Human Papillomavirus Type 16 and Immune Status in Human Immunodeficiency Virus-Seropositive Women

Strickler, Howard D.; Palefsky, Joel M.; Shah, Keerti V.; Anastos, Kathryn; Klein, Robert S.; Minkoff, Howard; Duerr, Ann; Massad, L. Stewart; Celentano, David D.; Hall, Charles B.; Fazzari, Melissa; Cu‐Uvin, Susan; Bacon, Melanie C.; Schuman, Paula; Levine, Alexandra M.; Durante, Amanda J.; Gange, Stephen J.; Melnick, Sandra; Burk, Robert D.

doi:10.1093/jnci/95.14.1062

Cited by 204 publications

(209 citation statements)

References 28 publications

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“…In particular, a meta-analysis of studies from around the world found that HPV 16 was significantly less prevalent in high grade squamous intraepithelial lesions (HSILs) from HIVseropositive women than in the general female population, 2 and two large, independent cohorts found that the prevalence of HPV 16 was more weakly associated with CD41 T-cell count than the prevalence of any other HPV type. 3 HPV 16's relative independence from immune status in these studies has been interpreted as evidence that HPV 16 may be innately better than other HPV types at avoiding the effects of immune surveillance and, thereby, less affected by changes in immune status.…”

Section: Dear Sirmentioning

confidence: 83%

HPV types present in invasive cervical cancers of HIV‐seropositive women

Strickler

Palefsky

Burk

2008

Intl Journal of Cancer

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A recent report by De Vuyst et al. 1 found that the prevalence of human papillomavirus (HPV) 16, the most important oncogenic HPV type, was similar in cervical cancer specimens obtained from HIV-seropositive and HIV-seronegative women in Kenya (41 and 44%, respectively). These data are important, since they suggest that current HPV vaccines containing HPV 16 and 18 (if effective in HIV-seropositive patients) have the potential to prevent many cancers in this and similar settings.The findings were also something of a surprise. Prior reports had led to predictions that HPV 16 would be under-represented (and other oncogenic HPV types overrepresented) in cervical cancer specimens among HIVseropositive compared with HIV-seronegative women. In particular, a meta-analysis of studies from around the world found that HPV 16 was significantly less prevalent in high grade squamous intraepithelial lesions (HSILs) from HIVseropositive women than in the general female population, 2 and two large, independent cohorts found that the prevalence of HPV 16 was more weakly associated with CD41 T-cell count than the prevalence of any other HPV type. 3 HPV 16's relative independence from immune status in these studies has been interpreted as evidence that HPV 16 may be innately better than other HPV types at avoiding the effects of immune surveillance and, thereby, less affected by changes in immune status.The disconnect between these prior reports and the study in Kenya can have several possible explanations, including: (i) The prior data showing a weak association of HPV 16 with host immune status were incorrect; (ii) The HPV 16-immune status association is (as reported) weak during the early stages of cervical tumorigenesis. However, it is the accumulation of relevant genetic mutations that is most important in the etiopathogenesis of frank carcinoma; (iii) The differences in HPV natural history between HIV-seropositive and HIV-seronegative women is not as strong in Kenya as it is in Europe and North America.The latter explanation may be the most likely (and most intriguing). Micronutrient deficiencies and chronic infections, especially helminthic infections, are common in many developing economic settings, and can create a relative immunosuppressive state. 4 This might make HIV-seronegative women less immunologically distinct from HIV-seropositive women, and could, in theory, contribute to the high cervical cancer rates common in such settings. The authors, in fact, correctly point out that studies in Africa have often found weaker associations between cervical cancer and HIV/AIDS than have been reported in Europe and North America.It is also possible, however, that technical issues have led to underestimation of the effects of HIV/AIDS on risk of cervical cancer in Africa. The only truly population-based study (e.g., involving linkage between a cancer registry and AIDS registry; similar to those conducted in the US 5,6 ) found a significant association between HIV/AIDS and risk of cervical cancer in Uganda. 7 Moreover, De Vuyst ...

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Section: Dear Sirmentioning

confidence: 83%

HPV types present in invasive cervical cancers of HIV‐seropositive women

Strickler

Palefsky

Burk

2008

Intl Journal of Cancer

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“…8,9 This data is also consistent with prior longitudinal studies that attributed the elevated prevalence of cervical HPV infection among HIV-infected women to both an increased risk of incident and persistent infection as severity of immunosuppression increased. 10,[18][19][20][21][22][23][24][25] Strickler and colleagues recently reported a strong interaction between serum HIV viral load and CD4 cell count on cervical HPV natural history in the WIHS study cohort. 24 Because of sample size constraints, a larger study will be needed to evaluate the interaction of HIV viral load and CD4 cell count on oral HPV natural history.…”

Section: Discussionmentioning

confidence: 99%

Six‐month natural history of oral versus cervical human papillomavirus infection

D’Souza

Fakhry

Sugar

et al. 2007

Intl Journal of Cancer

157

138

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Human papillomavirus (HPV) infection is etiologically associated with a subset of oral cancers, and yet, the natural history of oral HPV infection remains unexplored. The feasibility of studying oral HPV natural history was evaluated by collecting oral rinse samples on 2 occasions at a 6-month interval from 136 HIV-positive and 63 HIV-negative participants. Cervical vaginal lavage samples were concurrently collected for comparison. HPV genomic DNA was detected in oral and cervical samples by consensus primer PCR and type-specified for 37 HPV types. The sixmonth cumulative prevalence of oral HPV infection was significantly less than for cervical infection (p < 0.0001). HIV-positive women were more likely than HIV-negative women to have an oral (33 vs. 15%, p 5 0.016) or cervical (78 vs. 51%, p < 0.001) infection detected. Oral HPV infections detected at baseline were as likely as cervical infections to persist to 6 months among HIVnegative (60% vs. 51%, p 5 0.70) and HIV-positive (55% vs. 63%, p 5 0.27) women. Factors that independently elevated odds for oral HPV persistence differed from cervical infection and included current smoking (OR 5 8, 95% CI 5 1.3-53), age above 44 years (OR 5 20, 95% CI 5 4.1-83), CD4 < 500 (OR 5 6, 95% CI 5 1.1-26), use of HAART therapy (OR 5 12, 95% CI 5 1.0-156), and time on HAART therapy (trend p 5 0.04). The rate of oral HPV infections newly detected at follow-up was significantly lower than cervical infection among HIV-positive (p < 0.001) and HIV-negative women (p < 0.001). Our study not only demonstrates that it is feasible to study the natural history of oral HPV infection with oral rinse sampling, but also indicates that oral and cervical HPV natural history may differ. ' 2007 Wiley-Liss, Inc.Key words: oral; HPV; natural history; comparison; cervical; human papillomavirus; infectionThe majority of oral cancers are attributable to alcohol and tobacco use, however a subset are etiologically associated with human papillomavirus (HPV) infection.1 Case-control studies have shown that oral HPV infection elevates risk of oral cancer, 2,3 and therefore is likely a prerequisite for cancer development. Although natural history studies of oral infection are yet to be performed, seropositivity to HPV16 increases risk for incident oral cancer, supporting a temporal association between infection and cancer risk. While the natural history of cervical HPV infection is well studied, it is unclear whether it is appropriate to extrapolate data from the cervical literature to oral HPV infection. Unfortunately, 2 studies with consecutive measures of oral HPV infection provide limited insight into its natural history. One study evaluated persistence of oral HPV infection at baseline and a subsequent two and a half year time-point among only 4 subjects. 5 In a study of husband-wife pairs, only overall HPV infection status was considered.6 Because analysis of type-specific HPV infection was not performed, meaningful estimates of incidence and clearance could not be obtained. Our study was designed ...

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“…All subjects provided informed consent and each local institutional review board provided approval for the study. On an ongoing basis, the Women's Interagency HIV Study conducts semiannual study visits during which serum is obtained, and a cervicovaginal lavage specimen is collected for HPV DNA testing followed by a Papanicolaou smear (12)(13)(14). All Papanicolaou smears were interpreted centrally using the 1991 Bethesda System criteria (15).…”

Section: Methodsmentioning

confidence: 99%

Insulin-Like Growth Factor Axis and Oncogenic Human Papillomavirus Natural History

Harris

Burk

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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High serum levels of insulin-like growth factor-I (IGF-I) are reported to be a risk factor for several common cancers, and recent cross-sectional data suggest a possible additional association of IGF-I with cervical neoplasia. To prospectively assess whether circulating IGF-I levels influence the natural history of oncogenic human papillomavirus (HPV), the viral cause of cervical cancer, we conducted a pilot investigation of 137 women who underwent semiannual typespecific HPV DNA PCR testing and cervical cytology. Total IGF-I and IGF binding protein-3 (IGFBP-3), the most abundant IGFBP in circulation, were measured using baseline serum specimens. Having a high IGF-I/ IGFBP-3 ratio was associated with increased persistence of oncogenic HPV infection [that is, a lower rate of clearance; adjusted hazard ratio (AHR), 0.14; 95% confidence interval (95% CI), 0.04-0.57], whereas IGFBP-3 was inversely associated with both the incident detection of oncogenic HPV (AHR, 0.35; 95% CI, 0.13-0.93) and the incidence of oncogenic HPVpositive cervical neoplasia (that is, squamous intraepithelial lesions at risk of progression; AHR, 0.07; 95% CI, 0.01-0.66). These prospective data provide initial evidence that the IGF axis may influence the natural history of oncogenic HPV. (Cancer Epidemiol Biomarkers Prev 2008;17(1):245 -8)

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Human Papillomavirus Type 16 and Immune Status in Human Immunodeficiency Virus-Seropositive Women

Cited by 204 publications

References 28 publications

HPV types present in invasive cervical cancers of HIV‐seropositive women

HPV types present in invasive cervical cancers of HIV‐seropositive women

Six‐month natural history of oral versus cervical human papillomavirus infection

Insulin-Like Growth Factor Axis and Oncogenic Human Papillomavirus Natural History

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