Viral polymorphism in human papillomavirus types 33 and 35 and persistent and transient infection in the genital tract of women.

Abstract

Genetic polymorphism in human papillomavirus (HPV)-33 and -35 was investigated in 1055 sexually active women (732 human immunodeficiency virus [HIV] seropositive and 323 HIV seronegative). Consecutive genital specimens obtained at 6-month intervals were screened for HPV-33 and -35 by use of MY09-MY11. HPV-33 and -35 isolates from 95 women were analyzed by polymerase chain reaction sequencing of the long control region (LCR), E6, and E7. For HPV-33, 101 (20%) of 506 nucleotides in the LCR were variable, compared with 10 (2.1%) of 483 nucleotides in E6 (P<.001) and 6 (1.9%) of 324 nucleotides in E7 (P<.001). For HPV-35, the proportion of variable nucleotide sites was similar between the LCR and both E6 (P=.54) and E7 (P=.33). The presence of a 78-base pair deletion in HPV-33 (relative risk [RR], 1.8 [95% confidence interval [CI], 1.2-2.7]) and the presence of nonsynonymous E7 variations in HPV-35 (RR, 2.6 [95% CI, 1.4-4.6]) were associated with persistence. When the data for HPV-33 and -35 were combined, infection by HPV isolates with nonsynonymous E7 variations (RR, 2.3 [95% CI, 1.6-3.4]; P=.001) and ethnicity (P=.04) were associated with persistence, whereas age (P = .14) and HIV infection/CD4 cell count status (P=.12) were not significantly associated with persistence, by logistic regression analysis. HPV-33 and -35 polymorphism was different between types and was associated with persistence of HPV infection.