title: Type-specific distribution of HPV along the full spectrum of cervical carcinogenesis in Taiwan: an indication of viral oncogenic potential.
abstract: OBJECTIVE
  The distributional trend of different types of human papillomavirus (HPV) along the spectrum of cervical diseases from non-neoplastic HPV infection (Normal), cervical intraepithelial neoplasia 1 (CIN1), cervical intraepithelial neoplasia 2/3 (CIN2/3) to invasive cancer (CC) reflects the transformation potential of each HPV type.
  
  
  METHODS
  Type-specific distribution of HPV in four hospital- and population-based HPV surveys in Taiwan was analyzed.
  
  
  RESULTS
  Among the 1605 (out of 6356) women positive for HPV, the prevalence of HPV infection in Normal, CIN1, CIN2/3, and CC was 10%, 60%, 70%, and 86%, respectively. The order of type-specific prevalence was HPV 52 (20.9%), HPV 16 (16.9%), HPV 58 (9.0%), and HPV 18 (8.5%) in Normal; HPV 52 (16.5%), HPV 16 (10.2%), HPV 51 (8.4%), and HPV 58 (6.5%) in CIN1; HPV 16 (29.8%), HPV 52 (17.1%), HPV 58 (16.4%), and HPV 33 (10.3%) in CIN2/3; and HPV 16 (50.7%), HPV 18 (11.9%), HPV 58 (10.1%), and HPV 33 (8.4%) in CC. We compared the step-wise distributional changes of five major HPV types along the spectrum of cervical neoplasia. The CIN1 vs. Normal distributional ratio of each HPV type varied from 0.41 to 0.97, indicating a relatively similar chance of giving rise to CIN1. In the CIN2/3 vs. CIN1 and CC vs. CIN2/3 comparisons, the distributional changes varied dramatically among different HPV types. Upon progression to CIN2/3, the distributional proportions of HPV 16, 33, and 58 became 2.1- to 5.4-fold higher, and that of HPV 18 became 0.3- to 0.5-fold lower than their CIN1 and normal counterparts. In the CC vs. CIN2/3 comparison, the change in distributional proportion was highest in HPV 18 (5.7-fold), followed by HPV 16 (1.7-fold), HPV 33 (0.8-fold), HPV 58 (0.6-fold), and HPV 52 (0.18-fold).
  
  
  CONCLUSIONS
  The distribution-defined progression from subclinical infection to CC was highest for HPV 16, followed by HPV 33, 18, 58, and 52. The differential disease progression potential of different HPV types reflects their transformational capability at different steps of cervical carcinogenesis and warrants the clinical attention of HPV infection type specifically.
authors.affiliation: Department of Obstetrics and Gynecology, Buddhist Tzu Chi General Hospital, Tzu Chi University, Hualien, Taiwan.
authors.forename: Dah-Ching
authors.initials: DC
authors.lastname: Ding
authors.forename: Han-Chuan
authors.initials: HC
authors.lastname: Hsu
authors.forename: Rui-Lan
authors.initials: RL
authors.lastname: Huang
authors.forename: Hung-Cheng
authors.initials: HC
authors.lastname: Lai
authors.forename: Ching-Yu
authors.initials: CY
authors.lastname: Lin
authors.forename: Mu-Hsien
authors.initials: MH
authors.lastname: Yu
authors.forename: Tang-Yuan
authors.initials: TY
authors.lastname: Chu
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D052162:Human papillomavirus 16 / Q000235:genetics / Q000472:pathogenicity*; D052161:Human papillomavirus 18 / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D008875:Middle Aged; D030361:Papillomavirus Infections / Q000150:complications*; D013624:Taiwan; D002583:Uterine Cervical Neoplasms / Q000821:virology*; D055815:Young Adult; D002578:Uterine Cervical Dysplasia / Q000821:virology*