A few recent studies have suggested that other sexually transmitted infections may increase the likelihood of a human papillomavirus (HPV) infection progressing to high-grade cervical neoplasia and cancer.
The goal was to assess whether exposures to Chlamydia trachomatis, human T-cell lymphotrophic virus type 1 (HTLV-I), and/or human simplex virus type 2 (HSV-2) are greater in colposcopy patients with cervical intraepithelial neoplasia grade 3 or cancer (CIN3+) than in patients with low-grade cervical neoplasia (CIN1).
Sequential patients (n = 447) attending a colposcopy clinic in Kingston, Jamaica, a country with high cervical cancer rates and high HTLV-I prevalence, were tested for (1) HPV DNA by L1 consensus primer (MY09/11) polymerase chain reaction assays, (2) C trachomatis DNA by ligase chain reaction, (3) C trachomatis antibodies by both microimmunofluorescence and a peptide (VS4) enzyme linked immunosorbent assay (ELISA), (4) HTLV-I antibodies by ELISA confirmed by western blotting, and (5) HSV-2 antibodies by a recombinant HSV-2-specific ELISA. Odds ratios and 95% confidence intervals were estimated with use of multinomial logistic regression models.
HPV DNA detection was associated with grade of cervical neoplasia but other evaluated sexually transmitted infections were not.
HTLV-I, C trachomatis, and/or HSV-2 were not associated with severity of cervical neoplasia in Jamaican women.
Seroprevalence of C trachomatis, HSV-2, or HTLV-I was not associated with grade of cervical intraepithelial neoplasia among women attending a colposcopy clinic in Kingston, Jamaica.
From the *Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland; †University of the West Indies, Kingston, Jamaica; ‡Chlamydia Research Laboratory (Department of Laboratory Medicine) and the §Departments of Laboratory Medicine and Stomatology, University of California San Francisco, San Francisco, California; ∥Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, New York; and ¶Women's and Infants’ Hospital, Providence, Rhode Island
Some of the contents of this article were presented at the 20th International Papillomavirus Conference, in Paris, October 4–9, 2002.
The authors thank Roberta McClimens (IMS) for her role in data management and analysis in this study, Dr. Rhoda Ashley (University of Washington) for HSV-2 serologic testing, and Richard S. Stevens (University of California San Francisco).
Support for this research was provided by the Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute, including support for the collaborating clinical center, University of West Indies, Kingston, Jamaica. Additional support for Philip Castle was provided by a Cancer Prevention Fellowship from the Office of Preventive Oncology, NCI, and support for Howard Strickler was provided by DCEG and the Cancer Center of Albert Einstein College of Medicine (NCI grant number CA13330).
Reprint requests: Philip Castle, PhD, MPH, Division of Cancer Epidemiology and Genetics National Cancer Institute, 6120 Executive Boulevard, MSC 7234, Bethesda, MD 20892. E-mail: email@example.com
Received November 7, 2002,
revised December 31, 2002, and accepted January 28, 2003.