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Comparisons of high-risk cervical HPV infections in Caribbean and US populations

Comparisons of high-risk cervical HPV infections in Caribbean and US populations Background: Disparities in cervical cancer incidence and mortality rates exist among women of African ancestry (African-American, African-Caribbean and African). Persistent cervical infection with Human papillomavirus (HPV) is associated with cervical dysplasia and if untreated, could potentially progress to invasive cervical cancer. Very few studies have been conducted to examine the true prevalence of HPV infection in this population. Comparisons of cervical HPV infection and the type-specific distribution of HPV were performed between cancer-free Caribbean and US women. Results: The Caribbean population consisted of 212 women from Tobago and 99 women from Jamaica. The US population tested, consisted of 82 women from Pittsburgh. The majority of the US subjects was Caucasian, 74% (61/82) while 12% (10/82) and 13% (11/82) were African-American or other ethnic groups, respectively. The age-adjusted prevalence of any HPV infection among women from Tobago was 35%, while for Jamaica, it was 81% (p < 0.0001). The age-adjusted prevalence of HPV infection for Caribbean subjects was not statistically significantly different from the US (any Page 1 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 HPV: 47% vs. 39%, p > 0.1; high-risk HPVs: 27% vs. 25%, p > 0.1); no difference was observed between US-Blacks and Jamaicans (any HPV: 92% vs. 81%, p > 0.1; high-risk HPV: 50% vs. 53%, p > 0.1). However, US-Whites had a lower age-adjusted prevalence of HPV infections compared to Jamaican subjects (any HPV: 29% vs. 81%, p < 0.0001; high-risk HPV: 20% vs. 53%, p < 0.001). Subjects from Jamaica, Tobago, and US-Blacks had a higher proportion of high-risk HPV infections (Tobago: 20%, Jamaica: 58%, US-Blacks: 40%) compared to US-Whites (15%). Similar observations were made for the presence of infections with multiple high-risk HPV types (Tobago: 12%, Jamaica: 43%, US-Blacks: 30%, US-Whites: 8%). Although we observed similar prevalence of HPV16 infections among Caribbean and US-White women, there was a distinct distribution of high-risk HPV types when comparisons were made between the ethnic groups. Conclusion: The higher prevalence of cervical HPV infections and multiple high-risk infections in Caribbean and US-Black women may contribute to the high incidence and prevalence of cervical cancer in these populations. Evaluation of a larger sample size is currently ongoing to confirm the distinct distribution of HPV types between ethnic groups. Background Methods Disparities in cervical cancer incidence and mortality rates Study population exist among all women of African ancestry (African-Amer- The Caribbean populations consisted of 212 women from ican, African-Caribbean and African) [1,2]. The world Tobago [6] and 99 women from Jamaica [7]. The US pop- standardized age-adjusted incidence and mortality rates ulation consisted of 88 women from Pittsburgh. All of the per 100,000 for African-American women are 8.6 and 3.4, subjects from the three geographic areas were recruited respectively vs. 6.7 and 1.7 for Caucasians in the United from the general population and none were pregnant. The States (US) [1]. Furthermore, African and Caribbean women from Tobago were recruited between July and countries have the top two highest incidence and mortal- September 2004 by means of posters, flyers, public service ity rates, above Asia, the Americas and Europe [2]. announcements on television and radio, word of mouth, and a series of cancer information sessions conducted Almost all cases of invasive cancers of the cervix, most throughout the island. The Jamaican women were other anogenital tract cancers [3], and approximately 36% recruited during visits to a family practice in Western of oropharyngeal cancers [4], are associated with HPV Jamaica between January 2003 and October 2006. All infection. In addition to persistent HPV infection with Jamaican participants were recruited consecutively to high-risk genotypes, access to screening as well as behav- avoid selection bias. The US study population was iors such as early age of sexual intercourse, multiple sex enrolled from May 2007–Aug 2008 as part of a nested partners, and lifetime number of partners are risk factors cross-sectional study of the Epidemiologic STudy of associated with the development of cervical cancer. HEalth Risk (ESTHER) project, (an ongoing women's Although the HPV infection rate is high in the Caribbean study at the University of Pittsburgh). The ESTHER [5], very few studies have been conducted to measure the project's sample recruitment methodology attempted to true prevalence of HPV infection in this population. In address some of the biases related to use of a sample of addition, there are not enough data that describe the dis- convenience. The targeted recruitment for ESTHER was tribution of HPV types among cancer cases and healthy based on age, level of education, and race/ethnicity popu- controls from the many islands throughout the Carib- lation distributions. Recruitment strategies included bean. Since the HPV vaccine specifically prevents cancers attending women focused events, news items and adver- caused by HPV16 and 18, knowledge of the HPV type dis- tisements in women-focused news sources, and limited tribution in these populations is important in order to respondent driven sampling. evaluate the impact of the current HPV vaccine on these at-risk populations. All subjects from Jamaica and Tobago combined are referred to in this study as Caribbean. The majority of sub- We have previously reported the HPV type distribution in jects were African-Caribbean, although in Tobago, there two cancer-free Caribbean populations, Jamaica [6] and were 19 subjects who defined their ethnicity as East Tobago [7]. In this study, we have compared the preva- Indian. The self-reported ethnic groups in the US popula- lence and genotype distribution of cervical HPV infections tion were classified as White, Black or other ethnic groups. in these two Caribbean populations with that of US One subject did not define her ethnicity and was included women. in the other ethnic group category. Page 2 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 HPV testing and 58 individually, but positive for the cross-reactive Standardized protocols were implemented for sample col- probe are classified as HPV 52-positive. Samples that are lection, DNA extraction and HPV testing for all three sub- positive for HPV 33, 35, and/or 58 individually, as well as populations that were included in this analysis. A nurse or the cross-reactive probe have an uncertain HPV 52 status. clinician collected cervical brush samples and the DNA For our study these samples were considered negative for was extracted from these samples using the Puregene DNA HPV 52. purification kit (Qiagen, Germantown, MD, USA). The HPV genotyping was performed on these samples using HPV-risk classification was based on the epidemiological the Linear Array HPV Genotyping kit (Roche Diagnostics). classification of HPV types that are associated with cervi- All cervical samples were tested at the University of Pitts- cal cancer [8]. Briefly there are fifteen high-risk HPV types: burgh. The assay involved amplification of samples by 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, 82; PCR using a master mix which contained biotin-labeled three probable high-risk HPV types: 26, 53, 66 and twelve primers for the detection of the 37 most common HPV low-risk HPV types: 6, 11, 40, 42, 43, 44, 54, 61, 70, 72, genotypes as well as the human beta-globin gene. The 81, CP6108. For this analysis, we combined probable PCR products were chemically denatured and hybridized high-risk HPV types and high-risk HPV types into a single for 30 min at 53°C to linear array strips which contained group. The HPV types that do not fall into any of these specific and one cross-reactive oligonucleotide probe for aforementioned categories were classified as undeter- the HPV genotypes as well as a high and low concentra- mined risk. tion of a beta-globin probe. The HPV genotypes were identified when visualized using a streptavidin-horserad- Statistical analysis ish peroxidase conjugate and a substrate solution contain- All statistical analyses were performed using STATA SE ing hydrogen peroxide and 3,3',5,5'-tetramethylbenzidine (version 10), (StataCorp LP, College Station, TX). Age- which yielded a blue precipitate at the positions where the adjusted prevalence rates and confidence intervals were hybridization occurred. calculated using logistic regression estimates of infection with any HPV type or any high-risk HPV type, adjusted for For six samples from the US population, beta-globin was age. Observations with missing values of age were not positive, which indicated either poor quality or low dropped from the analysis before estimation. The chi- yield DNA samples. These samples were excluded. There- squared test of proportions was used to calculate p-values fore, HPV results were available for only 82 US samples. for the unadjusted differences in proportions as well as, p- All of the samples from Jamaica were tested with the values for the differences in adjusted proportions. AMPLICOR HPV method [7] prior to testing with the Lin- Although age and age at first sexual intercourse were both ear Array HPV Genotyping kit. Ten samples from the normally distributed, we rejected the hypothesis of equal Jamaican population tested HPV-negative using our assay, variances. Therefore, the comparisons of mean age and possibly due to a lower sensitivity. Therefore, for our age at first sexual intercourse were performed using two- study, these samples were classified as HPV X. sample t-tests on the equality of means adjusting for une- qual variances. The Linear Array protocol does not specifically detect HPV52. The cross-reactive probe in this assay detects HPV 33, 35, 52 and 58 combined. According to the manufac- turer's protocol, samples that are negative for HPV 33, 35, Table 1: Characteristics of the study population. Tobago Jamaica US Total Number of subjects 212 99 82 393 Population source GP GP GP GP Age (years, mean ± SD) 41 ± 11.6 36 ± 11.7 53 ± 9.0 42 ± 12.7 (n = 91) (n = 391) Age, first sexual intercourse 18 ± 3.5 17 ± 2.8 19 ± 3.8 18 ± 3.5 (years, mean ± SD) (n = 191) (n = 95) (n = 80) (n = 366) Number of sex partners N (%) 1–5 153 (79.7) 72 (74.2) 48 (60.8) 273 (74.2) 6–15 39 (20.3) 20 (20.6) 24 (30.4) 83 (22.6) 16+ 0 (0.0) 5 (5.2) 7 (8.9) 12 (3.3) GP = general population; SD = standard deviation; when there are subjects with missing data, the number of the subpopulation (n) used to calculate the overall means is indicated in each cell. Page 3 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 0.0001). Statistically significant differences were observed Results Study populations between the age-adjusted prevalence of high-risk HPV Table 1 summarizes the characteristics of each subpopula- infections among US Whites (20%) and Jamaican women tion. The overall study population consisted of 393 sub- (p = 0.001). In contrast, there was no statistically signifi- jects (mean age 42 ± 12.7 years) who were recruited from cant difference in the prevalence of high-risk infections the general population. The Caribbean subjects consisted among US-Blacks (50%) when compared to Jamaican of 212 women from Tobago [6] (mean age: 41 ± 11.6 subjects (p > 0.1). years). The 99 women from Jamaica [7] (mean age: 36 ± 11.7 years) were the youngest population, while the US Geographical distribution of high-risk HPV types and population, which consisted of 82 women (mean age: 53 multiple high-risk HPV infections ± 9.0 years) was the oldest (p < 0.0001). The majority of Figure 1 summarizes the HPV type distribution of high- subjects in the US population were White, 76% (67/88), risk HPV infections among all women infected with high- while 11% (10/88) and 13% (11/88) were African-Amer- risk HPV types. In both Caribbean islands, HPV 45 (over- ican or other ethnic groups, respectively. all: 26%, Tobago: 19% and Jamaica: 31%) rather than HPV 16 (overall: 13%, Tobago: 12% and Jamaica 14%) or The mean age at first sexual intercourse for each subpop- HPV 18 (overall: 14%, Tobago: 5% and Jamaica: 21%) ulation ranged from 17 to 19 years old, with an overall was the most common high-risk genotype detected. In mean of 18 ± 3.5 years. The age at first sexual intercourse contrast, US women had a different distribution of high- for Jamaican women was statistically significantly risk genotypes. HPV 33 infections were highest among the younger than women from Tobago (Jamaica: 17 ± 2.8 high-risk types in this population (overall: 29%, US- years vs. Tobago: 18 ± 3.5 years, p = 0.01) and US women Blacks: 25%, US-Whites: 22%) rather than HPV 16 (over- (vs. US: 19 ± 3.8 years, p = 0.0001). all: 7%, US-Blacks: 0%, US-Whites: 11%) or HPV 18 (overall: 7%, US-Blacks: 0%, US-Whites: 11%). Neverthe- Comparisons of cervical HPV prevalence between less, although not statistically significant, we observed a countries higher prevalence rate of HPV 16 and 18 infections among Thirty-five percent (75/212) of the women from Tobago, Caribbean subjects that were infected with high-risk HPV 84% (83/99) of the women from Jamaica and 32% (26/ types when compared to the US women (HPV 16: 13% vs. 82) of US women, tested positive for HPV infection of any 7%, p > 0.1 and HPV 18: 14% vs. 7%, p > 0.1). HPV type. Table 2 summarizes the age-adjusted preva- lence of HPV infections in our study population. The proportion of high-risk HPV infections appears to be Although the age-adjusted prevalence rate of any HPV highest among women of African ancestry. Jamaican infection was higher overall in the Caribbean (47%), it women had the highest proportion of high-risk HPV was not significantly different from the United States infections (58.6%), then US-Black (40%), Tobago (39%, p = 0.281). Similar observations were made when (20.3%) and US White (14.5%) women, followed by only high-risk HPV infections were considered (Carib- women from the US-other group (10%), (Table 3). Fifty bean: 27%, US 25%, p = 0.758). The highest prevalence of percent of US-black women, 40.4% of Jamaican women, high-risk HPV infections was observed in Jamaican 23.1% of Tobago women, 16.1% of US-white (40.4%) women (age-adjusted prevalence = 53%), while women and 10% of women from the US-other group had single from Tobago had a statistically significantly lower age- high-risk HPV infections. Similar observations were made adjusted prevalence of high-risk HPV infections (18%, p < for multiple high-risk HPV infections, US-whites and US- Table 2: Prevalence of HPV infection by geographic location. Country Test method Age-adjusted p-value, Country p-value, Ethnic Age-Adjusted p-value, Country p-value, Ethnic prevalence any group prevalence high- group HPV (%), 95% CI risk HPV (%), 95% CI Caribbean PCR 47.1 (41.3–53.0) ref 27.4 (22.3–33.3) ref Jamaica 80.5 (70.5–87.8) ref 52.7 (41.4–63.6) ref Tobago 34.5 (28.3–41.2) <0.0001 18.3 (13.5–24.2) <0.0001 United States PCR 39.4 (28.2–51.8) 0.281 25.3 (15.5–38.4) 0.758 US-Blacks 91.8 (58.3–98.9) 0.368 49.7 (21.4–78.2) 0.867 US-Whites 29.0 (18.0–43.0) <0.0001 20.2 (10.9–34.7) 0.001 US-Other 22.9 (5.9–58.5) 0.002 16.0 (2.3–61.0) 0.111 p-values for the differences in adjusted proportions. Page 4 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 tions. The inability to achieve statistical significance for high-risk HPV infections may be related to the small sam- ple size of the US population and consequently insuffi- cient statistical power to detect a difference between the two groups. Nevertheless, our findings suggest that the Caribbean higher rates of HPV infection in the Caribbean compared USA to the US, are likely to explain the higher incidence of cer- vical cancer reported in the region [2]. 0 The distribution of HPV types was similar in the two Car- 45 66 51 35 53 52 18 16 73 31 39 68 58 56 59 33 82 ibbean islands but was different from that observed in the High-risk HPV types US. This is not unexpected, since differences in the geo- graphical distribution of HPV infections have previously Distribution w Figure 1 omen with hi of high-risk HPV gh-risk HPV infe typ ctio es among ns Caribbean and US been reported [9]. We observed that HPV 16 and 18 were Distribution of high-risk HPV types among Caribbean and US not the predominant high-risk genotypes detected in can- women with high-risk HPV infections. cer-free Caribbean women. Our results show that Carib- bean women have a higher proportion of HPV 45 infections, the third most common high-risk HPV geno- other had lower proportions (8.1% and 10%, respec- type that drives cervical carcinogenesis [8,10]. Studies are tively). Higher proportions of multiple infections were currently ongoing to determine whether HPV 45 infec- observed among Jamaicans (43.4%), US-blacks (30%) tions might be driving cervical cancer development in the and women from Tobago (12.3%). In general, multiple Caribbean region. high risk infections among Caribbean women ranged from 2–6 high-risk HPV types whereas no more than two The current HPV vaccine prevents infections from HPV high-risk HPV types were detected among US Blacks. types 6, 11, 16 and 18 [11]. The low-risk genotypes, HPV 6 and 11, are responsible for the development of genital Discussion warts, while HPV 16 and 18 are the two most common This is the first study to report comparisons of the preva- high-risk genotypes and are reported to account for lence of cervical HPV infections and the specific HPV gen- almost 70% of cervical cancers worldwide [10]. We otypes between cancer-free Caribbean and US women. We observed that HPV 16 and 18 infections are not seen in have shown that the age-adjusted prevalence rate of any high proportions among cancer-free Caribbean women. HPV infection was higher in the Caribbean women (47%) However, Caribbean women still have a higher propor- than in women from the United States (39%), although tion of HPV 16 and 18 infections compared to their US the age-adjusted prevalence of high-risk HPV infections counterparts (HPV 16: 13% vs. 7%, and HPV 18: 14% vs. (Caribbean 27%, US 25%) was similar in both popula- 7%). These observed differences between the US and Car- Table 3: Characteristics of HPV infections according to ethnicity. Tobago N N (%) Jamaica N (%) US-Black N (%) US-White N (%) US-other N (%) Total N (%) Number of subjects 212 99 10 67 11 393 High-risk HPV infection 43 (20.3) 58 (58.6) 4 (40.0) 9 (14.5) 1 (10.0) 115 (29.3) Low-risk HPV infection 15 (7.1) 25 (25.3) 4 (40.0) 4 (6.5) 1 (10.0) 49 (12.5) Undetermined-risk infection 16 (7.6) 47 (47.5) 5 (50.0) 5 (8.1) 1 (10.0) 74 (18.3) Single high-risk infection* 49 (23.1) 40 (40.4) 5 (50.0) 10 (16.1) 1 (10.0) 105 (26.7) Multiple high-risk infection 26 (12.3) 43 (43.4) 3 (30.0) 5 (8.1) 1 (10.0) 78 (19.9) Number of high-risk HPV types per subject None** 169 (79.7) 41 (41.4) 6 (60.0) 53 (85.5) 9 (90.0) 278 (70.7) 1 33 (15.6) 34 (34.3) 3 (30.0) 7 (11.3) 1 (10.0) 78 (19.9) 2 7 (3.3) 11 (11.1) 1 (10.0) 2 (3.2) 0 (0.0) 21 (5.3) 3 2 (0.9) 7 (7.1) 0 (0.0) 0 (0.0) 0 (0.0) 9 (2.3) 4 1 (0.5) 2 (2.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (0.8) 5 0 (0.0) 3 (3.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (0.8) 6 0 (0.0) 1 (1.0) 0 (0.0) 0 (0.0) 0 (0.0) 1 (0.3) *Includes subjects infected with low-risk and undetermined-risk HPV types; **Includes subjects that were HPV-negative or had only low-risk HPV infections. Page 5 of 7 (page number not for citation purposes) Percent Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 ibbean may be due to immune resistance to HPV16 and Authors' contributions 18 genotypes in the US population (although we do not CR contributed to study design, sample/data collection have data to support these hypotheses). The evaluation of for Tobago and US populations, performed the data anal- serological status for HPV 16 and 18 and how these com- ysis and wrote the manuscript. JBW performed the sample pare to the prevalence of high-risk HPV infections in both and data collection of the Tobago population. ET, contrib- geographical regions are needed in order to test these uted to the overall study design and the writing of the hypotheses. Nevertheless, the higher incidence of cervical manuscript. AW, contributed to the study design, sample/ cancers in the Caribbean region compared to the US data collection of the Jamaican population and performed might be attributed to the higher proportions of HPV 16 the HPV testing. NM and RE: contributed to study design and 18 infections observed in the Caribbean. of the US population. AP, V W, CB and SMG: contributed to study design and sample/data collection for the Tobago Caribbean and US-Black subjects in comparison with US- population. SE: performed the HPV testing. HF, DG, MJ, Whites have higher prevalence rates of high-risk HPV MS, NY, NMA: contributed to the study design, sample/ infections and also a higher proportion of subjects with data collection of the Jamaican population. All co-authors multiple-high-risk HPV infections. This may be related to reviewed and approved the manuscript. sexual behaviour, social class (poverty and malnutrition), high parity, lack of barrier contraceptive protection and Acknowledgements This work is supported in part by NIH/R13 CA130596A, the UPCI Cancer use of steroidal contraception, [7,12-16]. However, these Education and Career Development grant R25CA089507, and a GLMA confounders could not be assessed in our study because foundation grant. This publication was also made possible by Grant these data were not available. Furthermore, the risk of cer- Number KL2 RR024154-03 to CCR, from the National Center for vical cancer among women with multiple high-risk infec- Research Resources (NCRR) [23], a component of the National Institutes tions has not been well studied; therefore additional of Health (NIH), and NIH Roadmap for Medical Research [24]. Its contents studies are warranted. are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. This publication was also supported by Studies show that younger age is associated with an funds received from the NIH/NCRR GCRC Grant MO1-RR000056 and/or the CTSA Grant 1 UL 1 RR024153-01. The authors wish to thank the increased risk of cervical HPV infection [17-20]. There- Tobago Branch of the Trinidad & Tobago Cancer Society for providing the fore, for comparisons of HPV infections between different facilities for subject recruitment and sample collection for the Tobago sub- populations, age must be standardized. A limitation in jects. our study is that although all subjects were recruited from the general population, the mean age for each country was This article has been published as part of Infectious Agents and Cancer. Vol- different. Pittsburgh subjects were the oldest (mean age = ume 4 Supplement 1, 2009: Second Annual International African-Caribbean 53 ± 9.0 years), and this was representative of the older Cancer Consortium Conference. The full contents of the supplement are population in the geographical region [21]. Jamaican available online at http://www.infectagentscancer.com/4/supplements/4/S1. women were the youngest population, also reflecting the References demographics for the country [22]. To address this limita- 1. Ries LAG, Melbert D, Krapcho M, Mariotto A, Miller BA, Feuer EJ, et tion, we have presented age-adjusted prevalence rates so al.: SEER Cancer Statistics Review, 1975–2004 National Cancer Institute. that these values might be compared. Another limitation Bethesda, MD; 2007. 2. Ferlay J, Bray F, Pisani P, Parkin DM: GLOBOCAN 2002 Cancer in this study is that only 11% (N = 10) of the US study Incidence, Mortality and Prevalence Worldwide IARC Can- population were African-American, which did not allow cerBase, Version 2.0 No. 5. Lyon, IARC Press; 2004. for adequate comparisons between African-American and 3. Steenbergen RD, de Wilde J, Wilting SM, Brink AA, Snijders PJ, Meijer CJ: HPV-mediated transformation of the anogenital tract. J Caribbean women. However, the proportion of African- Clin Virol 2005, 32(Suppl 1):S25-S33. American subjects is representative of the Pittsburgh 4. Kreimer AR, Clifford GM, Boyle P, Franceschi S: Human papillo- demographics. mavirus types in head and neck squamous cell carcinomas worldwide: a systematic review. Cancer Epidemiol Biomarkers Prev 2005, 14:467-475. Conclusion 5. Ragin CC, Kuo J, Taioli E: Prevalence of cancer-associated viruses in the Caribbean islands. Cancer Investigation 2008 in The higher prevalence of cervical HPV infections and mul- press. tiple high-risk infections in Caribbean and US-Black 6. Ragin CCR, Wheeler VW, Wilson JB, Bunker CH, Patrick AL, Gollin women may contribute to the high incidence and preva- SM, et al.: Distinct distribution of HPV types among cancer- free Afro-Caribbean women from Tobago. Biomarkers 2007, lence of cervical cancer in these populations. Further stud- 12:510-522. ies of the distribution of HPV types between ethnic groups 7. Watt A, Garwood D, Jackson M, Younger N, Ragin C, Smikle M, et al.: High-risk and multiple human papillomavirus (HPV) infec- and the risk of cervical cancer among women with multi- tions in cancer-free Jamaican women. Infectious Agents and Can- ple high-risk infections are currently ongoing. cer in press. 8. Munoz N, Bosch FX, de Sanjose S, Herrero R, Castellsague X, Shah KV, et al.: Epidemiologic classification of human papillomavi- Competing interests rus types associated with cervical cancer. N Engl J Med 2003, The authors declare that they have no competing interests. 348:518-527. Page 6 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 9. Clifford GM, Gallus S, Herrero R, Munoz N, Snijders PJ, Vaccarella S, et al.: Worldwide distribution of human papillomavirus types in cytologically normal women in the International Agency for Research on Cancer HPV prevalence surveys: a pooled analysis. Lancet 2005, 366:991-998. 10. Munoz N, Bosch FX, Castellsague X, Diaz M, de Sanjose S, Ham- mouda D, et al.: Against which human papillomavirus types shall we vaccinate and screen? The international perspec- tive. Int J Cancer 2004, 111:278-285. 11. FDA Licenses New Vaccine for Prevention of Cervical Can- cer and Other Diseases in Females Caused by Human Papil- lomavirus, Food & Drug Administration [http://www.fda.gov/ bbs/topics/NEWS/2006/NEW01385.html] 12. Fletcher HM, Hanchard B: Poverty eradication and decreased human papilloma virus related cancer of the penis and vulva in Jamaica. J Obstet Gynaecol 2008, 28:333-335. 13. Kahn JA, Lan D, Kahn RS: Sociodemographic Factors Associ- ated With High-Risk Human Papillomavirus Infection. Obstet Gynecol 2007, 110:87-95. 14. de Sanjose S, Bosch FX, Munoz N, Shah K: Social differences in sexual behaviour and cervical cancer. IARC Sci Publ; 1997:309-317. 15. McFarlane-Anderson N, Bazuaye PE, Jackson MD, Smikle M, Fletcher HM: Cervical dysplasia and cancer and the use of hormonal contraceptives in Jamaican women. BMC Womens Health 2008, 8:9. 16. Bazuaye PE, Fletcher H, McFarlane-Anderson N: Lifestyle and cer- vical dysplasia in Jamaica. Int J Gynaecol Obstet 2004, 84:175-177. 17. Kjaer SK, Breugelmans G, Munk C, Junge J, Watson M, Iftner T: Pop- ulation-based prevalence, type- and age-specific distribution of HPV in women before introduction of an HPV-vaccination program in Denmark. Int J Cancer 2008, 123:1864-1870. 18. Kitchener HC, Almonte M, Wheeler P, Desai M, Gilham C, Bailey A, et al.: HPV testing in routine cervical screening: cross sec- tional data from the ARTISTIC trial. Br J Cancer 2006, 95:56-61. 19. Dunne EF, Unger ER, Sternberg M, McQuillan G, Swan DC, Patel SS, et al.: Prevalence of HPV infection among females in the United States. JAMA 2007, 297:813-819. 20. Herrero R, Castle PE, Schiffman M, Bratti MC, Hildesheim A, Morales J, et al.: Epidemiologic profile of type-specific human papillo- mavirus infection and cervical neoplasia in Guanacaste, Costa Rica. J Infect Dis 2005, 191:1796-1807. 21. Pennsylvania Department of Health Annual Report of Vital Statistics, Pennsylvania Vital Statistics 2006 [http:// www.dsf.health.state.pa.us/health/cwp/view.asp?a=175&q=250106] 22. U.S.Census Bureau, Population Division/International Pro- grams Center, International Database Summary Demo- graphic Data [http://www.census.gov/ipc/www/idb/] 23. National Institutes of Health, National Institutes of Health, National Center for Research Resources [http:// www.ncrr.nih.gov/] 24. NIH Roadmap for Medical Research, NIH Roadmap for Med- ical Research, Re-engineering the Clinical Research Enter- prise [http://nihroadmap.nih.gov/clinicalresearch/overview- translational.asp] Publish with Bio Med Central and every scientist can read your work free of charge "BioMed Central will be the most significant development for disseminating the results of biomedical researc h in our lifetime." 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Comparisons of high-risk cervical HPV infections in Caribbean and US populations

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Springer Journals
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Copyright © 2009 by Ragin et al; licensee BioMed Central Ltd.
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Biomedicine; Cancer Research; Infectious Diseases; Oncology
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1750-9378
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10.1186/1750-9378-4-S1-S9
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19208214
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Abstract

Background: Disparities in cervical cancer incidence and mortality rates exist among women of African ancestry (African-American, African-Caribbean and African). Persistent cervical infection with Human papillomavirus (HPV) is associated with cervical dysplasia and if untreated, could potentially progress to invasive cervical cancer. Very few studies have been conducted to examine the true prevalence of HPV infection in this population. Comparisons of cervical HPV infection and the type-specific distribution of HPV were performed between cancer-free Caribbean and US women. Results: The Caribbean population consisted of 212 women from Tobago and 99 women from Jamaica. The US population tested, consisted of 82 women from Pittsburgh. The majority of the US subjects was Caucasian, 74% (61/82) while 12% (10/82) and 13% (11/82) were African-American or other ethnic groups, respectively. The age-adjusted prevalence of any HPV infection among women from Tobago was 35%, while for Jamaica, it was 81% (p < 0.0001). The age-adjusted prevalence of HPV infection for Caribbean subjects was not statistically significantly different from the US (any Page 1 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 HPV: 47% vs. 39%, p > 0.1; high-risk HPVs: 27% vs. 25%, p > 0.1); no difference was observed between US-Blacks and Jamaicans (any HPV: 92% vs. 81%, p > 0.1; high-risk HPV: 50% vs. 53%, p > 0.1). However, US-Whites had a lower age-adjusted prevalence of HPV infections compared to Jamaican subjects (any HPV: 29% vs. 81%, p < 0.0001; high-risk HPV: 20% vs. 53%, p < 0.001). Subjects from Jamaica, Tobago, and US-Blacks had a higher proportion of high-risk HPV infections (Tobago: 20%, Jamaica: 58%, US-Blacks: 40%) compared to US-Whites (15%). Similar observations were made for the presence of infections with multiple high-risk HPV types (Tobago: 12%, Jamaica: 43%, US-Blacks: 30%, US-Whites: 8%). Although we observed similar prevalence of HPV16 infections among Caribbean and US-White women, there was a distinct distribution of high-risk HPV types when comparisons were made between the ethnic groups. Conclusion: The higher prevalence of cervical HPV infections and multiple high-risk infections in Caribbean and US-Black women may contribute to the high incidence and prevalence of cervical cancer in these populations. Evaluation of a larger sample size is currently ongoing to confirm the distinct distribution of HPV types between ethnic groups. Background Methods Disparities in cervical cancer incidence and mortality rates Study population exist among all women of African ancestry (African-Amer- The Caribbean populations consisted of 212 women from ican, African-Caribbean and African) [1,2]. The world Tobago [6] and 99 women from Jamaica [7]. The US pop- standardized age-adjusted incidence and mortality rates ulation consisted of 88 women from Pittsburgh. All of the per 100,000 for African-American women are 8.6 and 3.4, subjects from the three geographic areas were recruited respectively vs. 6.7 and 1.7 for Caucasians in the United from the general population and none were pregnant. The States (US) [1]. Furthermore, African and Caribbean women from Tobago were recruited between July and countries have the top two highest incidence and mortal- September 2004 by means of posters, flyers, public service ity rates, above Asia, the Americas and Europe [2]. announcements on television and radio, word of mouth, and a series of cancer information sessions conducted Almost all cases of invasive cancers of the cervix, most throughout the island. The Jamaican women were other anogenital tract cancers [3], and approximately 36% recruited during visits to a family practice in Western of oropharyngeal cancers [4], are associated with HPV Jamaica between January 2003 and October 2006. All infection. In addition to persistent HPV infection with Jamaican participants were recruited consecutively to high-risk genotypes, access to screening as well as behav- avoid selection bias. The US study population was iors such as early age of sexual intercourse, multiple sex enrolled from May 2007–Aug 2008 as part of a nested partners, and lifetime number of partners are risk factors cross-sectional study of the Epidemiologic STudy of associated with the development of cervical cancer. HEalth Risk (ESTHER) project, (an ongoing women's Although the HPV infection rate is high in the Caribbean study at the University of Pittsburgh). The ESTHER [5], very few studies have been conducted to measure the project's sample recruitment methodology attempted to true prevalence of HPV infection in this population. In address some of the biases related to use of a sample of addition, there are not enough data that describe the dis- convenience. The targeted recruitment for ESTHER was tribution of HPV types among cancer cases and healthy based on age, level of education, and race/ethnicity popu- controls from the many islands throughout the Carib- lation distributions. Recruitment strategies included bean. Since the HPV vaccine specifically prevents cancers attending women focused events, news items and adver- caused by HPV16 and 18, knowledge of the HPV type dis- tisements in women-focused news sources, and limited tribution in these populations is important in order to respondent driven sampling. evaluate the impact of the current HPV vaccine on these at-risk populations. All subjects from Jamaica and Tobago combined are referred to in this study as Caribbean. The majority of sub- We have previously reported the HPV type distribution in jects were African-Caribbean, although in Tobago, there two cancer-free Caribbean populations, Jamaica [6] and were 19 subjects who defined their ethnicity as East Tobago [7]. In this study, we have compared the preva- Indian. The self-reported ethnic groups in the US popula- lence and genotype distribution of cervical HPV infections tion were classified as White, Black or other ethnic groups. in these two Caribbean populations with that of US One subject did not define her ethnicity and was included women. in the other ethnic group category. Page 2 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 HPV testing and 58 individually, but positive for the cross-reactive Standardized protocols were implemented for sample col- probe are classified as HPV 52-positive. Samples that are lection, DNA extraction and HPV testing for all three sub- positive for HPV 33, 35, and/or 58 individually, as well as populations that were included in this analysis. A nurse or the cross-reactive probe have an uncertain HPV 52 status. clinician collected cervical brush samples and the DNA For our study these samples were considered negative for was extracted from these samples using the Puregene DNA HPV 52. purification kit (Qiagen, Germantown, MD, USA). The HPV genotyping was performed on these samples using HPV-risk classification was based on the epidemiological the Linear Array HPV Genotyping kit (Roche Diagnostics). classification of HPV types that are associated with cervi- All cervical samples were tested at the University of Pitts- cal cancer [8]. Briefly there are fifteen high-risk HPV types: burgh. The assay involved amplification of samples by 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, 82; PCR using a master mix which contained biotin-labeled three probable high-risk HPV types: 26, 53, 66 and twelve primers for the detection of the 37 most common HPV low-risk HPV types: 6, 11, 40, 42, 43, 44, 54, 61, 70, 72, genotypes as well as the human beta-globin gene. The 81, CP6108. For this analysis, we combined probable PCR products were chemically denatured and hybridized high-risk HPV types and high-risk HPV types into a single for 30 min at 53°C to linear array strips which contained group. The HPV types that do not fall into any of these specific and one cross-reactive oligonucleotide probe for aforementioned categories were classified as undeter- the HPV genotypes as well as a high and low concentra- mined risk. tion of a beta-globin probe. The HPV genotypes were identified when visualized using a streptavidin-horserad- Statistical analysis ish peroxidase conjugate and a substrate solution contain- All statistical analyses were performed using STATA SE ing hydrogen peroxide and 3,3',5,5'-tetramethylbenzidine (version 10), (StataCorp LP, College Station, TX). Age- which yielded a blue precipitate at the positions where the adjusted prevalence rates and confidence intervals were hybridization occurred. calculated using logistic regression estimates of infection with any HPV type or any high-risk HPV type, adjusted for For six samples from the US population, beta-globin was age. Observations with missing values of age were not positive, which indicated either poor quality or low dropped from the analysis before estimation. The chi- yield DNA samples. These samples were excluded. There- squared test of proportions was used to calculate p-values fore, HPV results were available for only 82 US samples. for the unadjusted differences in proportions as well as, p- All of the samples from Jamaica were tested with the values for the differences in adjusted proportions. AMPLICOR HPV method [7] prior to testing with the Lin- Although age and age at first sexual intercourse were both ear Array HPV Genotyping kit. Ten samples from the normally distributed, we rejected the hypothesis of equal Jamaican population tested HPV-negative using our assay, variances. Therefore, the comparisons of mean age and possibly due to a lower sensitivity. Therefore, for our age at first sexual intercourse were performed using two- study, these samples were classified as HPV X. sample t-tests on the equality of means adjusting for une- qual variances. The Linear Array protocol does not specifically detect HPV52. The cross-reactive probe in this assay detects HPV 33, 35, 52 and 58 combined. According to the manufac- turer's protocol, samples that are negative for HPV 33, 35, Table 1: Characteristics of the study population. Tobago Jamaica US Total Number of subjects 212 99 82 393 Population source GP GP GP GP Age (years, mean ± SD) 41 ± 11.6 36 ± 11.7 53 ± 9.0 42 ± 12.7 (n = 91) (n = 391) Age, first sexual intercourse 18 ± 3.5 17 ± 2.8 19 ± 3.8 18 ± 3.5 (years, mean ± SD) (n = 191) (n = 95) (n = 80) (n = 366) Number of sex partners N (%) 1–5 153 (79.7) 72 (74.2) 48 (60.8) 273 (74.2) 6–15 39 (20.3) 20 (20.6) 24 (30.4) 83 (22.6) 16+ 0 (0.0) 5 (5.2) 7 (8.9) 12 (3.3) GP = general population; SD = standard deviation; when there are subjects with missing data, the number of the subpopulation (n) used to calculate the overall means is indicated in each cell. Page 3 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 0.0001). Statistically significant differences were observed Results Study populations between the age-adjusted prevalence of high-risk HPV Table 1 summarizes the characteristics of each subpopula- infections among US Whites (20%) and Jamaican women tion. The overall study population consisted of 393 sub- (p = 0.001). In contrast, there was no statistically signifi- jects (mean age 42 ± 12.7 years) who were recruited from cant difference in the prevalence of high-risk infections the general population. The Caribbean subjects consisted among US-Blacks (50%) when compared to Jamaican of 212 women from Tobago [6] (mean age: 41 ± 11.6 subjects (p > 0.1). years). The 99 women from Jamaica [7] (mean age: 36 ± 11.7 years) were the youngest population, while the US Geographical distribution of high-risk HPV types and population, which consisted of 82 women (mean age: 53 multiple high-risk HPV infections ± 9.0 years) was the oldest (p < 0.0001). The majority of Figure 1 summarizes the HPV type distribution of high- subjects in the US population were White, 76% (67/88), risk HPV infections among all women infected with high- while 11% (10/88) and 13% (11/88) were African-Amer- risk HPV types. In both Caribbean islands, HPV 45 (over- ican or other ethnic groups, respectively. all: 26%, Tobago: 19% and Jamaica: 31%) rather than HPV 16 (overall: 13%, Tobago: 12% and Jamaica 14%) or The mean age at first sexual intercourse for each subpop- HPV 18 (overall: 14%, Tobago: 5% and Jamaica: 21%) ulation ranged from 17 to 19 years old, with an overall was the most common high-risk genotype detected. In mean of 18 ± 3.5 years. The age at first sexual intercourse contrast, US women had a different distribution of high- for Jamaican women was statistically significantly risk genotypes. HPV 33 infections were highest among the younger than women from Tobago (Jamaica: 17 ± 2.8 high-risk types in this population (overall: 29%, US- years vs. Tobago: 18 ± 3.5 years, p = 0.01) and US women Blacks: 25%, US-Whites: 22%) rather than HPV 16 (over- (vs. US: 19 ± 3.8 years, p = 0.0001). all: 7%, US-Blacks: 0%, US-Whites: 11%) or HPV 18 (overall: 7%, US-Blacks: 0%, US-Whites: 11%). Neverthe- Comparisons of cervical HPV prevalence between less, although not statistically significant, we observed a countries higher prevalence rate of HPV 16 and 18 infections among Thirty-five percent (75/212) of the women from Tobago, Caribbean subjects that were infected with high-risk HPV 84% (83/99) of the women from Jamaica and 32% (26/ types when compared to the US women (HPV 16: 13% vs. 82) of US women, tested positive for HPV infection of any 7%, p > 0.1 and HPV 18: 14% vs. 7%, p > 0.1). HPV type. Table 2 summarizes the age-adjusted preva- lence of HPV infections in our study population. The proportion of high-risk HPV infections appears to be Although the age-adjusted prevalence rate of any HPV highest among women of African ancestry. Jamaican infection was higher overall in the Caribbean (47%), it women had the highest proportion of high-risk HPV was not significantly different from the United States infections (58.6%), then US-Black (40%), Tobago (39%, p = 0.281). Similar observations were made when (20.3%) and US White (14.5%) women, followed by only high-risk HPV infections were considered (Carib- women from the US-other group (10%), (Table 3). Fifty bean: 27%, US 25%, p = 0.758). The highest prevalence of percent of US-black women, 40.4% of Jamaican women, high-risk HPV infections was observed in Jamaican 23.1% of Tobago women, 16.1% of US-white (40.4%) women (age-adjusted prevalence = 53%), while women and 10% of women from the US-other group had single from Tobago had a statistically significantly lower age- high-risk HPV infections. Similar observations were made adjusted prevalence of high-risk HPV infections (18%, p < for multiple high-risk HPV infections, US-whites and US- Table 2: Prevalence of HPV infection by geographic location. Country Test method Age-adjusted p-value, Country p-value, Ethnic Age-Adjusted p-value, Country p-value, Ethnic prevalence any group prevalence high- group HPV (%), 95% CI risk HPV (%), 95% CI Caribbean PCR 47.1 (41.3–53.0) ref 27.4 (22.3–33.3) ref Jamaica 80.5 (70.5–87.8) ref 52.7 (41.4–63.6) ref Tobago 34.5 (28.3–41.2) <0.0001 18.3 (13.5–24.2) <0.0001 United States PCR 39.4 (28.2–51.8) 0.281 25.3 (15.5–38.4) 0.758 US-Blacks 91.8 (58.3–98.9) 0.368 49.7 (21.4–78.2) 0.867 US-Whites 29.0 (18.0–43.0) <0.0001 20.2 (10.9–34.7) 0.001 US-Other 22.9 (5.9–58.5) 0.002 16.0 (2.3–61.0) 0.111 p-values for the differences in adjusted proportions. Page 4 of 7 (page number not for citation purposes) Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 tions. The inability to achieve statistical significance for high-risk HPV infections may be related to the small sam- ple size of the US population and consequently insuffi- cient statistical power to detect a difference between the two groups. Nevertheless, our findings suggest that the Caribbean higher rates of HPV infection in the Caribbean compared USA to the US, are likely to explain the higher incidence of cer- vical cancer reported in the region [2]. 0 The distribution of HPV types was similar in the two Car- 45 66 51 35 53 52 18 16 73 31 39 68 58 56 59 33 82 ibbean islands but was different from that observed in the High-risk HPV types US. This is not unexpected, since differences in the geo- graphical distribution of HPV infections have previously Distribution w Figure 1 omen with hi of high-risk HPV gh-risk HPV infe typ ctio es among ns Caribbean and US been reported [9]. We observed that HPV 16 and 18 were Distribution of high-risk HPV types among Caribbean and US not the predominant high-risk genotypes detected in can- women with high-risk HPV infections. cer-free Caribbean women. Our results show that Carib- bean women have a higher proportion of HPV 45 infections, the third most common high-risk HPV geno- other had lower proportions (8.1% and 10%, respec- type that drives cervical carcinogenesis [8,10]. Studies are tively). Higher proportions of multiple infections were currently ongoing to determine whether HPV 45 infec- observed among Jamaicans (43.4%), US-blacks (30%) tions might be driving cervical cancer development in the and women from Tobago (12.3%). In general, multiple Caribbean region. high risk infections among Caribbean women ranged from 2–6 high-risk HPV types whereas no more than two The current HPV vaccine prevents infections from HPV high-risk HPV types were detected among US Blacks. types 6, 11, 16 and 18 [11]. The low-risk genotypes, HPV 6 and 11, are responsible for the development of genital Discussion warts, while HPV 16 and 18 are the two most common This is the first study to report comparisons of the preva- high-risk genotypes and are reported to account for lence of cervical HPV infections and the specific HPV gen- almost 70% of cervical cancers worldwide [10]. We otypes between cancer-free Caribbean and US women. We observed that HPV 16 and 18 infections are not seen in have shown that the age-adjusted prevalence rate of any high proportions among cancer-free Caribbean women. HPV infection was higher in the Caribbean women (47%) However, Caribbean women still have a higher propor- than in women from the United States (39%), although tion of HPV 16 and 18 infections compared to their US the age-adjusted prevalence of high-risk HPV infections counterparts (HPV 16: 13% vs. 7%, and HPV 18: 14% vs. (Caribbean 27%, US 25%) was similar in both popula- 7%). These observed differences between the US and Car- Table 3: Characteristics of HPV infections according to ethnicity. Tobago N N (%) Jamaica N (%) US-Black N (%) US-White N (%) US-other N (%) Total N (%) Number of subjects 212 99 10 67 11 393 High-risk HPV infection 43 (20.3) 58 (58.6) 4 (40.0) 9 (14.5) 1 (10.0) 115 (29.3) Low-risk HPV infection 15 (7.1) 25 (25.3) 4 (40.0) 4 (6.5) 1 (10.0) 49 (12.5) Undetermined-risk infection 16 (7.6) 47 (47.5) 5 (50.0) 5 (8.1) 1 (10.0) 74 (18.3) Single high-risk infection* 49 (23.1) 40 (40.4) 5 (50.0) 10 (16.1) 1 (10.0) 105 (26.7) Multiple high-risk infection 26 (12.3) 43 (43.4) 3 (30.0) 5 (8.1) 1 (10.0) 78 (19.9) Number of high-risk HPV types per subject None** 169 (79.7) 41 (41.4) 6 (60.0) 53 (85.5) 9 (90.0) 278 (70.7) 1 33 (15.6) 34 (34.3) 3 (30.0) 7 (11.3) 1 (10.0) 78 (19.9) 2 7 (3.3) 11 (11.1) 1 (10.0) 2 (3.2) 0 (0.0) 21 (5.3) 3 2 (0.9) 7 (7.1) 0 (0.0) 0 (0.0) 0 (0.0) 9 (2.3) 4 1 (0.5) 2 (2.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (0.8) 5 0 (0.0) 3 (3.0) 0 (0.0) 0 (0.0) 0 (0.0) 3 (0.8) 6 0 (0.0) 1 (1.0) 0 (0.0) 0 (0.0) 0 (0.0) 1 (0.3) *Includes subjects infected with low-risk and undetermined-risk HPV types; **Includes subjects that were HPV-negative or had only low-risk HPV infections. Page 5 of 7 (page number not for citation purposes) Percent Infectious Agents and Cancer 2009, 4(Suppl 1):S9 http://www.infectagentscancer.com/content/4/S1/S9 ibbean may be due to immune resistance to HPV16 and Authors' contributions 18 genotypes in the US population (although we do not CR contributed to study design, sample/data collection have data to support these hypotheses). The evaluation of for Tobago and US populations, performed the data anal- serological status for HPV 16 and 18 and how these com- ysis and wrote the manuscript. JBW performed the sample pare to the prevalence of high-risk HPV infections in both and data collection of the Tobago population. ET, contrib- geographical regions are needed in order to test these uted to the overall study design and the writing of the hypotheses. Nevertheless, the higher incidence of cervical manuscript. AW, contributed to the study design, sample/ cancers in the Caribbean region compared to the US data collection of the Jamaican population and performed might be attributed to the higher proportions of HPV 16 the HPV testing. NM and RE: contributed to study design and 18 infections observed in the Caribbean. of the US population. AP, V W, CB and SMG: contributed to study design and sample/data collection for the Tobago Caribbean and US-Black subjects in comparison with US- population. SE: performed the HPV testing. HF, DG, MJ, Whites have higher prevalence rates of high-risk HPV MS, NY, NMA: contributed to the study design, sample/ infections and also a higher proportion of subjects with data collection of the Jamaican population. All co-authors multiple-high-risk HPV infections. This may be related to reviewed and approved the manuscript. sexual behaviour, social class (poverty and malnutrition), high parity, lack of barrier contraceptive protection and Acknowledgements This work is supported in part by NIH/R13 CA130596A, the UPCI Cancer use of steroidal contraception, [7,12-16]. However, these Education and Career Development grant R25CA089507, and a GLMA confounders could not be assessed in our study because foundation grant. This publication was also made possible by Grant these data were not available. Furthermore, the risk of cer- Number KL2 RR024154-03 to CCR, from the National Center for vical cancer among women with multiple high-risk infec- Research Resources (NCRR) [23], a component of the National Institutes tions has not been well studied; therefore additional of Health (NIH), and NIH Roadmap for Medical Research [24]. Its contents studies are warranted. are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. This publication was also supported by Studies show that younger age is associated with an funds received from the NIH/NCRR GCRC Grant MO1-RR000056 and/or the CTSA Grant 1 UL 1 RR024153-01. The authors wish to thank the increased risk of cervical HPV infection [17-20]. There- Tobago Branch of the Trinidad & Tobago Cancer Society for providing the fore, for comparisons of HPV infections between different facilities for subject recruitment and sample collection for the Tobago sub- populations, age must be standardized. A limitation in jects. our study is that although all subjects were recruited from the general population, the mean age for each country was This article has been published as part of Infectious Agents and Cancer. Vol- different. Pittsburgh subjects were the oldest (mean age = ume 4 Supplement 1, 2009: Second Annual International African-Caribbean 53 ± 9.0 years), and this was representative of the older Cancer Consortium Conference. The full contents of the supplement are population in the geographical region [21]. Jamaican available online at http://www.infectagentscancer.com/4/supplements/4/S1. women were the youngest population, also reflecting the References demographics for the country [22]. To address this limita- 1. Ries LAG, Melbert D, Krapcho M, Mariotto A, Miller BA, Feuer EJ, et tion, we have presented age-adjusted prevalence rates so al.: SEER Cancer Statistics Review, 1975–2004 National Cancer Institute. that these values might be compared. Another limitation Bethesda, MD; 2007. 2. 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Pennsylvania Department of Health Annual Report of Vital Statistics, Pennsylvania Vital Statistics 2006 [http:// www.dsf.health.state.pa.us/health/cwp/view.asp?a=175&q=250106] 22. U.S.Census Bureau, Population Division/International Pro- grams Center, International Database Summary Demo- graphic Data [http://www.census.gov/ipc/www/idb/] 23. National Institutes of Health, National Institutes of Health, National Center for Research Resources [http:// www.ncrr.nih.gov/] 24. NIH Roadmap for Medical Research, NIH Roadmap for Med- ical Research, Re-engineering the Clinical Research Enter- prise [http://nihroadmap.nih.gov/clinicalresearch/overview- translational.asp] Publish with Bio Med Central and every scientist can read your work free of charge "BioMed Central will be the most significant development for disseminating the results of biomedical researc h in our lifetime." 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