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Oral Human Papillomavirus Infection: Differences in Prevalence Between Sexes and Concordance With Genital Human Papillomavirus Infection, NHANES 2011 to 2014

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Abstract

Background: The burden of human papillomavirus (HPV)-positive oropharyngeal squamous cell carcinoma (OPSCC) is disproportionately high among men, yet empirical evidence regarding the difference in prevalence of oral HPV infection between men and women is limited. Concordance of oral and genital HPV infection among men is unknown. Objective: To determine the prevalence of oral HPV infection, as well as the concordance of oral and genital HPV infection, among U.S. men and women. Design: Nationally representative survey. Setting: Civilian noninstitutionalized population. Participants: Adults aged 18 to 69 years from NHANES (National Health and Nutritional Examination Survey, 2011 to 2014). Measurements: Oral rinse, penile swab, and vaginal swab specimens were evaluated by polymerase chain reaction followed by type-specific hybridization. Results: The overall prevalence of oral HPV infection was 11.5% (95% CI, 9.8% to 13.1%) in men and 3.2% (CI, 2.7% to 3.8%) in women (equating to 11 million men and 3.2 million women nationwide). High-risk oral HPV infection was more prevalent among men (7.3% [CI, 6.0% to 8.6%]) than women (1.4% [CI, 1.0% to 1.8%]). Oral HPV 16 was 6 times more common in men (1.8% [CI, 1.3% to 2.2%]) than women (0.3% [CI, 0.1% to 0.5%]) (1.7 million men vs. 0.27 million women). Among men and women who reported having same-sex partners, the prevalence of high-risk HPV infection was 12.7% (CI, 7.0% to 18.4%) and 3.6% (CI, 1.4% to 5.9%), respectively. Among men who reported having 2 or more same-sex oral sex partners, the prevalence of high-risk HPV infection was 22.2% (CI, 9.6% to 34.8%). Oral HPV prevalence among men with concurrent genital HPV infection was fourfold greater (19.3%) than among those without it (4.4%). Men had 5.4% (CI, 5.1% to 5.8%) greater predicted probability of high-risk oral HPV infection than women. The predicted probability of high-risk oral HPV infection was greatest among black participants, those who smoked more than 20 cigarettes daily, current marijuana users, and those who reported 16 or more lifetime vaginal or oral sex partners. Limitation: Sexual behaviors were self-reported. Conclusion: Oral HPV infection is common among U.S. men. This study's findings provide several policy implications to guide future OPSCC prevention efforts to combat this disease. Primary funding source: National Cancer Institute.
Oral Human Papillomavirus Infection: Differences in Prevalence
Between Sexes and Concordance With Genital Human Papillomavirus
Infection, NHANES 2011 to 2014
Kalyani Sonawane, PhD; Ryan Suk, MS; Elizabeth Y. Chiao, MD, MPH; Jagpreet Chhatwal, PhD; Peihua Qiu, PhD;
Timothy Wilkin, MD, MPH; Alan G. Nyitray, PhD; Andrew G. Sikora, MD, PhD; and Ashish A. Deshmukh, PhD, MPH
Background: The burden of human papillomavirus (HPV)–
positive oropharyngeal squamous cell carcinoma (OPSCC) is dis-
proportionately high among men, yet empirical evidence re-
garding the difference in prevalence of oral HPV infection be-
tween men and women is limited. Concordance of oral and
genital HPV infection among men is unknown.
Objective: To determine the prevalence of oral HPV infection,
as well as the concordance of oral and genital HPV infection,
among U.S. men and women.
Design: Nationally representative survey.
Setting: Civilian noninstitutionalized population.
Participants: Adults aged 18 to 69 years from NHANES (Na-
tional Health and Nutritional Examination Survey, 2011 to 2014).
Measurements: Oral rinse, penile swab, and vaginal swab
specimens were evaluated by polymerase chain reaction fol-
lowed by type-specific hybridization.
Results: The overall prevalence of oral HPV infection was 11.5%
(95% CI, 9.8% to 13.1%) in men and 3.2% (CI, 2.7% to 3.8%) in
women (equating to 11 million men and 3.2 million women na-
tionwide). High-risk oral HPV infection was more prevalent
among men (7.3% [CI, 6.0% to 8.6%]) than women (1.4% [CI,
1.0% to 1.8%]). Oral HPV 16 was 6 times more common in men
(1.8% [CI, 1.3% to 2.2%]) than women (0.3% [CI, 0.1% to 0.5%])
(1.7 million men vs. 0.27 million women). Among men and
women who reported having same-sex partners, the prevalence
of high-risk HPV infection was 12.7% (CI, 7.0% to 18.4%) and
3.6% (CI, 1.4% to 5.9%), respectively. Among men who reported
having 2 or more same-sex oral sex partners, the prevalence of
high-risk HPV infection was 22.2% (CI, 9.6% to 34.8%). Oral HPV
prevalence among men with concurrent genital HPV infection
was fourfold greater (19.3%) than among those without it (4.4%).
Men had 5.4% (CI, 5.1% to 5.8%) greater predicted probability of
high-risk oral HPV infection than women. The predicted proba-
bility of high-risk oral HPV infection was greatest among black
participants, those who smoked more than 20 cigarettes daily,
current marijuana users, and those who reported 16 or more
lifetime vaginal or oral sex partners.
Limitation: Sexual behaviors were self-reported.
Conclusion: Oral HPV infection is common among U.S. men.
This study's findings provide several policy implications to guide
future OPSCC prevention efforts to combat this disease.
Primary Funding Source: National Cancer Institute.
Ann Intern Med. doi:10.7326/M17-1363 Annals.org
For author affiliations, see end of text.
This article was published at Annals.org on 17 October 2017.
Human papillomavirus (HPV) infection causes cancer
at several anatomical sites, including the orophar-
ynx, anus, and penis in men and the oropharynx, anus,
cervix, vagina, and vulva in women (1). Between 2008
and 2012, an average of 38 793 cases of HPV-related
cancer were diagnosed annually in the United States,
23 000 (59%) in women and 15 793 (41%) in men (2).
Among these cases, the most common cancer was
oropharyngeal squamous cell carcinoma (OPSCC), of
which there were 3100 cases in women and 12 638 in
men (2).
The incidence of HPV-related OPSCC among
women generally plateaued (with a statistically insignif-
icant increase of 0.57% per year) from 2002 to 2012 (3).
In contrast, the incidence among men (7.8 per 100 000)
has increased dramatically (2.89% per year) and has
already surpassed the incidence of cervical cancer in
women (7.4 per 100 000) (3). The increase in annual
incidence was particularly high in men aged 50 to 59
years: 7.75% from 2002 to 2004 and 2.44% from 2004
to 2010 (3). These incidence trends are projected to
continue and not reverse until after 2060, making
OPSCC a significant public health concern (4, 5).
Recent evidence shows that prophylactic HPV vac-
cination seems to protect against infection with
vaccine-covered oral HPV subtypes (6) and thus holds
promise for reversing the rising OPSCC incidence
among men in the long term; however, the low uptake
rate of the vaccine among boys remains a concern (7–
9). Furthermore, the great majority of persons at risk for
OPSCC are older than 26 years (4) and do not qualify
for HPV vaccination or may already have been exposed
to HPV. For this reason, epidemiologic studies on oral
HPV infection are needed to guide the design and de-
velopment of alternative OPSCC prevention strategies
targeted toward persons at high risk. Examining the re-
lationship between HPV infections occurring at differ-
ent anatomical sites also is crucial to understanding
HPV transmission dynamics. Therefore, our objective
was twofold: to estimate the population-based preva-
See also:
Web-Only
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lence and risk factors of oral HPV infection by sex and
sexual orientation and to characterize the concordance
of oral and genital HPV infection from the NHANES
(National Health and Nutrition Examination Survey).
METHODS
Survey Design and Population
The NHANES is conducted by the National Center
for Health Statistics of the Centers for Disease Control
and Prevention to monitor the health and nutritional
status of the U.S. population. Participants in NHANES
2011 to 2014 were noninstitutionalized U.S. civilians
identified through a stratified, multistage probability
sampling technique. Participants aged 18 to 69 years
had a physical examination at a mobile examination
center (MEC), followed by a household interview. His-
panic persons, African Americans, persons with low in-
come, and those aged 60 years and older were over-
sampled to allow sufficient sizes for subgroup analysis.
The medical examinations done at the MEC in-
cluded medical, dental, and physiologic measurements
and laboratory tests administered by highly trained
medical personnel. The household interview compo-
nent consisted of standardized questionnaires on de-
mographics, socioeconomic status, diet, and sexual
behavior administered through a personal or phone
interview.
Demographic and Behavioral Data
The NHANES collected demographic data through
a standard questionnaire administered in-home by
trained interviewers using a computer-assisted per-
sonal interviewing system. Data on cigarette, alcohol,
and marijuana use were collected during the MEC self-
interview. Demographic data included age at the time
of the interview, sex, race, marital status, and income.
Income-to-poverty ratio was calculated by dividing in-
come by the poverty guidelines of the U.S. Department
of Health and Human Services specific to the survey
year. Use of birth control pills and hormone therapy
was self-reported by female participants.
Self-reported sexual behavior data—for example,
ever having had sex (vaginal, anal, or oral), sexual ori-
entation, ever having had a same-sex sexual partner,
number of oral sex partners during the past 12 months,
age at first oral sex, and barrier use during oral sex in
the past 12 months—were collected at the MEC through
a standardized questionnaire. History of herpes or
warts and HPV infection also was self-reported. HIV
positivity was based on HIV-antibody test results.
Specimen Collection and Laboratory Methods
A dental hygienist collected oral rinse specimens in
sterile collection cups. Each participant was asked to
swish a 10-mL sample of a mouthwash or sterile solu-
tion in his or her mouth and then expectorate the sam-
ple into the sterile cup. The MEC laboratory technolo-
gist transferred each sample from the collection cup to
a 14-mL Falcon snap cap tube (Fisher Scientific) and
shipped it to the laboratory for testing. Detailed quality
control steps may be found in the MEC Laboratory Pro-
cedures Manual on the NHANES Web site (10).
Samples were then purified at the laboratory ac-
cording to the Puregene DNA purification kit (Qiagen)
protocol (11).
-Globin–positive samples were consid-
ered evaluable. Each purified DNA sample was ana-
lyzed by polymerase chain reaction assay for detection
of 37 HPV types, including high-risk types (HPV 16, 18,
26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68, 73,
and 82) and low-risk types (HPV 6, 11, 40, 42, 54, 55,
61, 62, 64, 67, 69, 70, 71, 72, 81, 82 IS39 subtype, 83,
84, and 89 [cp6108]) (12).
Concordance of Oral and Genital HPV
Concurrent overall genital and oral HPV infection
was defined as an infection in both the genital and oral
regions, regardless of HPV type. Concurrent high-risk
genital and oral HPV infection was defined as an infec-
tion with any high-risk type in both the genital and oral
regions. Similarly, concurrent type-specific infection
was defined as an infection with a specific HPV type
(such as HPV 16) in the genital and oral regions. Details
of specimen collection and laboratory methods for
genital HPV detection among men and women may be
found on the NHANES Web site and in previously pub-
lished studies (13, 14).
Statistical Analysis
We estimated the prevalence of overall, high-risk,
low-risk, and type-specific oral HPV, as well as preva-
lence by demographics and sexual behaviors, for men
and women aged 18 to 69 years by using NHANES
2011 to 2014. Concordance of genital and oral HPV
infection was estimated for adults aged 18 to 59 years
by using NHANES 2013 to 2014. A survey design–
adjusted Wald Ftest was used for bivariate analyses,
and the Cochran–Armitage test was performed to de-
tect trends in prevalence. Prevalence estimates with a
relative SE greater than 30% or based on 10 or fewer
positive cases are noted; these are considered unstable
and should be interpreted with caution. The differences
in predicted probability between levels of risk factors
for overall and high-risk oral HPV infection were esti-
mated by using logistic regression models. Variables in
logistic regression models were selected on the basis
of bivariate associations. Statistical significance was
tested at P< 0.05. All analyses were performed by us-
ing SAS 9.4 software (SAS Institute). For population es-
timates, we used SAS PROC SURVEY procedures, which
included weight, cluster, and strata statements, to in-
corporate sampling weights.
Role of the Funding Source
The funders had no role in the study design or con-
duct or in the reporting of results.
RESULTS
Analyses of overall and high-risk oral HPV infection
included 4493 men and 4641 women (Supplement Fig-
ure 1, available at Annals.org).
ORIGINAL RESEARCH Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV
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Prevalence of Oral HPV Infection Among Men
and Women
The prevalence of overall oral HPV infection among
men and women was 11.5% (95% CI, 9.8% to 13.1%)
and 3.2% (CI, 2.7% to 3.8%), respectively, equating to
11 million men and 3.2 million women nationwide. Sim-
ilarly, the prevalence of high-risk HPV infections was
higher among men (7.3% [CI, 6.0% to 8.6%]; 7 million)
than women (1.4% [CI, 1.0% to 1.8%]; 1.4 million) (P<
0.001). The type-specific prevalence of high-risk and
low-risk HPV infection is shown in Figure 1,Aand B,
respectively. Notably, the prevalence of HPV 16, the
most common type, was sixfold higher among men
(1.8% [CI, 1.3% to 2.2%]; 1.7 million) than women (0.3%
[CI, 0.1% to 0.5%]; 0.27 million) (P< 0.001). The preva-
lence of all high-risk and low-risk HPV types was consis-
tently higher in men than women. The age-specific
prevalence of vaccine-covered 9-valent, 4-valent,
Figure 1.
Type-specific prevalence of oral HPV infection among men and women, NHANES 2011–2014.
0
0.5
1.5
1.0
2.5
2.0
Prevalence, %
Prevalence, %
High-Risk HPV Types
Men
Women
16 66 59 51 35 56 18 53 39 52 33 58 31 68 73 45 82 26
Participants, nGenotype
Men 70 47 38 26 27 26 18 26 17 16 14 18 10 9 10 8 3 1
Women 13 8 10 5 10 6 3 11 7 7 0 1 0 3 4 3 1 1
62 55 84 6 61 89 81 83 72 42 69 54 67 71 11 70 IS39 40 64
Participants, n
Genotype
A
0
0.5
1.5
1.0
2.5
2.0
Low-Risk HPV Types
Men 48 42 36 34 37 18 19 14 20 13 11 4 5 10 5 2 4 1 1
Women 18 23 11 5 11 7 2 7 9 1 1 1 2 4 1 6 1 2 0
B
A. Weighted prevalence of high-risk type-specific oral HPV infection among men and women. B. Weighted prevalence of low-risk type-specific oral
HPV infection among men and women. Errors bars represent 95% CIs. HPV = human papillomavirus; NHANES = National Health and Nutrition
Examination Survey.
Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV ORIGINAL RESEARCH
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2-valent, and HPV 16 subtypes among men and women
is reported in Supplement Figure 2 (available at Annals
.org).
Prevalence of Overall and High-Risk Oral HPV
Infection by Demographic and Sexual
Characteristics
The prevalence of oral HPV infection by demo-
graphic characteristics is presented in Table 1. The
overall prevalence in men followed a bimodal pattern,
with prevalence peaks at ages 35 to 39 (12.2% [CI, 8.9%
to 15.7%]) and 50 to 54 years (15.4% [CI, 10.2% to
20.5%]). The prevalence of high-risk HPV infection in
men and overall and high-risk HPV infection in women
did not differ significantly with regard to age. Non-
Hispanic black men had the highest prevalence of over-
all (15.8%) and high-risk (8.8%) oral HPV infection, fol-
lowed by white (overall, 11.7%; HR, 7.8%) and Hispanic
(overall, 9.9%; high-risk, 5.5%) men.
The prevalence of overall and high-risk oral HPV
infection was significantly associated with cigarette and
marijuana use among men and women (Table 1). The
prevalence of overall oral HPV infection was highest
(overall, 23.6%; high-risk, 15.0%) among men who
smoked more than 20 cigarettes a day and was lowest
(overall, 8.3%; high-risk, 5.4%) among never-smokers
and former smokers. The prevalence was highest
among men who were former marijuana users (overall,
13.4%; high-risk, 9.4%). Among women, the highest
prevalence of oral HPV infection was in current mari-
juana users (overall, 7.9%; high-risk, 3.0%).
We found no significant difference in the preva-
lence of overall and high-risk HPV infection between
participants who received the HPV vaccine and those
who did not (Table 1). However, among HPV vaccine–
eligible persons who were reportedly vaccinated, we
found that the prevalence of 4-valent types was signifi-
cantly lower than in unvaccinated persons (0.18% vs.
1.47%; P< 0.001) (Supplement Figure 3, available at
Annals.org). Similarly, the difference remained statisti-
cally significant in men (0.41% vs. 1.97%; P= 0.019).
The prevalence of oral HPV infection was signifi-
cantly associated with sexual and behavioral character-
istics among men and women (Appendix Table, avail-
able at Annals.org). The prevalence of high-risk HPV
infection was 8, 10, and 4 times higher in men who
reported having more than 16 lifetime sex partners
(any, oral, or vaginal, respectively) than in those with 1
or no lifetime sex partners. Similarly, the prevalence in
women who reported such behavior was 7, 3, and 6
times higher than in those with 1 or no lifetime sex
partners (any, oral, and vaginal, respectively). When re-
stricted to number of sex partners in the past 12
months, the prevalence of oral HPV (both overall and
high-risk) was highest among men with 2 or more any
and oral sex partners. Results were similar for women
but not statistically significant.
Among men and women who reported having
same-sex partners, the prevalence of high-risk HPV in-
fection was 12.7% (CI, 7.0% to 18.4%) and 3.6% (CI,
1.4% to 5.9%), respectively; whereas among men and
women who did not report this behavior, it was 6.8%
and 1.2%, respectively. In particular, the prevalence of
high-risk HPV infection was highest (22.2% [CI, 9.6% to
34.8%]) among men who reported having 2 or more
lifetime same-sex oral sex partners. No statistically sig-
nificant difference in prevalence was found with regard
to lifetime number of anal sex partners among men
who reported having same-sex partners.
Prevalence of Oral HPV Infection Concurrent
With Genital HPV Infection
Figure 2 illustrates the prevalence of oral HPV in-
fection with and without concurrent genital HPV infec-
tion among men and women (overall and by age and
race). The prevalence of overall (Figure 2,A) and high-
risk (Figure 2,B) oral HPV infections among men with
concurrent genital overall or high-risk HPV infection
was 19.3% and 13.7%, respectively, whereas the prev-
alence among men without such infections was 4.4%
and 3.9%. Similarly, the prevalence of overall (5.1%)
and high-risk (3.2%) oral HPV infection was almost
threefold higher in women with concurrent genital HPV
infection than in those without such infections (overall,
2.1%; high-risk, 1.1%). We also present vaccine-
covered 9-valent, 4-valent, 2-valent, and HPV-16 oral
infection prevalence among men and women with or
without genital HPV infection in Supplement Figure 4
(available at Annals.org).
When stratified by age (Figure 2,Cand D), the
prevalence of oral HPV infection increased with age
among men with or without concurrent genital HPV in-
fection (P< 0.001 for trend). When stratified by race
(Figure 2,Eand F), we found no significant difference
in prevalence of oral HPV infection, regardless of the
presence or absence of genital HPV infection. Among
both men and women, when stratified by lifetime num-
ber of sexual partners, we found that regardless of the
presence or absence of concurrent genital HPV infec-
tion, the prevalence of oral HPV infection increased
with number of sexual partners (any, oral, or vaginal)
(Appendix Figure, available at Annals.org). We further
report prevalence of oral HPV among men and women
with genital HPV infection by age and lifetime number
of sexual partners in Supplement Figures 5 and 6(avail-
able at Annals.org).
Predicted Probability of Oral HPV Infection
The differences in predicted probability between
levels of risk factors for overall and high-risk oral HPV
infection are presented in Table 2. The predicted prob-
ability for overall oral HPV infection was 7.6% (CI, 7.1%
to 8.2%) and that for high-risk oral HPV infection was
5.4% (CI, 5.1% to 5.8%) greater for men than women.
Compared with white participants, black participants
had a greater risk for overall (predicted probability,
3.3% [CI, 2.7% to 3.9%] greater) and high-risk (pre-
dicted probability, 1.2% [CI, 0.8% to 1.6%] greater) oral
HPV infection. Hispanic participants had a greater risk
for overall oral HPV infection (predicted probability,
0.7% [CI, 0.1% to 1.3%] greater) than white participants;
however, their risk for high-risk oral HPV infection was
lower (predicted probability, 0.6% [CI, 1.0% to
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0.2%]). Increase in daily cigarette consumption was
associated with a greater risk for overall and high-risk
oral HPV infection. The risk for participants who
smoked more than 20 cigarettes daily was highest—
9.6% and 8.0% greater predicted probability for overall
and high-risk oral HPV infection, respectively, com-
pared with never or former smokers. Participants who
reported current marijuana use had a 6.4% greater risk
for overall and 4.5% greater risk for high-risk oral HPV
infection than those who never used marijuana. Partic-
ipants who reported having 16 or more lifetime vaginal
sex partners had the greatest risk for overall (predicted
probability, 11.1% greater) and high-risk (predicted
probability, 7.9% greater) oral HPV infection compared
with those who had 1 or no lifetime vaginal sex part-
ners. Similarly, the risk for overall (predicted probabil-
ity, 18.3% greater) and high-risk (predicted probability,
13.0% greater) oral HPV infection was highest for par-
ticipants with 16 or more lifetime oral sex partners. We
also report differences in predicted probability be-
tween levels of risk factors for concordant oral–genital
HPV infection in Supplement Table 3 (available at An-
nals.org).
DISCUSSION
The prevalence of high-risk oral HPV infection in
the United States is substantially higher in men than
women. We found that 7.3% of men and 1.4% of
women in the general population have high-risk oral
HPV infection, which equates to 7 million men and 1.4
million women, respectively. In particular, the preva-
lence of HPV 16, an oncogenic HPV type known to con-
tribute to increased risk for OPSCC, is 6 times greater in
men than women, equating to 1.7 million men and 0.27
million women with HPV 16 infection.
We found that when characterized by age, the
prevalence of high-risk oral HPV infection in both men
and women peaked at age 50 to 54 years. A large mul-
tinational cohort study—HIM (HPV Infection in Men)—
found that the acquisition of high-risk oral HPV infec-
tion was constant across age groups (15). Therefore,
the prevalence peak we observed in older participants
in our study may have been the result of a longer du-
ration of infection at older ages (15, 16). We found that
oncogenic HPV 16 was most prevalent in men aged 50
to 69 years. Data from the HIM study indicate that the
high HPV 16 prevalence among older men might be
attributed to longer persistence of infection (17). The
study reported that prevalent oral HPV 16 infection per-
sisted longer than newly acquired infections and that
the persistence of incident HPV 16 infection increased
significantly with age (17). Given that OPSCC incidence
is greatest in this age group of men (4), determining
whether persistent HPV 16 infection plays a role in the
observed excess prevalence of oral HPV 16 infection is
crucial, particularly because persistent infection might
be driving OPSCC carcinogenesis in older men.
We found that the prevalence of oral HPV infection
was high among men with concurrent genital HPV in-
fection. This finding is particularly important given the
recently reported high prevalence of genital HPV infec-
tion (45.2% [CI, 41.3% to 49.3%]) among U.S. men (13).
To our knowledge, only 1 study, from rural China, stud-
ied oral–genital HPV concordance and found that the
prevalence of oral HPV infection was higher among
men with concurrent genital HPV infection (11.4%) than
those without it (5.7%) (18). Steinau and colleagues (19)
studied oral and anal (another anatomical site) concor-
dance among men who have sex with men and found
that participants were more likely to have any oral HPV
if they also had any anal HPV (relative risk, 1.16 [CI, 1.05
to 1.28]).
The consistent association between sexual behav-
iors (such as lifetime number of sex partners) and the
high prevalence of oral HPV infection among adults
with genital HPV infection observed in our study im-
plies that transmission via genital–oral sex may be oc-
curring in this group (20–22). In addition, oral HPV in-
fection likely is acquired via autoinoculation from
genital HPV infection, or vice versa, through fingers in
the same individual (23). Further study of HPV transmis-
sion dynamics is crucial, because the bidirectional
transmission between genital and oral HPV likely is pro-
moting HPV-related cancer in the same individuals or
contributing to the increased risk of second primary
HPV-related cancer in men (24). Finally, the observed
discrepancy between oral–genital HPV concordance
rates among men and women may be the result of dif-
ferences in the size of HPV sampling area and circum-
cision status of their male partners (25).
The difference in burden of oral oncogenic infec-
tion and OPSCC among men and women is partially
explained by the strength of association between sex-
ual behaviors and HPV infection among men (26) and,
as observed in our study, a higher prevalence of HPV
16 infection in men. Another possibility is that serocon-
version rates after genital HPV infection are lower in
men than women, leading to greater protection against
subsequent oral HPV infection in women (1, 27). Our
findings indicate that association between HPV infec-
tions at oral and genital sites also might be contributing
to this heterogeneity between sexes. The incidence of
OPSCC in women, like that of cervical cancer, is de-
creasing in the United States (5). Because of increased
prevention efforts, such as screening, and given the
positive association between high-risk genital and oral
HPV, the decline in OPSCC incidence in women may be
mirroring the decline in cervical cancer incidence (28).
Likewise, OPSCC incidence trends paralleled increased
rates of genital warts and genital herpes among men
(29). Studies also attributed these incidence trends to a
birth cohort effect predicting that the relative incidence
of OPSCC among men will continue to increase for at
least 30 more years (28, 30).
We examined several risk factors for oral HPV infec-
tion. We found that smoking is associated with a higher
risk for overall oral HPV infection. The exact pathophys-
iologic mechanism of this association is unknown; how-
ever, that smoking induces proinflammatory and immu-
nosuppressive effects, increasing risk for HPV incidence
and persistence at the oropharynx, has been suggested
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Table 1. Prevalence of Overall and High-Risk Oral HPV Infection in Men and Women, by Demographic Characteristics,
NHANES 2011–2014
Characteristic Men
Overall Oral HPV Infection High-Risk Oral HPV Infection
Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
PValue Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
PValue
Age* 0.007 0.132
18–26 y 75/947 6.8 (4.5–9.1) 52/947 5.0 (3.0–7.1)
27–34 y 82/716 10.6 (7.8–13.4) 55/716 7.0 (4.5–9.6)
35–39 y 54/414 12.2 (8.8–15.7) 27/414 5.9 (2.9–8.9)
40–44 y 41/418 11.0 (7.2–14.8) 28/418 7.9 (4.3–11.4)
45–49 y 56/396 13.1 (8.7–17.5) 34/396 8.4 (4.8–12.0)
50–54 y 61/412 15.4 (10.2–20.5) 36/412 9.9 (5.4–14.3)
55–59 y 54/378 14.6 (9.5–19.6) 28/378 8.9 (5.0–12.7)
60–64 y 70/471 13.4 (8.5–18.4) 36/471 7.0 (3.8–10.2)
65–69 y 43/341 11.5 (6.8–16.2) 26/341 8.0 (4.1–12.0)
Marital status† 0.028 0.33
Never married 118/1052 11.4 (7.6–15.2) 74/1052 8.0 (4.5–11.4)
Married/living with partner 293/2567 10.9 (8.8–12.9) 183/2567 7.0 (5.4–8.5)
Widowed/separated/divorced 111/572 18.5 (13.6–23.3) 57/572 9.9 (6.6–13.2)
Race/ethnicity* <0.001 0.008
Non-Hispanic white 210/1655 11.7 (9.6–13.8) 139/1655 7.8 (6.1–9.5)
Non-Hispanic black 169/1081 15.8 (13.2–18.3) 95/1081 8.8 (7.0–10.5)
Hispanic 112/1009 9.9 (7.8–12.0) 60/1009 5.5 (3.8–7.3)
Other 45/748 7.0 (4.4–9.6) 28/748 4.6 (2.5–6.7)
Education† 0.115 0.105
Less than high school 137/1024 11.7 (9.5–14.0) 76/1024 6.8 (5.5–8.2)
High school diploma/GED 146/1054 14.5 (11.0–18.1) 76/1054 7.5 (5.0–10.1)
Some college 155/1235 12.0 (9.2–14.8) 110/1235 9.6 (6.9–12.3)
College graduate or higher 95/1075 9.0 (6.4–11.7) 58/1075 5.4 (3.6–7.2)
IPR*‡ 0.48 0.27
<1.0 182/1346 13.0 (10.4–15.5) 101/1346 6.5 (5.2–7.8)
1.0–1.9 131/1051 12.0 (9.4–14.6) 76/1051 7.2 (5.0–9.4)
2.0–2.9 60/543 12.0 (7.6–16.3) 41/543 9.7 (6.0–13.4)
≥3.0 163/1553 10.5 (8.2–12.7) 104/1553 7.0 (5.3–8.6)
Cigarette use†§ 0.003 0.011
Never/former smoker 203/2235 8.3 (6.9–9.6) 123/2235 5.4 (4.2–6.5)
≤10 cigarettes daily 79/549 13.5 (9.8–17.2) 44/549 9.2 (5.5–12.9)
11–20 cigarettes daily 64/337 19.4 (12.9–25.9) 39/337 10.2 (5.1–15.4)
>20 cigarettes daily 25/93 23.6 (12.4–34.8) 15/93 15.0 (3.8–26.2)
Alcohol use in past 12 mo† 0.161 0.013
0 drinks weekly 86/611 13.3 (9.3–17.3) 55/611 10.4 (6.3–14.5)
1–7 drinks weekly 77/734 8.8 (6.5–11.0) 48/734 4.8 (3.1–6.6)
8–14 drinks weekly 100/800 11.4 (7.5–15.4) 58/800 6.9 (3.9–9.9)
>14 drinks weekly 206/1650 12.7 (10.0–15.4) 122/1650 8.1 (6.0–10.3)
Marijuana use†円円<0.001 <0.001
Never-users 105/1344 6.6 (4.7–8.4) 57/1344 3.2 (2.1–4.4)
Former users 187/1400 13.4 (11.1–15.7) 122/1400 9.4 (7.5–11.2)
Current users 91/654 13.1 (9.4–16.8) 58/654 8.9 (5.4–12.5)
Oral contraceptive pill use†**
Yes NA NA NA NA
No NA NA NA NA
Hormone use†**††
Yes NA NA NA NA
No NA NA NA NA
HPV vaccination†¶ 0.69 0.89
Received vaccine 18/135 10.3 (4.8–15.8) 12/135 7.7 (2.0–13.4)
Did not receive vaccine 381/3299 11.5 (9.5–13.5) 235/3299 7.3 (5.7–8.9)
HPV = human papillomavirus; IPR = income–poverty ratio; NA = not applicable; NHANES = National Health and Nutrition Examination Survey.
* Prevalence estimates based on valid nonmissing results on oral HPV testing of male (n= 4493) and female (n= 4641) participants aged 18– 69 y.
† Sample size not equal to total sample size because of missing data.
‡ Calculated by dividing income by the poverty guidelines by the U.S. Department of Health and Human Services specific to the survey year.
§ A former smoker was defined as a person aged 18 or 19 y who ever tried cigarettes or a person aged 20– 69 y who smoked ≥100 cigarettes in
his or her lifetime but had not smoked a cigarette in the past 30 d.
兩兩 Current marijuana use was defined as use at least once within the past 30 d.
¶ Analyses restricted to participants aged 18–59 y.
** Data restricted to female participants only.
†† Data were available for women aged 20– 69 y.
ORIGINAL RESEARCH Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV
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Table 1—Continued
Women
Overall Oral HPV Infection High-Risk Oral HPV
Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
PValue Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
PValue
0.47 0.189
40/944 4.1 (2.8–5.3) 17/944 1.6 (0.6–2.6)
18/678 2.3 (1.0–3.6) 10/678 1.2 (0.4–2.0)
10/445 2.0 (0.8–3.3) 5/445 0.9 (0–2.0)
16/477 3.5 (1.2–5.9) 9/477 1.9 (0.2–3.6)
17/431 2.8 (0.9–4.8) 6/431 0.8 (0.1–1.6)
23/457 3.8 (1.3–6.4) 11/457 2.3 (0–4.6)
17/392 3.3 (0.9–5.8) 9/392 1.5 (0–3.1)
22/480 4.1 (1.4–6.8) 11/480 1.5 (0.1–2.8)
15/337 2.7 (0.9–4.6) 6/337 0.5 (0.1–1.0)
0.014 0.21
38/953 4.3 (2.9–5.7) 13/953 1.5 (0.4–2.7)
74/2418 2.5 (1.8–3.2) 37/2418 1.1 (0.6–1.6)
52/960 4.6 (3.1–6.1) 26/960 2.2 (1.1–3.2)
0.023 0.077
59/1653 2.9 (2.2–3.7) 27/1653 1.2 (0.7–1.8)
51/1155 4.5 (3.1–6.0) 21/1155 1.9 (1.1–2.7)
51/1070 4.0 (2.6–5.5) 27/1070 1.9 (1.1–2.8)
17/763 2.3 (0.9–3.6) 9/763 1.0 (0.4–1.7)
0.002 0.006
47/930 4.7 (2.9–6.4) 21/930 2.5 (1.1–3.9)
42/960 4.0 (2.8–5.1) 22/960 1.7 (0.7–2.6)
61/1484 3.7 (2.6–4.8) 27/1484 1.6 (0.8–2.4)
22/1168 1.6 (0.5–2.6) 10/1168 0.5 (0.1–0.8)
<0.001 0.25
81/1523 5.2 (4.4–6.0) 36/1523 2.0 (1.1–2.8)
46/1032 4.2 (2.4–6.1) 18/1032 1.5 (0.5–2.6)
19/550 2.8 (1.1–4.5) 12/550 1.8 (0.3–3.3)
32/1536 1.9 (0.9–2.8) 18/1536 0.9 (0.4–1.5)
0.048 0.101
82/3049 2.1 (1.4–2.7) 38/3041 0.7 (0.4–1.0)
24/394 5.1 (2.5–7.8) 11/394 2.4 (0.6–4.1)
15/222 4.7 (1.6–7.8) 6/222 1.9 (0.3–3.6)
2/33 7.0 (0–17.9) 2/33 7.0 (0–17.9)
0.58 0.162
23/578 3.3 (1.4–5.2) 12/578 2.2 (0.3–4.0)
42/1161 2.9 (1.6–4.2) 17/1161 1.0 (0.3–1.6)
36/845 3.5 (2.2–4.9) 17/845 1.2 (0.7–1.7)
39/762 4.6 (2.8–6.4) 22/762 2.7 (1.3–4.2)
0.015 0.032
45/1768 2.2 (1.3–3.0) 19/1768 0.9 (0.5–1.3)
45/1214 2.9 (1.5–4.3) 25/1214 1.8 (0.8–2.8)
34/396 7.9 (4.2–11.5) 16/396 3.0 (1.6–4.4)
0.24 0.41
123/2970 3.5 (2.7–4.2) 58/2970 1.5 (1.0–2.0)
39/1255 2.5 (1.3–3.8) 18/1255 1.1 (0.4–2.0)
0.57 0.69
26/564 3.7 (2.0–5.5) 16/564 1.6 (0.4–2.8)
123/3359 3.2 (2.4–3.9) 53/3359 1.4 (0.9–1.9)
0.54 0.94
22/498 3.8 (2.1–5.5) 11/498 1.5 (0.3–2.6)
114/3177 3.1 (2.2–4.0) 55/3177 1.5 (1.0–2.0)
Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV ORIGINAL RESEARCH
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Figure 2.
Prevalence of overall and high-risk oral HPV infection in persons with or without concurrent genital HPV infection, by
age and race, NHANES 2013–2014.
Men
Yes
No
Yes
No
Women
White
Black
Hispanic
Other
Men
Yes
No
Yes
No
Women
Prevalence of Oral HPV (Overall), %
Men
Yes
No
Yes
No
Women
Presence of
Genital HPV
(Overall)
Presence of
Genital HPV
(High-Risk)
Presence of
Genital HPV
(Overall)
Presence of
Genital HPV
(High-Risk)
Presence of
Genital HPV
(Overall)
Presence of
Genital HPV
(High-Risk)
Prevalence of Oral HPV (High-Risk), %
Prevalence of Oral HPV (Overall), %Prevalence of Oral HPV (High-Risk), %
Prevalence of Oral HPV (Overall), %Prevalence of Oral HPV (High-Risk), %
Men
Yes
No
Yes
No
Women
0102030405060
Men
Yes
No
Yes
No
Women
0102030405060
0 10 20 30 40 50 60 0 10 20 30 40 50 60
0 10 20 30 40 50 60 0 10 20 30 40 50 60
18–34 y
35–49 y
50–69 y
Men
Yes
No
Yes
No
Women
AB
C D
E F
Age
Race
P < 0.001
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P = 0.001
P = 0.09
P = 0.17
P = 0.35
P = 0.40
P = 0.07
P = 0.73
P = 0.66
P = 0.23
P = 0.003
P = 0.02
Prevalence of (A) overall and (B) high-risk oral HPV infection in men and women with or without concurrent genital HPV infection. Prevalence of (C)
overall and (D) high-risk oral HPV infection, by age, in men and women with or without concurrent genital HPV infection. Prevalence of (E) overall
and (F) high-risk oral HPV infection, by race, in men and women with or without concurrent genital HPV infection. Error bars represent 95% CIs.
HPV = human papillomavirus; NHANES = National Health and Nutrition Examination Survey.
*Pvalue for trend.
ORIGINAL RESEARCH Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV
8Annals of Internal Medicine Annals.org
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(31, 32). The predicted probability of oral HPV infection
was greatest among participants who had 16 or more
lifetime oral sex partners. This finding is consistent with
a previous study showing that persons who have had
many oral sex partners have greater odds of oral HPV
infection (33).
Similar to the findings of Hirth and colleagues (6),
our results suggest that HPV vaccination prevents oral
vaccine-covered HPV subtype infections in vaccine-
eligible persons. AIDS Clinical Trials Group protocol
A5298, a randomized double-blind trial of quadrivalent
HPV vaccination in HIV-infected adults older than 27
years, found that HPV vaccination reduced the risk for
persistent oral infection with vaccine types (hazard ra-
tio, 0.12 [CI, 0.02 to 0.98]), but the number of events
was low: 1 event among vaccine recipients compared
with 8 events among placebo recipients (34). Further
research is needed to determine whether HPV vaccina-
tion protects against oral HPV infection across all age
groups of the general population of men and whether
the incidence of HPV-related OPSCC is lower among
recipients of the HPV vaccine. Future decision analyses
also are needed to estimate the value of vaccinating
middle-aged men to reduce the expanding epidemic
of HPV-associated OPSCC.
The primary limitation of our study was insufficient
sample sizes to determine certain associations, such as
prevalence of 4-valent types by HPV vaccination doses.
However, the use of 2 NHANES panels allowed a sam-
ple large enough to report what we believe are the
most comprehensive data available to date on high-risk
oral HPV prevalence and genital–oral HPV concordance
among men and women. Concordance of oral–genital
HPV infection was studied by using only 1 NHANES
panel (2013 to 2014). Caveats exist regarding the sta-
bility of prevalence estimated by using 1 cycle of
NHANES data; therefore, our findings should be inter-
preted cautiously. Certain inherent limitations are asso-
ciated with NHANES data. Self-reported behaviors—for
example, sexual behaviors—likely are underreported
because of social stigma and recall bias. However, self-
report is the only way to obtain these data and is con-
sidered a standard practice. Finally, comparing our es-
timates with other non-NHANES studies should be
done cautiously, because other studies may have
Table 2. Difference in Predicted Probabilities of Overall and High-Risk Oral HPV Infection, NHANES 2011–2014*
Risk Factor Overall Oral HPV High-Risk Oral HPV
Predicted Probability
(95% CI), %
Difference in
Predicted Probability
(95% CI), %
Predicted Probability
(95% CI), %
Difference in
Predicted Probability
(95% CI), %
Sex
Men 10.1 (9.5 to 10.7) 7.6 (7.1 to 8.2) 6.5 (6.1 to 6.8) 5.4 (5.1 to 5.8)
Women 2.5 (2.4 to 2.6) Reference 1.1 (1.0 to 1.1) Reference
Race/ethnicity
Black 9.1 (8.6 to 9.6) 3.3 (2.7 to 3.9) 4.9 (4.6 to 5.3) 1.2 (0.8 to 1.6)
Mexican/Hispanic 6.5 (6.0 to 7.0) 0.7 (0.1 to 1.3) 3.1 (2.9 to 3.4) −0.6 (−1.0 to −0.2)
Other 4.4 (3.7 to 5.1) −1.4 (−2.3 to −0.5) 2.5 (2.1 to 3.0) −1.2 (−1.8 to −0.7)
White 5.8 (5.4 to 6.2) Reference 3.8% (3.5% to 4.1%) Reference
Cigarette use
Never/former smoker 4.6 (4.3 to 4.8) Reference 2.7 (2.5 to 2.8) Reference
≤10 cigarettes daily 10.4 (9.7 to 11.1) 5.9 (5.1 to 6.6) 6.8 (6.2 to 7.3) 4.1 (3.5 to 4.7)
11–20 cigarettes daily 12.3 (10.4 to 14.2) 7.7 (5.9 to 9.6) 6.4 (5.3 to 7.6) 3.8 (2.6 to 4.9)
>20 cigarettes daily 14.2 (11.9 to 16.5) 9.6 (7.3 to 11.9) 10.6 (8.6 to 12.7) 8.0 (5.9 to 10.0)
Marijuana use
Never 3.9 (3.6 to 4.2) Reference 1.6 (1.5 to 1.7) Reference
Current 10.3 (9.3 to 11.2) 6.4 (5.4 to 7.3) 6.2 (5.5 to 6.8) 4.5 (3.9 to 5.1)
Former 7.6 (7.1 to 8.0) 3.7 (3.2 to 4.2) 5.3 (5.0 to 5.6) 3.7 (3.3 to 4.0)
Lifetime number of vaginal sex partners
0–1 3.1 (2.8 to 3.5) Reference 1.8 (1.5 to 2.0) Reference
2–5 3.5 (3.3 to 3.7) 0.4 (0.0 to 0.7) 1.9 (1.7 to 2.1) 0.1 (-0.2 to 0.4)
6–10 7.2 (6.8 to 7.6) 4.1 (3.6 to 4.6) 4.7 (4.4 to 4.9) 2.9 (2.5 to 3.3)
11–15 11.5 (10.4 to 12.7) 8.4 (7.3 to 9.6) 4.9 (4.2 to 5.6) 3.1 (2.4 to 3.8)
≥16 14.2 (13.3 to 15.0) 11.1 (10.3 to 11.8) 9.7 (9.1 to 10.2) 7.9 (7.3 to 8.4)
Lifetime number of oral sex partners
0–1 2.5 (2.4 to 2.6) Reference 1.2 (1.1 to 1.3) Reference
2–5 5.6 (5.3 to 5.9) 3.1 (2.8 to 3.4) 3.3 (3.1 to 3.4) 2.1 (1.9 to 2.3)
6–10 8.9 (8.1 to 9.7) 6.4 (5.6 to 7.1) 4.9 (4.5 to 5.4) 3.7 (3.3 to 4.2)
11–15 17.5 (16.1 to 18.9) 15.0 (13.6 to 16.4) 11.8 (10.7 to 12.9) 10.6 (9.5 to 11.7)
≥16 20.8 (19.0 to 22.6) 18.3 (16.6 to 20.1) 14.2 (13.0 to 15.4) 13.0 (11.9 to 14.2)
HPV = human papillomavirus; NHANES = National Health and Nutrition Examination Survey.
* Models were simultaneously adjusted for variables in the table and for age as a linear term.
Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV ORIGINAL RESEARCH
Annals.org Annals of Internal Medicine 9
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used alternative methods (such as scraping) for sample
collection.
To our knowledge, our study provides the latest
national estimates of oral HPV infection prevalence
among men and women in the United States. Overall
prevalence of oral HPV infection was high among U.S.
men. Almost 2 million men had oncogenic HPV 16 in-
fection. The overall oral HPV infection prevalence was
particularly high among men who have had many (>16)
lifetime oral sexual partners (29.8%), men who reported
having sex with men (18.2%), and men with concurrent
genital HPV infection (19.3%). Future research needs to
be prioritized to improve targeted prevention and ad-
vances in screening and early detection procedures to
combat oropharyngeal cancer in this high-risk group.
From University of Florida, Gainesville, Florida; Baylor College
of Medicine and The University of Texas Health Science Cen-
ter at Houston School of Public Health, Houston, Texas; Har-
vard Medical School, Boston, Massachusetts; and Weill Cor-
nell Medicine, New York, New York.
Disclaimer: The content is solely the responsibility of the au-
thors and does not necessarily represent the official views of
the National Institutes of Health (NIH).
Acknowledgment: The authors thank Michael D. Swartz, PhD,
of The University of Texas School of Public Health at Houston
for constructive comments that improved the quality of the
manuscript.
Grant Support: By National Cancer Institute grant R01
CA163103.
Disclosures: Dr. Chiao reports grants from the NIH during the
conduct of the study. Dr. Chhatwal reports grants and per-
sonal fees from Merck and Gilead Sciences outside the sub-
mitted work. Dr. Wilkin reports grants from Gilead Sciences
and Bristol-Myers Squibb and grants and personal fees from
GlaxoSmithKline/ViiV Healthcare outside the submitted work.
Dr. Sikora reports grants from Advaxis outside the submitted
work. Authors not named here have disclosed no conflicts of
interest. Disclosures can also be viewed at www.acponline
.org/authors/icmje/ConflictOfInterestForms.do?msNum=M17
-1363.
Reproducible Research Statement: Study protocol: Not avail-
able. Statistical code: Available from Dr. Sonawane (e-mail,
ksonawane@phhp.ufl.edu). Data set: Available at www.cdc
.gov/nchs/nhanes/nhanes_questionnaires.htm.
Requests for Single Reprints: Ashish A. Deshmukh, PhD, MPH,
Department of Health Services Research, Management and
Policy, College of Public Health and Health Professions, Uni-
versity of Florida, P.O. Box 100195, 1225 Center Drive, HPNP
Room 3114, Gainesville, FL 32610; e-mail, aadeshmukh
@phhp.ufl.edu.
Current author addresses and author contributions are avail-
able at Annals.org.
References
1. Giuliano AR, Nyitray AG, Kreimer AR, Pierce Campbell CM, Good-
man MT, Sudenga SL, et al. EUROGIN 2014 roadmap: differences in
human papillomavirus infection natural history, transmission and hu-
man papillomavirus-related cancer incidence by gender and ana-
tomic site of infection. Int J Cancer. 2015;136:2752-60. [PMID:
25043222] doi:10.1002/ijc.29082
2. Viens LJ, Henley SJ, Watson M, Markowitz LE, Thomas CC,
Thompson TD, et al. Human papillomavirus-associated cancers—
United States, 2008-2012. MMWR Morb Mortal Wkly Rep. 2016;65:
661-6. [PMID: 27387669] doi:10.15585/mmwr.mm6526a1
3. Mourad M, Jetmore T, Jategaonkar AA, Moubayed S, Moshier E,
Urken ML. Epidemiological trends of head and neck cancer in the
United States: a SEER population study. J Oral Maxillofac Surg. 2017.
[PMID: 28618252] doi:10.1016/j.joms.2017.05.008
4. Gillison ML, Chaturvedi AK, Anderson WF, Fakhry C. Epidemiol-
ogy of human papillomavirus-positive head and neck squamous cell
carcinoma. J Clin Oncol. 2015;33:3235-42. [PMID: 26351338] doi:10
.1200/JCO.2015.61.6995
5. Chaturvedi AK, Engels EA, Pfeiffer RM, Hernandez BY, Xiao W,
Kim E, et al. Human papillomavirus and rising oropharyngeal cancer
incidence in the United States. J Clin Oncol. 2011;29:4294-301.
[PMID: 21969503] doi:10.1200/JCO.2011.36.4596
6. Hirth JM, Chang M, Resto VA; HPV Study Group. Prevalence of
oral human papillomavirus by vaccination status among young
adults (18-30 years old). Vaccine. 2017;35:3446-51. [PMID:
28526331] doi:10.1016/j.vaccine.2017.05.025
7. Voss DS, Wofford LG. Human papillomavirus vaccine uptake in
adolescent boys: an evidence review. Worldviews Evid Based Nurs.
2016;13:390-5. [PMID: 27458811] doi:10.1111/wvn.12172
8. Lu PJ, Yankey D, Jeyarajah J, O’Halloran A, Elam-Evans LD, Smith
PJ, et al. HPV vaccination coverage of male adolescents in the United
States. Pediatrics. 2015;136:839-49. [PMID: 26504124] doi:10.1542
/peds.2015-1631
9. Johnson KL, Lin MY, Cabral H, Kazis LE, Katz IT. Variation in hu-
man papillomavirus vaccine uptake and acceptability between fe-
male and male adolescents and their caregivers. J Community
Health. 2017;42:522-32. [PMID: 27778139] doi:10.1007/s10900
-016-0284-5
10. Centers for Disease Control and Prevention. National Health and
Nutrition Examination Survey 2013-2014 data documentation, code-
book, and frequencies. 2017. Accessed at wwwn.cdc.gov/Nchs
/Nhanes/2013-2014/DIQ_H.htm on 19 September 2017.
11. Broutian TR, He X, Gillison ML. Automated high throughput DNA
isolation for detection of human papillomavirus in oral rinse samples.
J Clin Virol. 2011;50:270-5. [PMID: 21273118] doi:10.1016/j.jcv.2010
.12.005
12. Mun˜oz N, Bosch FX, de Sanjose´ S, Herrero R, Castellsague´X,
Shah KV, et al; International Agency for Research on Cancer Multi-
center Cervical Cancer Study Group. Epidemiologic classification of
human papillomavirus types associated with cervical cancer. N Engl J
Med. 2003;348:518-27. [PMID: 12571259]
13. Deshmukh AA, Tanner RJ, Luetke MC, Hong YR, Sonawane
Deshmukh K, Mainous AG 3rd. Prevalence and risk of penile human
papillomavirus infection: evidence from the National Health and Nu-
trition Examination Survey 2013-2014. Clin Infect Dis. 2017;64:
1360-6. [PMID: 28205678] doi:10.1093/cid/cix159
14. Hariri S, Unger ER, Sternberg M, Dunne EF, Swan D, Patel S, et al.
Prevalence of genital human papillomavirus among females in the
United States, the National Health and Nutrition Examination Survey,
2003-2006. J Infect Dis. 2011;204:566-73. [PMID: 21791659] doi:10
.1093/infdis/jir341
15. Kreimer AR, Pierce Campbell CM, Lin HY, Fulp W, Papenfuss
MR, Abrahamsen M, et al. Incidence and clearance of oral human
papillomavirus infection in men: the HIM cohort study. Lancet.
2013;382:877-87. [PMID: 23827089] doi:10.1016/S0140-6736(13)
60809-0
16. Wood ZC, Bain CJ, Smith DD, Whiteman DC, Antonsson A. Oral
human papillomavirus infection incidence and clearance: a system-
ORIGINAL RESEARCH Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV
10 Annals of Internal Medicine Annals.org
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atic review of the literature. J Gen Virol. 2017;98:519-26. [PMID:
28150575] doi:10.1099/jgv.0.000727
17. Pierce Campbell CM, Kreimer AR, Lin HY, Fulp W, O’Keefe MT,
Ingles DJ, et al. Long-term persistence of oral human papillomavirus
type 16: the HPV Infection in Men (HIM) study. Cancer Prev Res
(Phila). 2015;8:190-6. [PMID: 25575501] doi:10.1158/1940-6207
.CAPR-14-0296
18. Liu F, Hang D, Deng Q, Liu M, Xi L, He Z, et al. Concurrence of
oral and genital human papillomavirus infection in healthy men: a
population-based cross-sectional study in rural China. Sci Rep. 2015;
5:15637. [PMID: 26503510] doi:10.1038/srep15637
19. Steinau M, Gorbach P, Gratzer B, Braxton J, Kerndt PR, Crosby
RA, et al. Concordance between anal and oral human papillomavirus
infections among young men who have sex with men. J Infect Dis.
2017;215:1832-5. [PMID: 28505338] doi:10.1093/infdis/jix232
20. Mbulawa ZZ, Johnson LF, Marais DJ, Coetzee D, Williamson AL.
Risk factors for oral human papillomavirus in heterosexual couples in
an African setting. J Infect. 2014;68:185-9. [PMID: 24184808] doi:10
.1016/j.jinf.2013.10.012
21. Vogt SL, Gravitt PE, Martinson NA, Hoffmann J, D’Souza G. Con-
cordant oral-genital HPV infection in South Africa couples: evidence
for transmission. Front Oncol. 2013;3:303. [PMID: 24377087] doi:10
.3389/fonc.2013.00303
22. Beachler DC, Sugar EA, Margolick JB, Weber KM, Strickler HD,
Wiley DJ, et al. Risk factors for acquisition and clearance of oral
human papillomavirus infection among HIV-infected and HIV-
uninfected adults. Am J Epidemiol. 2015;181:40-53. [PMID:
25480823] doi:10.1093/aje/kwu247
23. Hernandez BY, Wilkens LR, Zhu X, Thompson P, McDuffie K,
Shvetsov YB, et al. Transmission of human papillomavirus in hetero-
sexual couples. Emerg Infect Dis. 2008;14:888-94. [PMID: 18507898]
doi:10.3201/eid1406.070616
24. Sikora AG, Morris LG, Sturgis EM. Bidirectional association of
anogenital and oral cavity/pharyngeal carcinomas in men. Arch Oto-
laryngol Head Neck Surg. 2009;135:402-5. [PMID: 19380365] doi:10
.1001/archoto.2009.19
25. Wawer MJ, Tobian AA, Kigozi G, Kong X, Gravitt PE, Serwadda
D, et al. Effect of circumcision of HIV-negative men on transmission
of human papillomavirus to HIV-negative women: a randomised trial
in Rakai, Uganda. Lancet. 2011;377:209-18. [PMID: 21216000] doi:
10.1016/S0140-6736(10)61967-8
26. Chaturvedi AK, Graubard BI, Broutian T, Pickard RK, Tong ZY,
Xiao W, et al. NHANES 2009-2012 findings: association of sexual
behaviors with higher prevalence of oral oncogenic human papillo-
mavirus infections in U.S. men. Cancer Res. 2015;75:2468-77. [PMID:
25873485] doi:10.1158/0008-5472.CAN-14-2843
27. D’Souza G, Wentz A, Kluz N, Zhang Y, Sugar E, Youngfellow RM,
et al. Sex differences in risk factors and natural history of oral human
papillomavirus infection. J Infect Dis. 2016;213:1893-6. [PMID:
26908748] doi:10.1093/infdis/jiw063
28. Chaturvedi AK, Engels EA, Anderson WF, Gillison ML. Incidence
trends for human papillomavirus-related and -unrelated oral squa-
mous cell carcinomas in the United States. J Clin Oncol. 2008;26:
612-9. [PMID: 18235120] doi:10.1200/JCO.2007.14.1713
29. Louie KS, Mehanna H, Sasieni P. Trends in head and neck can-
cers in England from 1995 to 2011 and projections up to 2025. Oral
Oncol. 2015;51:341-8. [PMID: 25619734] doi:10.1016/j.oraloncology
.2015.01.002
30. Kreimer AR, Clifford GM, Boyle P, Franceschi S. Human papillo-
mavirus types in head and neck squamous cell carcinomas world-
wide: a systematic review. Cancer Epidemiol Biomarkers Prev. 2005;
14:467-75. [PMID: 15734974]
31. Arnson Y, Shoenfeld Y, Amital H. Effects of tobacco smoke on
immunity, inflammation and autoimmunity. J Autoimmun. 2010;34:
J258-65. [PMID: 20042314] doi:10.1016/j.jaut.2009.12.003
32. Castle PE. How does tobacco smoke contribute to cervical carci-
nogenesis? [Letter]. J Virol. 2008;82:6084-5. [PMID: 18497423] doi:
10.1128/JVI.00103-08
33. D’Souza G, Agrawal Y, Halpern J, Bodison S, Gillison ML. Oral
sexual behaviors associated with prevalent oral human papillomavi-
rus infection. J Infect Dis. 2009;199:1263-9. [PMID: 19320589] doi:
10.1086/597755
34. Wilkin T, Chen H, Cespedes M, Paczuski P, Godfrey C, et al.
ACTG A5298: a phase 3 trial of the quadrivalent HPV vaccine in older
HIV+ adults. Presented at Conference on Retroviruses and Opportu-
nistic Infections 2016, Boston, Massachusetts, 22–25 February 2016.
Abstract no. 161.
Sex Differences in Prevalence and Concordance of Oral vs. Genital HPV ORIGINAL RESEARCH
Annals.org Annals of Internal Medicine 11
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Current Author Addresses: Dr. Sonawane: Department of
Health Services Research, Management and Policy, College of
Public Health and Health Professions, University of Florida,
P.O. Box 100195, 1225 Center Drive, HPNP Room 3112,
Gainesville, FL 32610.
Ms. Suk: Department of Health Services Research, Manage-
ment and Policy, College of Public Health and Health Profes-
sions, University of Florida, P.O. Box 100195, 1225 Center
Drive, Gainesville, FL 32610.
Dr. Chiao: Michael E. DeBakey VA Medical Center, HSR&D
Center for Innovations, 2002 Holcombe Boulevard, Houston,
TX 77030.
Dr. Chhatwal: Institute for Technology Assessment, Massachu-
setts General Hospital, 101 Merrimac Street, 10th Floor, Bos-
ton, MA 02114.
Dr. Qiu: Department of Biostatistics, P.O. Box 117450, 2004
Mowry Road, 5th Floor CTRB, Gainesville, FL 32611.
Dr. Wilkin: Weill Cornell Medicine, 53 West 23rd Street, 6th
Floor, New York, NY 10010.
Dr. Nyitray: Center for Infectious Diseases, University of Texas
School of Public Health at Houston, 1200 Pressler, RAS-E707,
Houston, TX 77030.
Dr. Sikora: Bobby R. Alford Department of Otolaryngology–
Head and Neck Surgery, Baylor College of Medicine, One
Baylor Plaza, NA-504, Houston, TX 77030.
Dr. Deshmukh: Department of Health Services Research, Man-
agement and Policy, College of Public Health and Health Pro-
fessions, University of Florida, P.O. Box 100195, 1225 Center
Drive, HPNP Room 3114, Gainesville, FL 32610.
Author Contributions: Conception and design: K. Sonawane,
T. Wilkin, A.A. Deshmukh.
Analysis and interpretation of the data: K. Sonawane, R. Suk,
E.Y. Chiao, J. Chhatwal, P. Qiu, T. Wilkin, A.G. Nyitray, A.G.
Sikora, A.A. Deshmukh.
Drafting of the article: K. Sonawane, E.Y. Chiao, A.A.
Deshmukh.
Critical revision for important intellectual content: K.
Sonawane, R. Suk, E.Y. Chiao, J. Chhatwal, T. Wilkin, A.G. Nyi-
tray, A.G. Sikora, A.A. Deshmukh.
Final approval of the article: K. Sonawane, R. Suk, E.Y. Chiao,
J. Chhatwal, P. Qiu, T. Wilkin, A.G. Nyitray, A.G. Sikora, A.A.
Deshmukh.
Provision of study materials or patients: A.A. Deshmukh.
Statistical expertise: K. Sonawane, E.Y. Chiao, P. Qiu, A.A.
Deshmukh.
Obtaining of funding: E.Y. Chiao, A.A. Deshmukh.
Administrative, technical, or logistic support: K. Sonawane,
E.Y. Chiao, A.A. Deshmukh.
Collection and assembly of data: K. Sonawane, R. Suk, A.A.
Deshmukh.
Annals.org Annals of Internal Medicine
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Appendix Table. Prevalence of Overall and High-Risk Oral HPV Infection in Men and Women, by Sexual and Behavioral
Characteristics, NHANES 2011–2014
Characteristic Men Women
Overall Oral HPV Infection High-Risk Oral HPV Infection Overall Oral HPV Infection High-Risk Oral HPV Infection
Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
Ever had sex*†
Yes 3896 (474) 11.6 (9.7–13.4) 3896 (290) 7.4 (6.0–8.9) 3917 (156) 3.3 (2.7–4.0) 3917 (74) 1.5 (1.0–1.9)
No 254 (14) 3.2 (1.2–5.3) 254 (3) 0.9 (0–2.0) 217 (4) 1.5 (0–3.6) 217 (1) 0.2 (0–0.6)
Pvalue <0.001 <0.001 0.129 <0.001
Ever had oral sex*‡
Yes 3210 (425) 12.1 (10.2–14.0) 3210 (261) 7.8 (6.3–9.3) 3092 (133) 3.6 (2.8–4.3) 3092 (64) 1.6 (1.0–2.1)
No 923 (63) 6.9 (3.9–9.8) 923 (33) 4.0 (2.0–5.9) 1037 (28) 1.9 (1.0–2.8) 1037 (12) 0.9 (0.2–1.6)
Pvalue 0.004 <0.001 0.007 0.142
Ever had vaginal sex*§
Yes 3778 (457) 11.5 (9.7–13.3) 3778 (278) 7.4 (6.0–8.8) 3875 (156) 3.3 (2.7–4.0) 3875 (74) 1.5 (1.0–1.9)
No 374 (32) 6.8 (3.0–10.6) 374 (16) 3.9 (1.3–6.5) 264 (4) 1.3 (0–3.0) 264 (1) 0.2 (0–0.5)
Pvalue 0.026 0.012 0.046 <0.001
Ever had anal sex*円円
Yes 1587 (238) 14.5 (12.1–16.9) 1587 (152) 9.3 (7.4–11.2) 1357 (62) 4.0 (2.8–5.1) 1357 (34) 2.0 (1.1–3.0)
No 2554 (251) 9.0 (7.1–10.9) 2554 (142) 5.8 (4.3–7.3) 2768 (99) 2.9 (2.2–3.5) 2768 (42) 1.1 (0.7–1.6)
Pvalue <0.001 <0.001 0.068 0.102
Lifetime number of sex
partners (any)*¶
0–1 754 (39) 3.6 (1.7–5.4) 754 (17) 1.7 (0.6–2.9) 961 (19) 1.2 (0.5–2.0) 961 (7) 0.5 (0.0–1.0)
2–5 1017 (941) 7.1 (4.8–9.3) 1017 (46) 4.3 (2.7–5.8) 1681 (52) 2.2 (1.6–2.8) 1681 (22) 0.7 (0.4–1.1)
6–10 850 (111) 10.8 (7.2–14.4) 850 (71) 7.1 (4.1–9.9) 850 (49) 4.8 (3.1–6.5) 850 (22) 2.0 (1.0–2.9)
11–15 394 (50) 14.0 (9.0–18.9) 394 (30) 7.8 (3.9–11.6) 257 (15) 5.4 (1.6–9.2) 257 (8) 2.6 (0.2–4.9)
≥16 1087 (208) 20.1 (16.8–23.5) 1087 (125) 13.8 (10.8–16.9) 362 (24) 5.6 (2.5–8.7) 362 (16) 3.4 (1.1–5.7)
Pvalue <0.001 <0.001 0.002 0.023
Lifetime number of sex
partners (oral)* **
0–1 1457 (85) 4.7 (3.2–6.3) 1457 (41) 2.1 (1.2–3.0) 1788 (43) 1.7 (1.2–2.3) 1788 (20) 0.9 (0.5–1.3)
2–5 1262 (132) 8.4 (6.2–10.6) 1262 (80) 5.5 (3.9–7.0) 1426 (58) 3.0 (1.9–4.1) 1426 (27) 1.4 (0.7–2.1)
6–10 413 (61) 13.5 (9.1–18.0) 413 (36) 7.7 (4.8–10.6) 274 (18) 5.5 (2.2–8.8) 274 (8) 2.3 (0.3–4.4)
11–15 162 (32) 21.0 (10.9–31.1) 162 (22) 14.6 (5.3–24.0) 71 (5) 3.9 (0–14.4) 71 (4) 2.7 (0.0–5.6)
≥16 307 (93) 29.8 (21.6–37.9) 307 (64) 21.8 (14.9–28.8) 112 (9) 7.2 (1.6–12.9) 112 (4) 2.5 (0.0–5.3)
Pvalue <0.001 <0.001 0.042 0.182
Lifetime number of sex
partners (vaginal)*††
0–1 820 (60) 5.6 (3.3–7.8) 820 (31) 3.1 (1.4–4.8) 952 (21) 1.8 (0.7–2.9) 952 (7) 0.6 (0.0–1.2)
2–5 885 (63) 6.0 (3.8–8.1) 885 (39) 4.0 (1.9–6.0) 1256 (38) 2.3 (1.4–3.1) 1256 (15) 0.8 (0.5–1.2)
6–10 630 (78) 11.1 (7.7–14.5) 630 (51) 7.3 (4.3–10.4) 702 (34) 3.8 (2.3–5.3) 702 (20) 2.1 (1.1–3.1)
11–15 321 (40) 15.1 (9.6–20.7) 321 (23) 7.1 (3.1–11.2) 208 (11) 4.5 (0.8–8.2) 208 (5) 1.8 (0.0–3.7)
≥16 760 (151) 20.7 (17.2–24.2) 760 (95) 14.8 (11.7–17.9) 291 (18) 5.7 (1.8–9.6) 291 (11) 3.5 (0.7–6.3)
Pvalue <0.001 <0.001 0.074 0.074
Number of sex
partners during the
past 12 months (any)*
0 276 (17) 5.2 (1.4–9.0) 276 (6) 3.2 (0.0–6.9) 255 (9) 3.9 (0.1–7.7) 255 (3) 2.0 (0.0–5.2)
1 79 (10) 10.5 (1.7–19.4) 79 (6) 4.3 (0.0–9.1) 158 (10) 4.0 (1.0–7.1) 158 (6) 1.9 (0.0–3.9)
≥2 788 (119) 14.8 (11.2–18.4) 788 (73) 9.8 (6.8–12.8) 512 (35) 6.9 (3.2–10.6) 512 (20) 3.3 (1.4–5.2)
Pvalue <0.001 0.003 0.47 0.62
Number of sex
partners during the
past 12 months (oral)*
0 917 (59) 6.4 (3.6–9.2) 917 (31) 3.6 (1.7–5.4) 1059 (32) 2.4 (1.3–3.6) 1059 (14) 1.3 (0.3–2.3)
1 25 (3) 8.2 (0–19.6) 25 (2) 6.8 (0.0–17.8) 325 (17) 4.4 (1.6–7.1) 325 (3) 0.4 (0.0–1.0)
≥2 469 (91) 18.3 (13.0–23.5) 469 (55) 12.4 (8.2–16.6) 325 (21) 6.7 (2.5–10.9) 325 (9) 1.9 (0.2–3.5)
Pvalue <0.001 0.001 0.057 0.133
Number of sex
partners during the
past 12 months
(vaginal)*
0 615 (49) 7.8 (4.7–10.8) 615 (30) 5.8 (2.9–8.7) 718 (23) 2.3 (1.0–3.6) 718 (8) 1.0 (0.0–2.0)
1 1929 (216) 11.1 (8.8–13.5) 1929 (131) 7.1 (5.3–8.9) 2159 (71) 2.9 (1.9–3.9) 2159 (33) 1.4 (0.8–2.0)
≥2 765 (106) 12.6 (9.8–15.3) 765 (65) 8.2 (5.4–8.9) 485 (30) 6.1 (2.6–9.7) 485 (18) 2.9 (1.1–4.7)
Pvalue 0.023 0.45 0.140 0.21
Continued on following page
Annals of Internal Medicine Annals.org
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Appendix Table—Continued
Characteristic Men Women
Overall Oral HPV Infection High-Risk Oral HPV Infection Overall Oral HPV Infection High-Risk Oral HPV Infection
Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
Age first had any sex*
<18 years 2416 (354) 14.6 (12.0–17.1) 2416 (210) 9.2 (7.1–11.4) 2162 (108) 4.6 (3.5–5.6) 2162 (52) 2.0 (1.2–2.8)
≥18 years 1480 (120) 6.8 (5.3–8.4) 1480 (80) 4.6 (3.4–5.8) 1755 (48) 1.8 (1.2–2.3) 1755 (22) 0.8 (0.4–1.2)
Pvalue <0.001 <0.001 <0.001 0.011
Age first had oral sex*
<18 years 3160 (415) 12.0 (10.1–13.9) 3160 (255) 7.8 (6.3–9.3) 1335 (64) 3.8 (2.6–4.9) 1335 (37) 1.9 (0.8–3.1)
≥18 years 50 (10) 16.2 (4.2–28.2) 50 (6) 11.0 (1.0–20.9) 1757 (69) 3.4 (2.2–4.6) 1757 (27) 1.2 (0.7–1.8)
Pvalue 0.50 0.52 0.69 0.30
Time since last oral
sex*
Never had oral sex 923 (63) 6.9 (3.9–9.8) 923 (33) 4.0 (2.0–5.9) 1037 (28) 1.9 (1.0–2.8) 1037 (12) 0.9 (0.2–1.6)
<12 months 781 (113) 13.6 (10.5–16.6) 781 (75) 9.6 (6.7–12.4) 724 (33) 3.6 (2.0–5.1) 724 (20) 2.1 (0.9–3.3)
12–24 months 210 (33) 18.6 (11.5–25.8) 210 (18) 11.4 (5.6–17.2) 210 (5) 2.4 (0–5.2) 210 (0) NR
>24 months 89 (13) 11.6 (3.3–20.0) 89 (9) 7.5 (0.8–14.2) 88 (3) 2.3 (0.1–4.5) 88 (2) 2.1 (0–4.2)
Pvalue 0.002 0.0002 0.177 NA
Used barrier during
oral sex during past
12 months*
Never/rarely 1807 (247) 13.0 (10.7–15.3) 1807 (155) 8.5 (6.7–10.3) 1744 (64) 2.9 (2.0–3.8) 1744 (36) 1.5 (0.9–2.1)
Usually/always 275 (30) 9.7 (5.2–14.2) 275 (18) 6.9 (2.8–11.0) 193 (14) 8.1 (2.8–13.4) 193 (6) 3.0 (0.6–5.4)
Pvalue 0.115 0.38 0.072 0.23
History of
herpes/warts*
Yes 137 (22) 15.5 (6.3–24.8) 137 (16) 12.0 (2.2–21.7) 310 (12) 4.1 (0.7–7.5) 310 (2) 0.8 (0–2.3)
No 3031 (351) 11.2 (9.3–13.1) 3031 (217) 7.2 (5.7–8.7) 2880 (106) 3.0 (2.3–3.7) 2880 (55) 1.5 (1.1–2.0)
Pvalue 0.34 0.34 0.47 0.38
History of
chlamydia/
gonorrhea‡‡
Yes 29 (12) 28.0 (5.7–50.3) 29 (8) 20.7 (0.2–41.1) 73 (4) 3.8 (0.0–7.9) 73 (1) 1.1 (0.0–3.4)
No 3139 (362) 11.3 (9.4–13.2) 3139 (226) 7.4 (5.9–8.9) 3118 (115) 3.1 (2.3–3.9) 3118 (56) 1.4 (1.0–1.9)
Pvalue 0.113 0.196 0.72 0.79
History of HPV§§
Yes NA NA NA NA 287 (12) 4.3 (1.1–7.5) 287 (9) 2.7 (0.5–5.0)
No NA NA NA NA 2906 (107) 3.0 (2.1–3.9) 2906 (48) 1.3 (0.9–1.7)
Pvalue 0.43 0.23
HIV status円円 円円
HIV-positive 28 (9) 29.7 (6.0–53.4) 28 (7) 24.8 (2.9–46.7) 8 (0) NR 8 (0) NR
HIV-negative 3412 (380) 10.9 (9.3–12.5) 3412 (231) 7.0 (5.7–8.3) 3582 (128) 3.1 (2.4–3.8) 3582 (60) 1.4 (1.0–1.9)
Pvalue 0.105 0.110 NR NR
Self-reported sexual
orientation*
Heterosexual 3211 (356) 10.8 (9.0–12.5) 3211 (217) 6.9 (5.5–8.2) 3035 (101) 2.9 (2.0–3.7) 3035 (46) 1.3 (0.8–1.7)
Homosexual/bisexual 119 (21) 17.1 (7.5–26.7) 119 (16) 13.9 (5.7–22.1) 207 (16) 6.3 (3.1–9.5) 207 (8) 3.2 (1.0–5.5)
Pvalue 0.157 0.073 0.043 0.097
Ever had any sex with
partner of same sex*¶¶
Yes 212 (38) 18.2 (10.8–25.6) 212 (25) 12.7 (7.0–18.4) 374 (31) 6.6 (3.6–9.7) 374 (17) 3.6 (1.4–5.9)
No 3934 (451) 10.8 (9.1–12.4) 3934 (269) 6.8 (5.5–8.1) 3762 (130) 2.9 (2.3–3.5) 3762 (59) 1.2 (0.8–1.6)
Pvalue 0.045 0.041 0.020 0.043
Lifetime number of
same-sex oral sex
partners*
0 3934 (451) 10.7 (9.1–12.4) 3934 (269) 6.8 (5.5–8.1) 3762 (130) 2.9 (2.3–3.5) 3762 (59) 1.2 (0.8–1.6)
1 134 (14) 8.3 (3.3–13.2) 134 (8) 5.1 (0.2–9.9) 310 (24) 6.8 (3.3–10.2) 310 (14) 3.9 (1.2–6.6)
≥2 75 (22) 30.3 (15.2–45.5) 75 (16) 22.2 (9.6–34.8) 44 (5) 6.9 (2.3–11.5) 44 (1) 1.6 (0.0–5.0)
Pvalue 0.029 0.038 0.026 0.146
Number of same-sex
oral sex partners
during the past 12
months‡‡
0 4018 (463) 10.8 (9.2–12.4) 4018 (277) 12.1 (2.3–21.8) 3816 (136) 3.1 (2.4–3.7) 3816 (61) 1.3 (0.9–1.7)
≥1 91 (16) 15.6 (4.3–26.9) 19 (12) 6.9 (5.5–8.2) 112 (10) 8.6 (2.5–14.8) 112 (3) 3.3 (0.0–7.4)
Pvalue 0.37 0.28 0.080 0.36
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Appendix Table—Continued
Characteristic Men Women
Overall Oral HPV Infection High-Risk Oral HPV Infection Overall Oral HPV Infection High-Risk Oral HPV Infection
Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %Participants With
Infection/Total
Participants, n/N
Prevalence
(95% CI), %
Lifetime number of
same-sex anal sex
partners***
0 3934 (451) 10.8 (9.1–12.4) 3934 (269) 6.8 (5.5–8.1) NA NA NA NA
1 90 (14) 12.7 (3.6–21.9) 90 (8) 6.5(0.8–12.2) NA NA NA NA
≥2 65 (16) 26.1 (12.4–39.8) 65 (12) 19.9 (8.2–31.7) NA NA NA NA
Pvalue 0.108 0.083
Number of same-sex
anal sex partners
during the past 12
months***
0 3994 (462) 10.9 (9.3–12.6) 3994 (276) 6.9 (5.6–8.3) NA NA NA NA
≥1 75 (15) 15.7 (4.1–27.4) 75 (12) 14.2 (3.2–25.1) NA NA NA NA
Pvalue 0.39 0.193
HPV = human papillomavirus; NA = not applicable; NHANES = National Health and Nutrition Examination Survey; NR = not reported.
* Prevalence estimates based on valid nonmissing oral HPV results for participants aged 18-69 years who responded to the audio, computer-
assisted self-interview.
If a man answered “yes” to having had any of the following types of sex, he was coded as “yes”: ever had vaginal sex with a woman, ever
performed oral sex on a woman, ever had anal sex with a woman, or ever had any sex with a man (anal, oral). Similarly for women.
‡ Men were asked, “Have you ever performed oral sex on a woman? This means putting your mouth on a woman's vagina or genitals.” Women were
asked, “Have you ever performed oral sex on a man? This means putting your mouth on a man's penis or genitals.”
§ Men were asked, “Have you ever had vaginal sex, also called sexual intercourse, with a woman? This means your penis in a woman's vagina.”
Women were asked, “Have you ever had vaginal sex, also called sexual intercourse, with a man? This means a man's penis in your vagina.”
兩兩 Men were asked, “Have you ever had anal sex with a woman? Anal sex means contact between your penis and a woman's anus or butt.” Women
were asked, “Have you ever had anal sex? This means contact between a man's penis and your anus or butt.”
¶ Men were asked, “In your lifetime, with how many women have you had any kind of sex?'” Women were asked, “In your lifetime, with how many
men have you had any kind of sex?”
** Men and women were asked, “In your lifetime, on how many women have you performed oral sex?” and “In your lifetime, on how many men have
you performed oral sex?”
†† Men were asked, “In your lifetime, with how many women have you had vaginal sex?” Women were asked, “In your lifetime, with how many men
have you had vaginal sex?”
‡‡ Restricted to participants aged 18-59 years.
§§ Restricted to female participants aged 18-59 years.
兩兩兩兩 Restricted to participants aged 18-59 years with valid nonmissing HIV antibody test results.
¶¶ Men were asked, “Have you ever had any kind of sex with a man, including oral or anal?” Women were asked, “Have you ever had any kind of
sex with a woman? By sex, we mean sexual contact with another woman's vagina or genitals.”
*** Restricted to male participants aged 18-59 years.
Annals of Internal Medicine Annals.org
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Appendix Figure.
Prevalence, by sexual behavior, of overall and high-risk oral HPV infection in persons with or without
concurrent genital HPV infection, NHANES 2013–2014.
Men
Yes
No
Yes
No
Women
Men
Yes
No
Yes
No
Women
Men
Yes
No
Yes
No
Women
Men
Yes
No
Yes
No
Women
0 1020304050
Prevalence of Oral HPV (High-Risk), %
60
Men
Yes
No
Yes
No
Women
0 102030405060
0 102030405060
0 102030405060
0 102030405060
0 102030405060
Prevalence of Oral HPV (Overall), %
Prevalence of Oral HPV (High-Risk), %
Prevalence of Oral HPV (Overall), %
Prevalence of Oral HPV (High-Risk), %
Prevalence of Oral HPV (Overall), %
0–5
6–10
11–15
16
Men
Yes
No
Yes
No
Women
Presence of
Genital HPV
(Overall)
Presence of
Genital HPV
(High-Risk)
Presence of
Genital HPV
(Overall)
Presence of
Genital HPV
(High-Risk)
Presence of
Genital HPV
(Overall)
Presence of
Genital HPV
(High-Risk)
AB
CD
E F
Lifetime Number of Any Sex Partners
Lifetime Number of Oral Sex Partners
Lifetime Number of Vaginal Sex Partners
P < 0.001*
P < 0.001*
P < 0.001*
NR
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001* P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001*
P < 0.001* P < 0.001*
NR
Prevalence of (A) overall and (B) high-risk oral HPV infection, by lifetime number of any sex partners, in men and women with or without concurrent
genital HPV infection. Prevalence of (C) overall and (D) high-risk oral HPV infection, by lifetime number of oral sex partners, in men and women with
or without concurrent genital HPV infection. Prevalence of (E) overall and (F) high-risk oral HPV infection, by lifetime number of vaginal sex partners,
in men and women with or without concurrent genital HPV infection. Errors bars represent 95% CIs. HPV = human papillomavirus; NHANES =
National Health and Nutrition Examination Survey; NR = not reported.
*Pvalue for trend.
Annals.org Annals of Internal Medicine
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... HPV-16 is detected in 60-80% of head and neck cancers, while HPV-18 has been identified in 34% of oral cavity squamous cell cancers and 17% of laryngeal squamous cell cancers [32]. Men have a higher prevalence of oral HPV infections (11.5% vs. 3.2%) and HPV-16 infections (1.8% vs. 0.3%) compared to women [33]. A systematic review highlighted geographic variability in HPV-positive oropharyngeal cancers, with higher rates in North America, Northern Europe, and Oceania [34]. ...
... HPV-18 has been identified in 34% of oral cavity squamous cell cancers and 17% of laryngeal squamous cell cancers [32]. Men have a higher prevalence of oral HPV infections (11.5% vs. 3.2%) and HPV-16 infections (1.8% vs. 0.3%) compared to women [33]. A systematic review highlighted geographic variability in HPV-positive oropharyngeal cancers, with higher rates in North America, Northern Europe, and Oceania [34]. ...
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... Moreover, the incidence of HPV-positive OPSCC in men has surpassed that of cervical cancer in women, which is closely associated with HPV. In addition, risky sexual behaviors such as having two or more lifetime sex partners and oral sex were consistent with HPV exposure, and were established as risk factors for HPVpositive OPSCC, suggesting directions for future disease prevention [39][40][41][42]. However, a study conducted in Germany reported different results, which by showing a low prevalence of risky sexual behaviors in OPSCC patients, confirmed findings from other European studies that differed substantially from North American case-control studies [43]. ...
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... 20 Men with a genital HPV infection were found to be four times more likely to present with an oral HPV infection. 21 However, another study found no higher risk of oral HPV in female participants with cervical HPV. 22 Studies investigating the prevalence of HPV in the Extended Middle East and North Africa (EMENA) region have focused mainly on cervical HPV rather than oral HPV. ...
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Subclinical oral HPV infection that persists for decades is likely to precede a HPV-driven HNSCC, however little is known about the natural history of oral HPV. We systematically reviewed and abstracted data from nine manuscripts that examined HIV-negative and cancer-free subjects for oral HPV DNA to determine the pooled baseline prevalence and incidence of newly acquired oral HPV infections, and specifically for HPV-16. We also documented the clearance rate and the median time to clearance, where data existed. Of 3,762 individuals, 7.5% had an oral infection with any HPV type (1.6% for HPV-16). Meta-regression analysis estimated the 12-month cumulative incidence to be 4.8% (95% CI 3.2-7.3%). The overall oral HPV clearance was reported to be 0% to 80% between studies, and the median time to clearance from 6.5 months to 18 months. Oral HPV-16 clearance was 43%-83%, and median time to clearance for HPV-16 was 7 to 22 months. Oral HPV prevalence, incidence and clearance vary considerably between published studies from different geographical regions. Further research is required to identify predictors of persistent oral HPV infection. Measurable baseline prevalence was observed in all studies, as well non-trivial incidence of newly acquired oral HPV infections and incomplete clearance.
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Background: Despite evidence-based guidelines recommending routine vaccination against human papillomavirus (HPV) for adolescent boys, ages 11-12 years, vaccine uptake among this population remains low. Aims: To examine reasons for low HPV quadrivalent vaccine uptake and methods available to increase vaccine uptake among adolescent males, ages 11-12 years. Methods and results: Of 341 identified studies, 30 were included from three databases. The 30 studies were grouped into six categories: population-specific, problem-specific, educational interventions, theory-specific, political implications, and foundational guidelines and Websites. Discussion: Among eight studies, low vaccine uptake was attributed to lack of parental, adolescent, and physician knowledge of HPV4 vaccine availability and recommendations. HPV4 vaccine educational interventions for parents and adolescents were the most effective for promoting vaccine uptake. Theory applications and gain-framed messages were shown to be effective for assessing HPV vaccine attitudes and perceptions. Political implication studies reveal the need for political and financial measures to encourage HPV vaccine acceptability among the population. Implications for clinicians: To promote HPV vaccine uptake among adolescent males, providers must remain current with HPV vaccine recommendations and offer parental and adolescent HPV education focusing on benefits of vaccine acceptance and risks of vaccine refusal. Linking evidence to action: The results of this review inform our understanding of effective educational strategies to positively impact HPV vaccine uptake in adolescent males. Based on this review, clinicians can employ several evidence-based educational strategies to facilitate HPV vaccine uptake.
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Oral HPV16 infection causes oropharyngeal squamous cell carcinoma (OPSCC), and prevalence is higher among men than women in the United States. In a cohort study of oral HPV infection among 409, 18-25 year-olds, risk significantly increased with recent (prior three months) number of oral sexual partners among men, but not women (p-interaction [pI]=0.05). In contrast, risk significantly declined with lifetime number of vaginal sexual partners among women, but not men (pI= 0.037). Men were also significantly less likely to clear an oral HPV infection than women. Our data contribute to understanding gender differences in risk for HPV-positive OPSCC.