interval,
1.32–2.08; ). Significant risk factors included AfricanP
! .001
American race, age, and presence of children 3 years old
in the home.
2.95). Each additional year of age was associated with a 1.1
times increased risk of CMV (95% CI, 1.00–1.28).
To examine whether there were an increased risk of CMV
infection in subjects with multiple risk factors, the 3 significant
factors were evaluated in an additive fashion with respect to
CMV antibody. Number of lifetime sexual partners was not
included, because the data was limited to those 14 years of
age who had a history of sexual contact. Table 4 displays the
relationship of the number of risk factors to CMV infection.
It is interesting that of 40 subjects with no risk factors, only 8
(20%) were CMV seropositive. However, of 88 adolescents with
all 3 risk factors, 51 (58%) were seropositive. As the number
of risk factors increased, so did the percentage of adolescents
who were CMV positive (OR, 1.6; 95% CI, 1.32–2.08).
DISCUSSION
CMV infections are common in adolescent males. Forty-seven
percent of males in this study were CMV seropositive, which
is comparable with prior US estimates (41%–89%) [1, 2, 7, 8,
11, 22]. Given that approximately half of all males are becoming
infected with CMV by adolescence, it is important to under-
stand what factors, exposures, and personal behaviors may be
associated with infection.
Previous reports (about both females and males) indicated
that both African Americans and Hispanics may have higher
rates of positive CMV antibody [1, 4, 22–24] than do white
subjects. Our study supported higher rates in African Ameri-
cans but did not detect higher rates in Hispanic participants.
The literature suggests that the 2 main periods of CMV ac-
quisition are in early childhood (as documented in day care
studies [9, 25–27]) and in young adulthood (presumed to be
linked to sexual exposure because CMV has been isolated from
saliva, cervical specimens [28], and semen [29]). Studies of
young women have supported the significance of sexual trans-
mission, because increased CMV infection rates have been
found in those with heterosexual contact [13], early sexual
debut [4, 25], an increased number of partners [5], and a
history of sexually transmitted infections [12].
Our study indicates that seroprevalence increases with age
in males; 36% of 12-year-olds had evidence of CMV, whereas
by age 17 years, 57% showed antibody. However, we did not
find a direct link to sexual exposure (either kissing or intimate
sexual contact). Yet, among those with a history of sexual in-
tercourse, an increasing number of sexual partners did increase
risk. Whether this association represents increased sexual ex-
posure, identifies those who engage in more numerous risky
behaviors or perhaps in riskier behaviors, or selects individuals
who are exposed to a different partner pool is unknown. In a
recent comprehensive study [24], several sexual activity markers
were evaluated in both young women and young men. Al-
though associations between CMV infection and sexual activity
were detected in non-Hispanic females, little or no association
was detected within each racial and/or ethnic group of males.
The associations between CMV infection and sexual activity in
women may be related more to efficient transmission from the
receptive nature of vaginal intercourse, biologic differences,
and/or high viral titer in semen, which may account for the
finding that females have higher rates of CMV infection [1,
29–32] than do males.
It is also possible that the gender difference in CMV se-
roprevalence reflects females’ exposure to young children. In
our study, 42% of adolescent males had children 3 years of
age in the household, and these adolescents were more likely
to be CMV seropositive. Although the relationship of child
care to CMV infection has been presumed to be attributable
to the presence of CMV at high titers in urine and/or saliva,
we were not able to find specific behaviors that increase ex-
posure that were associated with a greater likelihood of CMV
infection in males. Nevertheless, the study presented here sug-
gests that, similar to females, adolescent males are at an in-
creased risk of CMV infection when exposed to young chil-
dren in the household.
Previous studies have also noted that both group living and
living in crowded situations have been positively associated with
Page 4
e80 CID 2010:51 (15 November) Stadler et al
CMV infection [1, 33–36]. In our study, we examined group
living exposure without a precise assessment of how much close
contact that involved. After evaluating various types of group
living situations and varied durations of exposure to those set-
tings individually, this variable was not significant. Therefore,
the specific types and durations were combined as a group living
variable; however, it still was not statistically significant.
One of the possible sources of transmission is saliva, and
saliva-sharing behaviors increase during adolescence. These be-
haviors are common, with 57% of adolescents having shared
items and 74% having a history of kissing. When evaluated
collectively, the relationship was not significant; however, this
could have been a sample size issue, because the relationship
approached significance. It may be that kissing is a key behavior,
but the cross-sectional design, older age of our subjects (mean
age, 14.4 years), and limited assessment of the amount and
type of kissing did not allow us to capture the impact of this
behavior. Lastly, when placed in a multivariate analysis, African
American race and age remained in the model, and exposure
to young children did not. Furthermore, there appeared to be
an additive effect of various risk factors, such that seropositivity
increased with the number of risk factors that were present.
There are a number of limitations to this study, including a
sample size that may have been unable to detect small differ-
ences between groups and to evaluate differences in frequency
and amount of specific behaviors. Given that only 262 of 397
participants were 14 years of age and thus eligible to answer
questions regarding sexual activity, our ability to fully assess
sexual activity was limited. Factors related to the postinfancy
years and early childhood (such as country of origin, breast-
feeding, and day care) were not evaluated, because we wanted
to focus on issues pertinent to adolescents. Lastly, the cross-
sectional design of this study limits the analysis to associations
and does not allow us to pair the timing of increases in risk
behavior in adolescence with new infections. Future studies
should examine these relationships in a longitudinal design of
sufficient sample size to evaluate these exposures and individual
behaviors in adolescent males in preparation for a CMV vaccine
targeted at adolescents.
Acknowledgments
We thank Dick Ward and Jesse LePage, for performing the CMV antibody
assays; study coordinators Tara Foltz, Danielle Shoreman (CCHMC), and
Heather Meza (UTMB), as well as Lisa Sherden, Matt Urmy, and Mary
Vozar (VUMC), for their efforts in recruitment and sound advice; Jennifer
Kissner and Emily Foster (VUMC), for their involvement in the study; and
Heather Hill (Emmes), for help in developing the CASI.
Financial support. National Institute of Allergy and Infectious Diseases
(grants N01-AI-25459, AI-80006 to Cincinnati Children’s Hospital, and
N01-AI-8007 to Vanderbilt University); Molecular Epidemiology Child En-
vironmental Health–National Institute of Environmental Health Sciences
(training grant 5-T32-ES010957-08 to L.P.S.); National Institutes of Health
(loan repayment extramural grant funding 2L30AI066732-02 for clinical
research from October 2005 through July 2008 to L.P.S.).
Potential conflicts of interest. K.M.E. participates in research with
Novartis for meningococcal vaccines and with Sanofi Pasteur for serologic
studies for pertussis, serves as a consultant to NexBio, and receives contract
support from National Institutes of Health and Centers for Disease Control
and Prevention. All other authors: no conflicts.
References
1. Staras SA, Dollard SC, Radford KW, Flanders WD, Pass RF, Cannon
MJ. Seroprevalence of cytomegalovirus infection in the United States,
1988–1994. Clin Infect Dis 2006; 43(9):1143–1151.
2. Bate SL, Dollard SC, Cannon MJ. Cytomegalovirus seroprevalence in
the United States: the National Health and Nutrition Examination
Surveys, 1988–2004. Clin Infect Dis 2010; 50(11):1439–1447.
3. Kumar ML, Nankervis GA, Cooper AR, Gold E. Postnatally acquired
cytomegalovirus infections in infants of CMV-excreting mothers. J Pe-
diatr 1984; 104(5):669–673.
4. Chandler SH, Holmes KK, Wentworth BB, et al. The epidemiology of
cytomegaloviral infection in women attending a sexually transmitted
disease clinic. J Infect Dis 1985; 152(3):597–605.
5. Sohn YM, Oh MK, Balcarek KB, Cloud GA, Pass RF. Cytomegalovirus
infection in sexually active adolescents. J Infect Dis 1991; 163(3):460
463.
6. Nesmith JD, Pass RF. Cytomegalovirus infection in adolescents. Ado-
lesc Med 1995; 6(1):79–90.
7. Rosenthal SL, Stanberry LR, Biro FM, et al. Seroprevalence of herpes
simplex virus types 1 and 2 and cytomegalovirus in adolescents. Clin
Infect Dis 1997; 24(2):135–139.
8. Stanberry LR, Rosenthal SL, Mills L, et al. Longitudinal risk of her-
pes simplex virus (HSV) type 1, HSV type 2, and cytomegalovirus in-
fections among young adolescent girls. Clin Infect Dis 2004; 39(10):
1433–1438.
9. Bale JF Jr, Zimmerman B, Dawson JD, Souza IE, Petheram SJ, Murph
JR. Cytomegalovirus transmission in child care homes. Arch Pediatr
Adolesc Med 1999; 153(1):75–79.
10. Pass RF, Hutto C, Ricks R, Cloud GA. Increased rate of cytomegalovirus
infection among parents of children attending day-care centers. N Engl
JMed1986; 314(22):1414–1418.
11. Zanghellini F, Boppana SB, Emery VC, Griffiths PD, Pass RF. Asymp-
tomatic primary cytomegalovirus infection: virologic and immunologic
features. J infect Dis 1999; 180(3):702–707.
12. Jordan MC, Rousseau WE, Noble GR, Steward JA, Chin TD. Associ-
ation of cervical cytomegaloviruses with venereal disease. N Engl J Med
1973; 288(18):932–934.
13. Handsfield HH, Chandler SH, Caine VA, et al. Cytomegalovirus in-
fection in sex partners: evidence for sexual transmission. J Infect Dis
1985; 151(2):344–348.
14. Lang DJ, Kummer JF. Demonstration of cytomegalovirus in semen. N
Engl J Med 1972; 287(15):756–758.
15. Cannon MJ, Davis KF. Washing our hands of the congenital cyto-
megalovirus disease epidemic. BMC Public Health 2005; 5:70.
16. Fowler KB, Stagno S, Pass RF, Britt WJ, Boll TJ, Alford CA. The
outcome of congenital cytomegalovirus infection in relation to ma-
ternal antibody status. N Engl J Med 1992; 326(10):663–667.
17. Fowler KB, McCollister FP, Dahle AJ, Boppana S, Britt WJ, Pass RF.
Progressive and fluctuating sensorineural hearing loss in children with
asymptomatic congenital cytomegalovirus infection. J Pediatr 1997;
130(4):624–630.
18. Stagno S, Pass RF, Dworsky ME, Alford CA Jr. Maternal cytomegalovirus
infection and perinatal transmission. Clin Obstet Gynecol 1982; 25(3):
563–576.
19. Stratton KR, Durch JS, Lawrence RS, eds; Institute of Medicine (US)
Committee to Study Priorities for Vaccine Development, Division of
Health Promotion and Disease Prevention, Institute of Medicine. Vac-
cines for the 21st century: a tool for decision making. Washington,
DC: National Academy Press, 2000.
20. Dobbins JG, Stewart JA, Demmler GJ. Surveillance of congenital cyto-
Page 5
CMV Infections in Adolescent Males CID 2010:51 (15 November) e81
megalovirus disease, 1990–1991. Collaborating Registry Group. MMWR
CDC Surveill Summ 1992; 41(2):35–39.
21. Pass RF, Zhang C, Evans A, et al. Vaccine prevention of maternal
cytomegalovirus infection. N Engl J Med 2009; 360(12):1191–1199.
22. Sohn YM, Oh MK, Balcarek KB, Cloud GA, Pass RF. Cytomegalovirus
infection in sexually active adolescents. J Infect Dis 1991; 163(3):460
463.
23. Tookey PA, Ades AE, Peckham CS. Cytomegalovirus prevalence in
pregnant women: the influence of parity. Arch Dis Child 1992;67(7
Spec No):779–783.
24. Staras SA, Flanders WD, Dollard SC, Pass RF, McGowan JE Jr, Cannon
MJ. Influence of sexual activity on cytomegalovirus seroprevalence in
the United States, 1988–1994. Sex Transm Dis 2008; 35(5):472–479.
25. Fowler KB, Pass RF. Risk factors for congenital cytomegalovirus in-
fection in the offspring of young women: exposure to young children
and recent onset of sexual activity. Pediatrics 2006; 118(2):e286–e292.
Epub 2006 Jul 17.
26. Adler SP, Finney JW, Manganello AM, Best AM. Prevention of child-
to-mother transmission of cytomegalovirus among pregnant women.
J Pediatr 2004; 145(4):485–491.
27. Adler SP. Cytomegalovirus transmission among children in day care,
their mothers and caretakers. Pediatr Infect Dis J 1988; 7(4):279–285.
28. Jordan MC, Rousseau WE, Noble GR, Steward JA, Chin TD. Associ-
ation of cervical cytomegaloviruses with venereal disease. N Engl J Med
1973; 288(18):932–934.
29. Lang DJ, Kummer JF. Demonstration of cytomegalovirus in semen. N
Engl J Med 1972; 287(15):756–758.
30. Demmler GJ, Schydlower M, Lampe RM. Texas, teenagers, and CMV.
J Infect Dis 1985; 152(6):1350.
31. Green MS, Cohen D, Slepon R, Robin G, Wiener M. Ethnic and gender
differences in the prevalence of anticytomegalovirus antibodies among
young adults in Israel. Int J Epi 1993; 22(4):720–723.
32. Hecker M, Qiu D, Marquardt K, Bein G, Hackstein H. Continuous
cytomegalovirus seroconversion in a large group of healthy blood do-
nors. Vox Sang 2004; 86(1):41–44.
33. Sarov B, Naggan L, Rosenzveig R, Katz S, Haikin H, Sarov I. Prevalence
of antibodies to human cytomegalovirus in urban, kibbutz, and Bed-
ouin children in southern Israel. J Med Virol 1982; 10(3):195–201.
34. Clarke LM, Duerr A, Feldman J, Sierra MF, Daidone BJ, Landesman
SH. Factors associated with cytomegalovirus infection among human
immunodeficiency virus type 1–seronegative and –seropositive women
from an urban minority community. J Infect Dis 1996; 173(1):77–82.
35. Palacios O, Cabau N, Horaud F, Plotkin S. Serologic survey of anti-
bodies to cytomegalovirus in women and infants in Lima, Peru. J Infect
Dis 1983; 147(4):777.
36. Kothari A, Ramachandran VG, Gupta P, Singh B, Talwar V. Seroprev-
alence of cytomegalovirus among voluntary blood donors in Delhi,
India. J Health Popul Nutr 2002; 20(4):348–351.
Page 6
  • Source
    • "The mean titer of anti-EBV nuclear-antigen antibodies was significantly higher in Sjögren's syndrome patients than in normal people. [48] Cytomegalovirus Cytomegalovirus (CMV) is a common infection with a seroprevalence among adolescents ranging from 47% to 89%. [49] The persistence of CMV with alteration of cell surface expression in certain tissues may initiate the tissue destruction that leads to the clinical manifestations of Sjögren's syndrome. Ductal cells of salivary and lacrimal glands are immunologically attacked due to CMV antigenic expression. "
    [Show abstract] [Hide abstract] ABSTRACT: Xerostomia is a common complaint of nearly half of the elderly population and about one-fifth of younger adults. It causes several signs and symptoms, and compromise oral functions and health-related quality-of-life. Multiple reasons are proposed to describe the etiology of xerostomia such as local factors, psychogenic factors, and systemic diseases. In order to manage xerostomia effectively, identification of the main causality is mandatory. The aim of this review was to present systemic diseases leading to xerostomia with their mechanisms of action. We used various general search engines and specialized databases such as Google, Google Scholar, Yahoo, PubMed, PubMed Central, MedLine Plus, Medknow, EBSCO, ScienceDirect, Scopus, WebMD, EMBASE, and authorized textbooks to find relevant topics by means of Medical Subject Headings keywords such as "xerostomia," "hyposalivations," "mouth dryness," "disease," and "systemic." We appraised 97 English-language articles published over the last 40 years in both medical and dental journals including reviews, meta-analysis, original papers, and case reports. Upon compilation of relevant data, it was concluded that autoimmune diseases most frequently involve salivary glands and cause xerostomia followed by diabetes mellitus, renal failure, and graft-versus-host disease. Moreover, the underlying mechanisms of systemic disease-related xerostomia are: autoimmunity, infiltration of immunocompetent cells, granuloma formation, fibrosis and dehydration, deposition of proteinaceous substances, bacterial infection, and side-effects of medications.
    Full-text · Article · Jul 2014
  • Source
    [Show abstract] [Hide abstract] ABSTRACT: Human cytomegalovirus (HCMV) is an undisputed pathogen in humans with severe immune compromise, which has historically been thought to carry little consequence in immunocompetent hosts. During the past decade, however, accumulating data suggest that significant numbers of immunocompetent humans reactivate HCMV during critical illness, and that these reactivation episodes are associated with worsened outcomes. Because most people are infected with this ubiquitous virus by adulthood, confirming pathogenicity has now become a clinical priority. In this article, we will review the incidence and implications of reactivation, the relevant immune responses and reactivation triggers relevant to the immunocompetent host. We will summarize the progress made during the past ten years, outline the work ongoing in this field, and identify the major gaps remaining in our emerging understanding of this phenomenon.
    Full-text · Article · Mar 2011 · Antiviral research
  • No preview · Article · Jan 2012 · Critical care medicine
Show more