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Obstetrics & Gynecology 1999;94:653-658
© 1999 by The American College of Obstetricians and Gynecologists
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ORIGINAL RESEARCH

Seroprevalence of Human Papillomavirus Type 16 in Pregnant Women

MICHAEL E. HAGENSEE, MD, PhD, JOSEPH SLAVINSKY, III, CHRISTOPHER M. GAFFGA, JOSE SUROS, PATRICIA KISSINGER, PhD and DAVID H. MARTIN, MD

From the Department of Medicine, Louisiana State University Medical Center, New Orleans, Louisiana.

Address reprint requests to: Michael E. Hagensee, MD, PhD, Department of Medicine, Section of Infectious Diseases, LSUMC, 1542 Tulane Avenue, New Orleans, LA 70112, E-mail: mhagen{at}lsumc.edu


   Abstract
Top
Abstract
Materials and Methods
 Results
 Discussion
 References
 
Objective: To determine the seroprevalence of and risk factors for human papillomavirus (HPV) type 16 capsid antibodies in a large cohort of pregnant women.

Methods: Antibodies against in vitro produced HPV-16 capsids were measured in stored sera from 2597 pregnant women enrolled from 1984 through 1989 in the Vaginal Infection and Prematurity Study, New Orleans site.

Results: Women in this study were primarily black (83.4%) with a mean age of 23.4 years (standard deviation [SD], 5.1), mean number of sexual partners in lifetime was 3.3 (SD, 6.6), and the mean age at sexual debut was 16.7 years (SD, 2.2). Overall, 28.0% (n = 727) of these women were positive for HPV-16 capsid antibodies. In bivariate analysis, the presence of antibodies against HPV-16 was correlated with numerous demographic characteristics as well as history of various sexually transmitted diseases. However, neither current cervical or vaginal infection nor adverse obstetric outcome was associated with increased detection of HPV-16 antibodies. In multivariate logistic regression analysis, factors predictive of HPV-16 seropositivity were: more than five lifetime sexual partners (odds ratio [OR], 1.80; 95% confidence interval [CI], 1.28, 2.52), 6 or more years of sexual activity (OR, 1.84; 95% CI, 1.22, 2.78), level of education (OR, 1.26; 95% CI, 1.03, 1.55), and history of Neisseria gonorrhoeae infection (OR, 1.53; 95% CI, 1.20, 1.96).

Conclusion: HPV-16 seropositivity correlates with measures of sexual activity, confirming its role as a sexually transmitted disease, and its prevalence is similar to that in nonpregnant populations. HPV-16 seropositivity does not predict an adverse obstetric outcome

Infection by human papillomavirus (HPV) is the most common viral sexually transmitted disease. Human papillomavirus is the causative agent of genital warts, and high-risk HPV infection (types 16, 18, and others) has been linked to the majority of cases of anogenital malignancy.1 Due to the relative inability to propagate HPV in the laboratory, little is known about the seroepidemiology of this disease. The recent in vitro production of HPV capsids,2–4 has led to the development of immunoassays to detect serum antibodies against HPV capsid antigens. Use of these assays has demonstrated that HPV DNA in genital secretions as well as HPV-related disease (genital warts and squamous intraepithelial lesions)5 are associated with HPV serum antibodies.

Seroprevalence of HPV-16 in cohort studies has varied from 10% to 52%, depending on the population studied.6–9 Risk-factor analyses have shown that HPV seropositivity correlates with increased numbers of sexual partners.6,10 Numerous studies have also demonstrated that HPV-16 seropositivity is associated with the presence of HPV-16 DNA6,11–13 in specimens taken from the genital tract. The prevalence of serum antibodies against HPV capsid antigens in pregnant women has not been studied in detail. One investigation reported seropositivity of 16% for antibodies to HPV-6,10,14 whereas no reports on the seroprevalence of HPV-16 capsid antibodies in pregnant women have been issued. Although infection with HPV may increase during pregnancy,15–20 high-risk HPV-related disease, namely squamous intraepithelial lesions and cervical cancer, is not detected more often21 in pregnant than in nonpregnant women. In general, HPV is not thought to be a teratogen, but this has not been studied in detail. One recent report noted an increase in HPV E6 and E7 DNA in spontaneous abortion material as compared with elective abortion material22; however, the significance of this finding is not clear at this time.

Our study examined the seroprevalence of capsid antibodies to HPV-16 in a large group of pregnant women enrolled in the Vaginal Infection and Prematurity study in the late 1980s in New Orleans. Additionally, antibody positivity was correlated to the demographic data collected from those women, to the presence of sexually transmitted diseases at the time of enrollment, and to eventual obstetric outcome.


   Materials and Methods
Top
Abstract
 Materials and Methods
Results
 Discussion
 References
 
The women enrolled were part of the Vaginal Infections and Prematurity study conducted at Louisiana State University Medical Center, New Orleans, LA, from November 1984 until March 1989 (n = 3341). Women, who were aged 18 to 40, between 23 and 26 weeks’ gestation, and attending the prenatal clinics at the medical center, were asked to enroll in this study. Women were excluded if they had a severe medical condition (hypertension, severe cardiac or renal condition requiring medication, and diabetes requiring insulin), obstetric condition associated with premature labor (erythroblastosis, multiple gestation, and cervical cerclage), used antibiotics within the previous 2 weeks, and were using tocolytics or steroids. The demographics of this population, the physical exam protocol, and collection of vaginal, urine, and blood specimens have been detailed elsewhere.23,24 The local Institutional Review Board approved this study, and subjects signed informed consent prior to its initiation. First-visit sera that were available from the New Orleans subset of the Vaginal Infections and Prematurity study were included in this study and tested for antibodies against HPV-16 capsid antigens (n = 2597). The 744 subjects who were excluded from this study either did not have a first-visit serum sample stored at the New Orleans site or this specimen was no longer available and assumed to have been consumed in other studies.

The culture of cervical and vaginal specimens for cervicovaginal pathogens were as previously reported.24 In addition, a vaginal smear was evaluated for the presence of bacterial vaginosis by morphotype scoring.25 Gestational age at initial visit was determined by physical examination, last menstrual period, and any ultrasonography results. Gestational age at delivery was determined from this initial estimate and the elapsed time since the initial estimate. Premature rupture of membranes (PROM) was defined as any rupture of membranes prior to the onset of labor, regardless of gestational age. Preeclampsia was defined either as blood pressure higher than 140/90 on two occasions more than 6 hours apart, an increase in systolic blood pressure of more than 30 mmHg, an increase in diastolic blood pressure of more than 15 mmHg after the first 20 weeks of pregnancy, and/or proteinuria of greater than 300 mg/L in a 24-hour collection or greater than 1 g/L in two urine samples at least 6 hours apart (dipstick 1+ or greater). Eclampsia was defined as signs of preeclampsia coexistent with tonic-clonic seizures or coma.

The HPV-16 capture enzyme-linked immunosorbent assay (ELISA) was performed as described by Carter et al.6 The necessary amounts of monoclonal antibody H16.V5 (provided by N. Christensen, Pennsylvania State Medical Center, Hershey, PA) and capsids (produced in the vaccinia-virus system) needed were predetermined with positive control sera to maximize the signal and minimize the background.8 These fixed amounts of reagents were used to assay the test population sera. For each sample, the median of activity in three wells without capsids was subtracted from the median of activity in three wells with capsids.

The cutpoint for the ELISA was determined by assayed sera from a group of 28 children (under age 10) with no reported sexual activity or history of sexual abuse. Two standard deviations above the means of their response were used as the cutpoint (optical density = 0.286) for positivity. Cutpoint determination using a population thought to be at low risk for HPV infection has been used extensively6–8,10 and has compared favorably with population-derived methods.8 Variables were compared by the Pearson {chi}2 test with the level of statistical significance defined by a two-sided P <.05. Multivariate logistic regression analysis was employed to test for parameters independently associated with HPV-16 seropositivity while adjusting for possible confounding factors. Variables that showed a bivariate association with P < .1 were entered into the multivariate model. Appropriate stepwise procedures utilizing the likelihood ratio method were performed to determine the most parsimonious regression model. Adjusted odds ratios and 95% confidence intervals were calculated. Data analysis was completed with the use of SPSS for Windows statistical software (SPSS for Windows, Release 9.0.0; SPSS Inc., Chicago, IL).


   Results
Top
Abstract
 Materials and Methods
 Results
Discussion
 References
 
In New Orleans, 3341 women were enrolled in the Vaginal Infections and Prematurity study. Sera for HPV-16 antibody testing were available from 2597 of these women. The women who were tested for HPV-16 antibodies were slightly older but otherwise identical in age, number of pregnancies, ethnicity, and numbers of sexual partners to the overall New Orleans Vaginal Infections and Prematurity study group (Table 1Go). Overall, HPV-16 capsid antibodies were found in 727 (28.0%) women in the study population. The seroprevalence of HPV-16 antibodies did not change significantly over the course of this study (year-% seropositive; 1984-33.3, 1985-25.0, 1986-32.4, 1987-27.6, 1988-26.2, and 1989-31.5, P < .11), and finally, the HPV-16 seroprevalence and the gestational age of the fetus at the time of serologic screen did not differ significantly (data not shown).


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  		Table 1. Descriptive Characteristics of the Human Papillomavirus Study Group and Those for Whom Sera Were not Available
 
Significant bivariate associations between HPV-16 seropositivity and various demographic criteria are shown in Table 2Go. Age, number of pregnancies, mother’s education level, smoking, alcohol intake, number of years of sexual activity, and number of lifetime sexual partners were all found to be bivariate risk factors for HPV-16 seropositivity. In addition, alcohol intake within the past 3 months and a lifetime history of smoking were associated with HPV-16 antibodies. Demographic characteristics that were not significantly associated with the presence of HPV-16 capsid antibodies included marital status, household income, use of birth control pills, history of douching, and age at sexual debut (data not shown).


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  		Table 2. Significant Bivariate Associations of Human Papillomavirus-16 Seropositivity With Demographic Characteristics
 
The association between HPV-16 serum antibodies and history of sexual transmitted diseases was also examined (Table 3Go). Women enrolled in this study who had a self-reported history of Neisseria gonorrhoeae, cone biopsy (usually associated with an abnormal Papanicolaou test), Trichomonas vaginalis, or yeast infection were more likely to be HPV-16 seropositive. On a percentage basis, a higher number of women with a history of Chlamydia trachomatis, genital herpes, or syphilis infection had HPV-16 antibodies, but this did not reach statistical significance. In addition, the presence of HPV-16 antibodies did not correlate with history of postpartum endometritis. Finally, HPV-16 antibodies did not consistently correlate with concurrent Candida, T vaginalis, group B streptococcus, bacterial vaginosis, C trachomatis, N gonorrhoeae, or genital tract mycoplasma (data not shown). Papanicolaou test, HPV DNA detection, herpes simplex virus (HSV) culture or serology, and syphilis serology were not performed.


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  		Table 3. Bivariate Associations of Human Papillomavirus-16 Seropositivity and Self-Reported History of Sexually Transmitted Diseases and Other Gynecologic Infections
 
The associations between HPV-16 and obstetric outcome are shown in Table 4Go. There was no association with HPV-16 antibody detection and gestational age, birth weight, preeclampsia or eclampsia, method of delivery, spontaneous labor, preterm PROM, Apgar scores at 5 minutes, or delivery outcome. This suggests that previous or concurrent HPV infection of the mother does not adversely effect obstetric outcome.


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  		Table 4. Associations of Human Papillomavirus Type-16 Seropositivity and Obstetric Outcome
 
The parameters that were found to be significant at a level of P < .1 in the bivariate analysis were entered into a multivariate model (Table 5Go). This analysis demonstrated that women who have more education, who have been sexually active longer, with increased numbers of sexual partners, and who have a history of N gonorrhoeae infection, were more likely to test seropositive for HPV-16.


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  		Table 5. Predictors of Human Papillomavirus Type-16 Seropositivity in Multivariate Logistic Regression Analysis
 

   Discussion
Top
Abstract
 Materials and Methods
 Results
 Discussion
References
 
This study examined HPV-16 seropositivity in a large cohort of pregnant women observed in the Vaginal Infections and Prematurity study of the late 1980s. The rate of HPV-16 seropositivity in this cohort was 28.0%. The women were mainly low-income and black with a relatively long history of sexual activity (7 years) and a moderate number of lifetime sexual partners (3.3). Studies of nonpregnant women have demonstrated that the seroprevalence rate for HPV-16 capsid antibodies is correlated with sexual activity. Carter et al6 reported 9.5% HPV-16 seroprevalence in a cohort of college-aged women who had an average number of two lifetime sexual partners. Other studies found seroprevalence of 24% in college-aged women with an average of four lifetime partners,7 49% in sexually transmitted disease (STD) clinic attendees with 20–25 lifetime partners9 and 44% in gay men with more than 50 lifetime partners.8 Although these study populations did differ in terms of age and race, the 28.0% rate found in pregnant women suggests that the extent of sexual activity determines the rate of HPV-16 antibodies and that pregnancy does not greatly influence this rate.

Our bivariate analysis found that a number of demographic and behavioral risk factors were associated with HPV-16 seropositivity. These included age, number of lifetime sexual partners, duration of sexual activity, mother’s education level, and tobacco and alcohol use. Only the level of education, the number of lifetime sexual partners, and the length of sexual activity were significant in multivariate analysis. In studies of non-pregnant women, the number of sexual partners also has correlated with the HPV-16 seropositivity in both bivariate6,7,9,26 or multivariate analysis.27 Our data, in addition to these studies, clearly confirm the fact that HPV is an STD.

A self-reported history of cervical infection with N gonorrhoeae was found independently associated with HPV-16 antibodies in the multivariate model. In contrast, a self-reported history of C trachomatis infection, genital herpes, or syphilis were not associated; however, the number of patients with a history of these STDs was quite small (Table 3Go). The fact that, in the mid-1980s, tests for C trachomatis and HSV were not done routinely in New Orleans and the prevalence of syphilis was relatively low may help explain these findings. It is interesting that determination of STD by culture or Gram stain in this cohort of pregnant women was not associated with HPV-16 seropositivity. The absence of HPV-16 seropositivity when recent high-risk sexual behavior results in concurrent C trachomatis, N gonorrhoeae, may occur because HPV-16 seropositivity requires a mean of 9 months to seroconvert.6

Not surprisingly serum antibodies to HPV-16 in the serum were not associated with an adverse obstetric outcome, such as eclampsia, premature delivery, PROM, preterm PROM, or abnormal Apgar scores. Low-risk HPV types, especially HPV-6 and -11, have been found to cause respiratory papillomatosis in young children, and these agents have been implicated in potential vertical transmission.1 In addition, studies have shown persistent detection of high-risk HPV types in young children, who presumably acquired this infection perinatally.28,29 The significance of these findings is unclear. Unfortunately, follow-up infant serum is not available from this study.

This survey of pregnant women demonstrates that markers of sexual activity are associated with the detection of HPV-16 serum antibodies. The local subset of subjects was predominantly black and all were pregnant, which will limit the generalizability of the data. The performance of a study examining similarly risked pregnant and nonpregnant women is necessary to better define this. Patient enrollments at other Vaginal Infections and Prematurity study sites had different racial mixes. To more closely examine the role of regional or ethnic differences in HPV-16 antibody detection, the assay of sera from the other study sites might prove useful. In addition, measurement of HPV antibodies in a newly enrolled cohort of pregnant women from New Orleans would better define the current status of HPV infection and address changes in seroprevalence.


   Footnotes
 
Financial support National Institutes of Health contract number NO1 HD 3-2834. CMG supported by National Cancer Institute CA47877.

PII S0029-7844(99)00454-8

Received October 7, 1998. Received in revised form March 3, 1999. Accepted March 11, 1999.


   References
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 Materials and Methods
 Results
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1. Koutsky LA, Galloway DA, Holmes KK. The epidemiology of genital papillomavirus infections. Epidemiol Rev 1988;10:122–63.[Free Full Text]

2. Hagensee ME, Yaegashi N, Galloway DA. Self-assembly of human papillomavirus type 1 capsids by expression of the L1 protein alone or by coexpression of the L1 and L2 capsid proteins. J Virol 1993;67:315–22.[Abstract/Free Full Text]

3. Kirnbauer R, Booy F, Cheng N, Lowy DR, Schiller JT. Papilloma-virus L1 major capsid protein self-assembles into virus-like particles that are highly immunogenic. Proc Natl Acad Sci USA 1992;89:12180–4.[Abstract/Free Full Text]

4. Hofmann KJ, Cook JC, Joyce JG, Brown DR, Schultz LD, George HA, et al. Sequence determination of human papillomavirus type 6a and assembly of virus-like particles in Saccharomyces cerevisiae. Virology 1995;209:506–18.[Medline]

5. Carter JJ, Galloway DA. Humoral immune response to human papillomavirus infection. Clin Dermatol 1997;15:249–59.[Medline]

6. Carter JJ, Koutsky LA, Wipf GC, Christensen ND, Lee S-K, Kuypers J, et al. The natural history of HPV-16 capsid antibodies among a cohort of university women. J Infect Dis 1996;174:927–36.[Medline]

7. Viscidi RP, Kotloff K, Clayman B, Russ K, Shapiro S, Shah KV. Prevalence of antibodies to human papillomavirus (HPV) type 16 virus-like particles in relation to cervical HPV infection among college women. Clin Diagn Lab Immunol 1997;4:122–6.[Abstract]

8. Hagensee ME, Kiviat NB, Critchlow CW, Hawes S, Kuypers J, Holte S, et al. Seroprevalence of HPV 6 and 16 capsid antibodies in homosexual men. J Infect Dis 1997;176:625–31.[Medline]

9. Nonnenmacher B, Kjaer S, Svare E, Scott J, Hubbert N, van den Brule A, et al. Seroreactivity to HPV16 virus-like particles as a marker for cervical cancer risk in high-risk populations. Int J Cancer 1996;68:704–9.[Medline]

10. Carter JJ, Wipf GC, Hagensee ME, McKnight B, Habel LA, Lee SK, et al. Use of human papillomavirus type 6 capsids to detect antibodies in people with genital warts. J Infect Dis 1995;172:11–8.[Medline]

11. Wideroff L, Schiffman MH, Nonnenmacher B, Hubbert N, Kirnbauer R, Greer CE, et al. Evaluation of seroreactivity to human papillomavirus type 16 virus-like particles in an incident case-control study of cervical neoplasia. J Infect Dis 1995;172:1425–30.[Medline]

12. Nonnenmacher B, Hubbert NL, Kirnbauer R, Shah KV, Munoz N, Bosch FX, et al. Serologic response to human papillomavirus type 16 (HPV-16) virus-like particles in HPV-16 DNA-positive invasive cervical cancer and cervical intraepithelial neoplasia grade III patients and controls from Colombia and Spain. J Infect Dis 1995;172:19–24.[Medline]

13. Kirnbauer R, Hubbert NL, Wheeler CM, Becker TM, Lowy DR, Schiller JT. A virus-like particle enzyme-linked immunosorbent assay detects serum antibodies in a majority of women infected with human papillomavirus type 16. J Natl Cancer Inst 1994;86: 494–9.[Abstract/Free Full Text]

14. Heim K, Christensen ND, Hoepfl R, Wartusch B, Pinzger G, Zeimet A, et al. Serum IgG, IgM, and IgA reactivity to human papilloma-virus types 11 and 6 virus-like particles in different gynecologic patient groups. J Infect Dis 1995;172:395–402.[Medline]

15. Schneider A, Hotz M, Gissmann L. Increased prevalence of human papillomaviruses in the lower genital tract of pregnant women. Int J Cancer 1987;40:198–201.[Medline]

16. Fife KH, Katz B, Roush J, Handy VD, Brown DR, Hansell R. Cancer-associated human papillomavirus types are selectively increased in cervix of women in the first trimester of pregnancy. Am J Obstet Gynecol 1996;174:1487–93.[Medline]

17. Morrison EAB, Gammon MD, Goldberg GL, Verumund SH, Burk RD. Pregnancy and cervical infection with human papillomavi-ruses. Int J Obstet Gynecol 1996;54:125–30.

18. de Roda Husman AM, Walboomers JMM, Hopman E, Bleker OP, Helmerhorst TJM, Rozendaal L, et al. HPV prevalence in cytomor-phologically normal cervical scrapes of pregnant women as determined by PCR: The age-related pattern. J Med Virol 1995;46:97–102.[Medline]

19. Kemp EA, Hakenwerth AM, Laurent SL, Gravitt PE, Stoerker J. Human papillomavirus prevalence in pregnancy. Obstet Gynecol 1992;79:649–56.[Abstract/Free Full Text]

20. Tenti P, Zappatore R, Migliora P, Spinillo A, Maccarini U, De Benedittis M, et al. Latent human papillomavirus infection in pregnant women at term: A case-control study. J Infect Dis 1997;176:277–80.[Medline]

21. Malone JM, Sokol RJ, Ager JW. Pregnancy, human papillomavirus and cervical intraepithelial neoplasia. Eur J Gynaecol Oncol 1988; 9:120–30.[Medline]

22. Hermonat PL, Han L, Wendel PJ, Quirk JG, Stern S, Lowery CL, et al. Human papillomavirus is more prevalent in the first trimester spontaneously aborted products of conception compared to elective specimens. Virus Genes 1997;14:13–7.[Medline]

23. Cotch MF, Pastorek JG, Nugent R, Yerg DE, Martin DH, Eschenbach DA. Demographic and behavioral predictors of Trichomonas vaginalis infection among pregnant women. Obstet Gynecol 1991; 78:1087–92.[Abstract/Free Full Text]

24. Eschenbach DA, Nugent R, Rao V, Cotch MF, Gibbs RS, Lipscomb KA, et al. A randomized placebo-controlled trial of erythromycin for the treatment of Ureaplasma urealyticum to prevent premature delivery. Am J Obstet Gynecol 1991;164:734–52.[Medline]

25. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. J Clin Microbiol 1991;29:297–301.[Abstract/Free Full Text]

26. Andersson-Ellstrom A, Dillner J, Hagmar B, Schiller J, Sapp M, Forssman L, et al. Comparison and development of serum antibodies to HPV 16 and HPV 33 and acquisition of cervical HPV DNA among sexually experienced and virginal young girls. Sex Transm Dis 1995;23:234–8.

27. Olson A, Dillner J, Gjoen K, Magnus P. Seropositivity against HPV 16 capsids: A better marker of past sexual behaviour than presence of HPV DNA. Genitourin Med 1997;73:131–5.[Medline]

28. Cason J, Kaye JN, Jewers RJ, Kambo PK, Bible JM, Kell B, et al. Perinatal infection and persistence of human papillomavirus types 16 and 18 in infants. J Infect Dis 1995;172:395–402.

29. Puranen M, Yliskoski M, Saarikoski S, Syrjanen K, Syranen S. Vertical transmission of human papillomavirus from infected mothers to their newborn and persistence of the virus in childhood. Am J Obstet Gynecol 1996;174:694–9.[Medline]




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