PERSISTENT GENITAL HUMAN PAPILLOMAVIRUS INFECTION AS A RISK FACTOR FOR PERSISTENT CERVICAL DYSPLASIA

Background: Cervical dysplasia, also referred to as squamous intraepit helial lesion (SIL) in cytology or cervical intraepithelial neoplasia in histopathology, is thought to have the potential to advance in prog ressive stages to cervical cancer. However, not all cases of SIL progr ess, and most of the mild lesions spontaneously regress. Factors that govern regression, persistence, and progression of SIL are poorly unde rstood. Purpose: Our analysis sought to identify factors that determin ed persistence or regression of SIL. Methods: Seventy subjects with hi stopathologically confirmed cervical dysplasia were followed at 3-mont h intervals for 15 months. At each visit, the cervix was evaluated by Pap smear and colposcopy, and exfoliated cervicovaginal cells were ana lyzed for human papillomavirus (HPV) DNA. For each subject, data from every two consecutive visits were grouped as a pair. Persistent SIL wa s considered present if a lesion was detected at a visit (t) as well a s at the next visit (t + 1) and absent if a lesion was detected at vis it t but not at visit t + 1. A statistical model for time-dependent da ta correlated persistent SIL with various risk factors. Results: Age, ethnicity, education, sexual behavior, smoking, and the use of oral co ntraceptives did not correlate with persistent SIL. The risk of persis tent SIL was associated with continual HPV infection in visits t and t + 1 (HPV positive by Southern blot analysis: odds ratio [OR] = 3.91, and 95% confidence interval [CI] = 1.58-9.65; HPV positive by polymera se chain reaction [PCR]: OR = 2.42, and 95% CI = 1.03-5.67) and a pers istent high viral load (OR = 4.07, and 95% CI = 1.35-12.30). When type d by PCR, individuals with type-specific persistent infection in visit s t and t + 1, and particularly those with a continual high viral load (OR = 4.97; 95% CI = 1.45-17.02), had the highest risk for persistent SIL compared with those with a low level of type-specific persistent infection or non-type-specific persistent infection. The presence of p ersistent HPV infection in visits t - 1 and t (the preceding time inte rval) was also predictive of persistent SIL in visits t and t + 1, alt hough the strength of association was weaker, suggesting that persiste nt HPV and SIL occur synchronously. Conclusion: HPV infection and its associated cervical lesions tend to occur concurrently, and type-speci fic persistent HPV infection, particularly with a high viral load, pro duces chronic cervical dysplasia. Implications: The natural history of genital HPV infection directly influences the prognosis of cervical d ysplasia as measured by persistence of the lesion. Testing for HPV inf ection may be valuable in the clinical management of women with cervic al dysplasia.