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.

A human papillomavirus (HPV) type 16 virus-like particle-based ELISA was used to assess antivirion immune responses in 300 women participating in cervical cancer case-control studies in Colombia and Spain. Virion IgG antibodies were detected in the sera of 51% and 59% of women with HPV-16 DNA-positive invasive cervical cancer and 81% and 73% of women with HPV-16 DNA-positive cervical intraepithelial neoplasia grade III (CIN III) in Colombia and Spain, respectively. Capsid antibodies were detected in 22% and 3% of cancer controls (P < .001) and in 43% and 10% of CIN III controls (P = .010) from Colombia and Spain, respectively. Since Colombia has an 8-fold higher incidence of cervical cancer, these results demonstrate an association between ELISA positivity and cancer risk. Capsid antibody responses did not correlate with humoral responses of the same women to HPV-16 E6 and E7 oncoproteins.

[1]  D. Lowy,et al.  A virus-like particle enzyme-linked immunosorbent assay detects serum antibodies in a majority of women infected with human papillomavirus type 16. , 1994, Journal of the National Cancer Institute.

[2]  B. McKnight,et al.  Use of HPV 1 capsids produced by recombinant vaccinia viruses in an ELISA to detect serum antibodies in people with foot warts. , 1994, Virology.

[3]  F. X. Bosch,et al.  Sexually transmitted agents and cervical neoplasia in colombia and Spain , 1994, International journal of cancer.

[4]  T. Iftner,et al.  The predominant mRNA class in HPV16‐infected genital neoplasias does not encode the e6 or the E7 protein , 1993, International journal of cancer.

[5]  B. Dawson-Saunders,et al.  Basic and Clinical Biostatistics , 1993 .

[6]  F. X. Bosch,et al.  Human papillomavirus and cervical intraepithelial neoplasia grade III/carcinoma in situ: a case-control study in Spain and Colombia. , 1993, Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology.

[7]  S Wacholder,et al.  Epidemiologic evidence showing that human papillomavirus infection causes most cervical intraepithelial neoplasia. , 1993, Journal of the National Cancer Institute.

[8]  R. Garcea,et al.  Expression of human papillomavirus type 11 L1 protein in insect cells: in vivo and in vitro assembly of viruslike particles , 1993, Journal of virology.

[9]  J. Kaldor,et al.  Risk factors for cervical cancer in Colombia and Spain , 1992, International journal of cancer.

[10]  J. Kaldor,et al.  The causal link between human papillomavirus and invasive cervical cancer: A population‐based case‐control study in colombia and spain , 1992, International journal of cancer.

[11]  F. X. Bosch,et al.  Comparison of ViraPap, Southern hybridization, and polymerase chain reaction methods for human papillomavirus identification in an epidemiological investigation of cervical cancer , 1992, Journal of clinical microbiology.

[12]  K. Holmes,et al.  A cohort study of the risk of cervical intraepithelial neoplasia grade 2 or 3 in relation to papillomavirus infection , 1992, The New England journal of medicine.

[13]  H. zur Hausen,et al.  Human papillomavirus type 16 (HPV 16) gene expression and DNA replication in cervical neoplasia: analysis by in situ hybridization. , 1992, Virology.

[14]  R Reid,et al.  Human papillomavirus infection of the cervix: relative risk associations of 15 common anogenital types. , 1992, Obstetrics and gynecology.

[15]  Steven Wolinsky,et al.  Human papillomavirus type 16 and 18 gene expression in cervical neoplasias. , 1992, Human pathology.

[16]  D. Lowy,et al.  The full-length E6 protein of human papillomavirus type 16 has transforming and trans-activating activities and cooperates with E7 to immortalize keratinocytes in culture , 1991, Journal of virology.

[17]  D. McCance,et al.  Immortalization and altered differentiation of human keratinocytes in vitro by the E6 and E7 open reading frames of human papillomavirus type 18 , 1990, Journal of virology.

[18]  R. Schlegel,et al.  The E6 and E7 genes of the human papillomavirus type 16 together are necessary and sufficient for transformation of primary human keratinocytes , 1989, Journal of virology.

[19]  D. Lowy,et al.  The E7 open reading frame of human papillomavirus type 16 encodes a transforming gene. , 1988, Oncogene research.

[20]  K. Münger,et al.  The human papillomavirus type 16 E7 gene encodes transactivation and transformation functions similar to those of adenovirus E1A , 1988, Cell.

[21]  A. Schneider-Gädicke,et al.  Different human cervical carcinoma cell lines show similar transcription patterns of human papillomavirus type 18 early genes. , 1986, The EMBO journal.

[22]  F. Wettstein,et al.  Transcription of human papillomavirus type 16 early genes in a cervical cancer and a cancer-derived cell line and identification of the E7 protein. , 1986, Proceedings of the National Academy of Sciences of the United States of America.

[23]  Galloway Da.  Serological assays for the detection of HPV antibodies. , 1992 .