A longitudinal study of human papillomavirus 16 L1, E6, and E7 seropositivity and oral human papillomavirus 16 infection

Daniel C. Beachler, Raphael Viscidi, Elizabeth A. Sugar, Howard Minkoff, Howard Strickler, Ross D. Cranston, Dorothy J. Wiley, Lisa P. Jacobson, Kathleen M. Weber, Joseph B. Margolick, Susheel Reddy, Maura L. Gillison, Gypsyamber D'Souza

Research output: Contribution to journalArticle

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Abstract

Individuals with human papillomavirus (HPV) infections can develop IgG antibodies to HPV proteins including the L1 capsid and E6 and E7 oncoproteins. Evidence on whether L1 antibodies reduce the risk of cervical HPV infection is mixed, but this has not been explored for oral HPV infections. Antibodies to HPV16's E6 oncoprotein have been detected in some oropharyngeal cancer cases years before cancer diagnosis, but it is unknown if these antibodies are associated with oral HPV16 DNA. METHODS: Enzyme-linked immunosorbent assays tested for serum antibodies to HPV16's L1 capsid in 463 HIV-infected and 293 HIV-uninfected adults, and for antibodies to recombinantly expressed E6 and E7 oncoproteins to HPV16 in 195 HIV-infected and 69 HIV-uninfected cancer-free participants at baseline. Oral rinse samples were collected semiannually for up to 3 years and tested for HPV DNA using PGMY 09/11 primers. Adjusted Poisson, logistic, and Wei-Lin-Weissfeld regression models were used. RESULTS: Human papillomavirus 16 L1 seroreactivity did not reduce the subsequent risk of incident oral HPV16 infection in unadjusted (hazard ratio, 1.4; 95% confidence interval, 0.59-3.3) or adjusted (adjusted hazard ratio = 1.1; 95% confidence interval, 0.41-3.0) analysis. Antibodies to HPV16 E6 and E7 oncoproteins were detected in 7.6% and 3.4% of participants, respectively, but they were not associated with baseline oral HPV16 DNA prevalence or oral HPV16 persistence (each P > 0.40). CONCLUSIONS: Naturally acquired HPV16 L1 antibodies did not reduce the risk of subsequent oral HPV16 infection. Human papillomavirus 16 E6 and E7 seropositivity was not a marker for oral HPV16 infection in this population without HPV-related cancer.

Original languageEnglish (US)
Pages (from-to)93-97
Number of pages5
JournalSexually Transmitted Diseases
Volume42
Issue number2
DOIs
StatePublished - Feb 2 2015

Fingerprint

Papillomavirus Infections
Human papillomavirus 16
Longitudinal Studies
Antibodies
Oncogene Proteins
HIV
Capsid
DNA
Infection
Confidence Intervals
Oropharyngeal Neoplasms
Neoplasms
Immunoglobulin G
Enzyme-Linked Immunosorbent Assay
Serum

ASJC Scopus subject areas

  • Dermatology
  • Public Health, Environmental and Occupational Health
  • Microbiology (medical)
  • Infectious Diseases

Cite this

A longitudinal study of human papillomavirus 16 L1, E6, and E7 seropositivity and oral human papillomavirus 16 infection. / Beachler, Daniel C.; Viscidi, Raphael; Sugar, Elizabeth A.; Minkoff, Howard; Strickler, Howard; Cranston, Ross D.; Wiley, Dorothy J.; Jacobson, Lisa P.; Weber, Kathleen M.; Margolick, Joseph B.; Reddy, Susheel; Gillison, Maura L.; D'Souza, Gypsyamber.

In: Sexually Transmitted Diseases, Vol. 42, No. 2, 02.02.2015, p. 93-97.

Research output: Contribution to journalArticle

Beachler, DC, Viscidi, R, Sugar, EA, Minkoff, H, Strickler, H, Cranston, RD, Wiley, DJ, Jacobson, LP, Weber, KM, Margolick, JB, Reddy, S, Gillison, ML & D'Souza, G 2015, 'A longitudinal study of human papillomavirus 16 L1, E6, and E7 seropositivity and oral human papillomavirus 16 infection', Sexually Transmitted Diseases, vol. 42, no. 2, pp. 93-97. https://doi.org/10.1097/OLQ.0000000000000236
Beachler, Daniel C. ; Viscidi, Raphael ; Sugar, Elizabeth A. ; Minkoff, Howard ; Strickler, Howard ; Cranston, Ross D. ; Wiley, Dorothy J. ; Jacobson, Lisa P. ; Weber, Kathleen M. ; Margolick, Joseph B. ; Reddy, Susheel ; Gillison, Maura L. ; D'Souza, Gypsyamber. / A longitudinal study of human papillomavirus 16 L1, E6, and E7 seropositivity and oral human papillomavirus 16 infection. In: Sexually Transmitted Diseases. 2015 ; Vol. 42, No. 2. pp. 93-97.
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abstract = "Individuals with human papillomavirus (HPV) infections can develop IgG antibodies to HPV proteins including the L1 capsid and E6 and E7 oncoproteins. Evidence on whether L1 antibodies reduce the risk of cervical HPV infection is mixed, but this has not been explored for oral HPV infections. Antibodies to HPV16's E6 oncoprotein have been detected in some oropharyngeal cancer cases years before cancer diagnosis, but it is unknown if these antibodies are associated with oral HPV16 DNA. METHODS: Enzyme-linked immunosorbent assays tested for serum antibodies to HPV16's L1 capsid in 463 HIV-infected and 293 HIV-uninfected adults, and for antibodies to recombinantly expressed E6 and E7 oncoproteins to HPV16 in 195 HIV-infected and 69 HIV-uninfected cancer-free participants at baseline. Oral rinse samples were collected semiannually for up to 3 years and tested for HPV DNA using PGMY 09/11 primers. Adjusted Poisson, logistic, and Wei-Lin-Weissfeld regression models were used. RESULTS: Human papillomavirus 16 L1 seroreactivity did not reduce the subsequent risk of incident oral HPV16 infection in unadjusted (hazard ratio, 1.4; 95{\%} confidence interval, 0.59-3.3) or adjusted (adjusted hazard ratio = 1.1; 95{\%} confidence interval, 0.41-3.0) analysis. Antibodies to HPV16 E6 and E7 oncoproteins were detected in 7.6{\%} and 3.4{\%} of participants, respectively, but they were not associated with baseline oral HPV16 DNA prevalence or oral HPV16 persistence (each P > 0.40). CONCLUSIONS: Naturally acquired HPV16 L1 antibodies did not reduce the risk of subsequent oral HPV16 infection. Human papillomavirus 16 E6 and E7 seropositivity was not a marker for oral HPV16 infection in this population without HPV-related cancer.",
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AU - Minkoff, Howard

AU - Strickler, Howard

AU - Cranston, Ross D.

AU - Wiley, Dorothy J.

AU - Jacobson, Lisa P.

AU - Weber, Kathleen M.

AU - Margolick, Joseph B.

AU - Reddy, Susheel

AU - Gillison, Maura L.

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N2 - Individuals with human papillomavirus (HPV) infections can develop IgG antibodies to HPV proteins including the L1 capsid and E6 and E7 oncoproteins. Evidence on whether L1 antibodies reduce the risk of cervical HPV infection is mixed, but this has not been explored for oral HPV infections. Antibodies to HPV16's E6 oncoprotein have been detected in some oropharyngeal cancer cases years before cancer diagnosis, but it is unknown if these antibodies are associated with oral HPV16 DNA. METHODS: Enzyme-linked immunosorbent assays tested for serum antibodies to HPV16's L1 capsid in 463 HIV-infected and 293 HIV-uninfected adults, and for antibodies to recombinantly expressed E6 and E7 oncoproteins to HPV16 in 195 HIV-infected and 69 HIV-uninfected cancer-free participants at baseline. Oral rinse samples were collected semiannually for up to 3 years and tested for HPV DNA using PGMY 09/11 primers. Adjusted Poisson, logistic, and Wei-Lin-Weissfeld regression models were used. RESULTS: Human papillomavirus 16 L1 seroreactivity did not reduce the subsequent risk of incident oral HPV16 infection in unadjusted (hazard ratio, 1.4; 95% confidence interval, 0.59-3.3) or adjusted (adjusted hazard ratio = 1.1; 95% confidence interval, 0.41-3.0) analysis. Antibodies to HPV16 E6 and E7 oncoproteins were detected in 7.6% and 3.4% of participants, respectively, but they were not associated with baseline oral HPV16 DNA prevalence or oral HPV16 persistence (each P > 0.40). CONCLUSIONS: Naturally acquired HPV16 L1 antibodies did not reduce the risk of subsequent oral HPV16 infection. Human papillomavirus 16 E6 and E7 seropositivity was not a marker for oral HPV16 infection in this population without HPV-related cancer.

AB - Individuals with human papillomavirus (HPV) infections can develop IgG antibodies to HPV proteins including the L1 capsid and E6 and E7 oncoproteins. Evidence on whether L1 antibodies reduce the risk of cervical HPV infection is mixed, but this has not been explored for oral HPV infections. Antibodies to HPV16's E6 oncoprotein have been detected in some oropharyngeal cancer cases years before cancer diagnosis, but it is unknown if these antibodies are associated with oral HPV16 DNA. METHODS: Enzyme-linked immunosorbent assays tested for serum antibodies to HPV16's L1 capsid in 463 HIV-infected and 293 HIV-uninfected adults, and for antibodies to recombinantly expressed E6 and E7 oncoproteins to HPV16 in 195 HIV-infected and 69 HIV-uninfected cancer-free participants at baseline. Oral rinse samples were collected semiannually for up to 3 years and tested for HPV DNA using PGMY 09/11 primers. Adjusted Poisson, logistic, and Wei-Lin-Weissfeld regression models were used. RESULTS: Human papillomavirus 16 L1 seroreactivity did not reduce the subsequent risk of incident oral HPV16 infection in unadjusted (hazard ratio, 1.4; 95% confidence interval, 0.59-3.3) or adjusted (adjusted hazard ratio = 1.1; 95% confidence interval, 0.41-3.0) analysis. Antibodies to HPV16 E6 and E7 oncoproteins were detected in 7.6% and 3.4% of participants, respectively, but they were not associated with baseline oral HPV16 DNA prevalence or oral HPV16 persistence (each P > 0.40). CONCLUSIONS: Naturally acquired HPV16 L1 antibodies did not reduce the risk of subsequent oral HPV16 infection. Human papillomavirus 16 E6 and E7 seropositivity was not a marker for oral HPV16 infection in this population without HPV-related cancer.

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