Serum Immunoglobulin G Response to Human Papillomavirus Type 16 Virus‐Like Particles in Human Immunodeficiency Virus (HIV)–Positive and Risk‐Matched HIV‐Negative Women

Viscidi, Raphael P.; Ahdieh‐Grant, Linda; Clayman, Barbara; Fox, Kelly; Massad, L. Stewart; Cu‐Uvin, Susan; Shah, Keerti V.; Anastos, Kathryn; Squires, Kathleen; Duerr, Ann; Jamieson, Denise J.; Burk, Robert D.; Klein, Robert S.; Minkoff, Howard; Palefsky, Joel M.; Strickler, Howard D.; Schuman, Paula; Piessens, Eva; Miotti, Paolo

doi:10.1086/346052

Cited by 52 publications

(38 citation statements)

References 33 publications

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“…HPV-16, HPV-18, and HPV-33 immunoglobulin G antibody serostatus were assessed by three in-house ELISAs in the laboratory of Dr. Raphael P. Viscidi (31). These assays detect immunoglobulin G antibodies against HPV-16, HPV-18, and HPV-33 virus-like particles, respectively.…”

Section: Methodsmentioning

confidence: 99%

Plasma Antibodies against Chlamydia trachomatis, Human Papillomavirus, and Human Herpesvirus Type 8 in Relation to Prostate Cancer: A Prospective Study

Sutcliffe

Giovannucci

Gaydos

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Traditionally, case-control studies of sexually transmitted infections and prostate cancer have focused on gonorrhea and syphilis, with overall positive associations. More recently, researchers have begun to expand their focus to include additional sexually transmitted infections, such as Chlamydia trachomatis, human papillomavirus (HPV), and human herpesvirus type 8 (HHV-8) infections. Continuing this investigation, we examined each of these infections in relation to incident prostate cancer in a nested case-control study within the Health Professionals Follow-up Study. Prostate cancer cases were men diagnosed with prostate cancer between the date of blood draw (1993)(1994)(1995) and 2000 (n = 691). Controls were men free of cancer and alive at the time of case diagnosis who had had at least one prostatespecific antigen test between the date of blood draw and case diagnosis. One control was individually matched to each case by age; year, time of day, and season of blood draw; and prostate-specific antigen screening history before blood draw (n = 691). C. trachomatis and HPV-16, HPV-18, and HPV-33 antibody serostatus were assessed by enzyme-based immunoassays and HHV-8 antibody serostatus was assessed by an immunofluorescence assay. No associations were observed between C. trachomatis [odds ratio (OR), 1.13; 95% confidence interval (95% CI), 0.65-1.96], HPV-16 (OR, 0.83; 95% CI, 0.57-1.23), HPV-18 (OR, 1.04; 95% CI, 0.66-1.64), and HPV-33 (OR, 1.14; 95% CI, 0.76-1.72) antibody seropositivity and prostate cancer. A significant inverse association was observed between HHV-8 antibody seropositivity and prostate cancer (OR, 0.70; 95% CI, 0.52-0.95). As this study is the first, to our knowledge, to observe such an inverse association, similar additional studies are warranted. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1573 -80)

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Section: Methodsmentioning

confidence: 99%

Plasma Antibodies against Chlamydia trachomatis, Human Papillomavirus, and Human Herpesvirus Type 8 in Relation to Prostate Cancer: A Prospective Study

Sutcliffe

Giovannucci

Gaydos

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Virus-like particles were purified from cell pellets by density-gradient ultracentrifugation and column chromatography techniques as described previously (Studentsov et al, 2002;Viscidi et al, 2003). For the VLP-based ELISA, 96-well flat bottom PolySorp plates (Nunc, Naperville, IL, USA) were coated overnight at 41C with 0.4 -0.5 mg total VLP protein per millilitre of phosphate-buffered saline (PBS), pH 7.2.…”

Section: Serological Measurementsmentioning

confidence: 99%

Seroprevalence of human papillomavirus-16, -18, -31, and -45 in a population-based cohort of 10 000 women in Costa Rica

et al. 2003

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Human papillomavirus (HPV) seroprevalence and determinants of seropositivity were assessed in a 10 049-woman population-based cohort in Guanacaste, Costa Rica. Serologic responses based on VLP-based ELISA were obtained from the plasma collected at study enrollment in 1993/1994 for HPV-16 (n ¼ 9949), HPV-18 (n ¼ 9928), HPV-31 (n ¼ 9932), and HPV-45 (n ¼ 3019). Seropositivity was defined as five standard deviations above the mean optical density obtained for studied virgins (n ¼ 573). 15, 16, and 11%, respectively. Of women DNA-positive for , seropositivity was 45, 34, 51, and 28%, respectively. Peak HPV seroprevalence occurred a decade after DNA prevalence; lifetime number of sexual partners was the key determinant of seropositivity independent of DNA status and age. DNA-and sero-positive women showed the highest risk for concurrent CIN3/cancer, followed by DNA-positive, sero-negative women. British Journal of Cancer (2003) (Ho et al, 1995). The prevalence of HPV DNA therefore underestimates the cumulative incidence of infection in a population, particularly where the majority of women will not develop persistent infection or cervical neoplasia. Measurement of serum antibody to HPV capsids (or virus-like particles (VLPs)) has been demonstrated as a useful although imperfect marker of past and cumulative HPV exposure, thus complementing the assessment of HPV DNA (Kirnbauer et al, 1994;Wideroff et al, 1995Wideroff et al, , 1999Carter et al, 1996;Sasagawa et al, 1998;Touze et al, 2001).As part of a large population-based study of the natural history of HPV infection and cervical neoplasia in Guanacaste, Costa Rica, we report here the population-based seroprevalence in Guanacaste women of four oncogenic HPV types found in the majority of cervical cancers worldwide Munoz et al, 2003). The data presented document the baseline burden of HPV exposure in Guanacaste, Costa Rica. As a major objective, we determined the association of risk for concurrent diagnosis of CIN3/cancer with HPV assessed jointly by serology and PCR-based DNA testing. As only about half of all HPV-DNA-positive women are seropositive using available VLP assays (Kirnbauer et al, 1994;Le Cann et al, 1995), we also investigated determinants of seropositivity in our population. METHODS Study populationThis study was conducted in an on-going population-based cohort study of 10 049 women in Guanacaste, Costa Rica (Herrero et al, 1997;Hildesheim et al, 2001) who were enrolled in 1993 -1994 with the approval of the National Cancer Institute (NCI) and local institutional review boards; all participants provided written informed consent. Briefly, the cohort was a representative sample of the adult population based on selection by cluster sampling, with oversampling for cancer. Participation among eligible women exceeded 90%, and participants completed a risk factor questionnaire that addressed demographic, behavioural, and sexual practices. Women were screened using three cytologic and one visual test at enrollment; colposcopy referral with biopsy was perform...

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“…Plasma samples were tested for antibodies against HPV16 VLPs by ELISA 18 and results were dichotomized as seropositive or seronegative as described previously. 1 …”

Section: Detection Of Antibodies Against Hpv16 Vlpsmentioning

confidence: 99%

HPV16 semiquantitative viral load and serologic biomarkers in oral and oropharyngeal squamous cell carcinomas

Kreimer

Clifford

Snijders

et al. 2005

Intl Journal of Cancer

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A considerable subset of oropharyngeal squamous cell carcinomas (SCCs) are positive for human papillomavirus (HPV); however, delineating etiologically-associated HPV infections from SCCs with concurrent HPV infection unrelated to tumorigenesis is challenging. Viral load assessment in biopsy specimens may help facilitate such differentiation. HPV16 viral load and serologic markers were assessed among oral and oropharyngeal cases from a multinational study conducted by the International Agency for Research on Cancer (IARC). HPV16 viral load, measured semiquantitatively by PCR-enzyme immunoassay, was dichotomized as high or low based on the median optical density value. Serologic antibodies to HPV16 virus-like particles (VLPs) and to HPV16 E6 and E7 proteins were measured by ELISA. Compared to HPV DNA-negative cases (n = 852), HPV16 DNA-positive cases with high viral load (n = 26) were significantly more likely to originate in the oropharynx (odds ratio [OR], 12.0; 95% confidence interval [CI], 5.2-27.5) and, after adjustment for tumor site (AdjOR), have antibodies against HPV16 VLPs (AdjOR, 14.6; 95% CI, 6.0-35.6), E6 (AdjOR, 57.6; 95% CI, 21.4-155.3) and E7 (AdjOR, 25.6; 95% CI, 9.3-70.8). HPV16 DNA-positive cases with low viral load (n = 27) were more commonly oropharyngeal (OR, 2.7; 95% CI, 1.1-6.2) and seropositive for HPV16 VLPs (AdjOR, 2.7; 95% CI, 1.1-6.9), E6 (AdjOR, 3.0; 95% CI, 0.7-14.0) and E7 (AdjOR, 3.5; 95% CI, 0.7-16.3), compared to HPV DNA-negative cases; the associations, however, were neither as strong nor as significant as the associations for high viral load. As there appears to be a strong association between HPV16 serologic markers and viral load, in the absence of data on serologic markers, HPV16 viral load may be used to help delineate the subset of HPV16 DNA-positive oral and oropharyngeal cancers that may be the consequence of HPV infection. ' 2005 Wiley-Liss, Inc.Key words: human papillomavirus; HPV16 viral load; oral cancer; oropharyngeal cancer Numerous studies have provided consistent evidence that human papillomavirus (HPV), the necessary cause of cervical cancer, is present in tumor biopsies from approximately 20-50% of oropharyngeal squamous cell carcinomas (SCCs) and a smaller subset of oral SCCs. 1-4 Among HPV DNA-positive oropharyngeal SCCs, 90% are positive for HPV16. 1-4 Nonetheless, HPV DNA detection in tumor biopsies may not be sufficient evidence of causation. HPV16 DNA from tumor specimens analyzed jointly with markers of expression of the viral oncogene E6, mutational patterns of the cancer suppressor gene TP53 and levels of allelic loss, have helped identify a subset of these cancers that may be the consequence of HPV infection. 1,2,[5][6][7][8] HPV viral load, a measure of the amount of viral DNA in biopsy specimens, alone or in conjunction with well-characterized HPV serologic assays, may clarify the role of HPV among oral and oropharyngeal cases. Antibodies against HPV E6 and E7 are markers of an invasive HPV-associated malignancy 9,10 and are rarely present among ind...

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Serum Immunoglobulin G Response to Human Papillomavirus Type 16 Virus‐Like Particles in Human Immunodeficiency Virus (HIV)–Positive and Risk‐Matched HIV‐Negative Women

Cited by 52 publications

References 33 publications

Plasma Antibodies against Chlamydia trachomatis, Human Papillomavirus, and Human Herpesvirus Type 8 in Relation to Prostate Cancer: A Prospective Study

Plasma Antibodies against Chlamydia trachomatis, Human Papillomavirus, and Human Herpesvirus Type 8 in Relation to Prostate Cancer: A Prospective Study

Seroprevalence of human papillomavirus-16, -18, -31, and -45 in a population-based cohort of 10 000 women in Costa Rica

HPV16 semiquantitative viral load and serologic biomarkers in oral and oropharyngeal squamous cell carcinomas

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