Table 5.
Specific application to non-16/18 HPV genotypes in different geographical areas.
| Study | Country | Specific application | Population | HPV testing assay | Distribution of HPV genotypes in descending order | Main findings | Specific application to non-16/18 HPV genotypes in NILM women |
|---|---|---|---|---|---|---|---|
| Khuna-mornpong et al. (78) | Thailand | 16/18+addition | N = 226, age ≥ 25 y, NILM women positive for HPV | HC2 and Linear Array (Roche Molecular System, Inc., Branchburg, NJ, USA) | HPV52 (74, 32.7%), HPV39 (38, 16.8%), HPV68 (25, 11.1%), HPV16 (24, 10.6%), HPV51 (17, 7.5%), HPV56 (17, 7.5%), HPV31 (15, 6.6%), HPV18 (12, 5.3%) | The rate of histologic HSIL+ in each genotype was above 10% for HPV16 (16.7%), HPV31 (13.3%), HPV52 (14.9%), and HPV58 (16.7%) | Addition of genotyping for HPV52/58 or HPV31/52/58 to HPV16/18 in NILM women |
| Stoler et al. (76, 77) | USA | 16/18+addition | N = 22,383, age ≥ 30 y, NILM women | Onclarity (Becton, Dickinson and Company, BD Life Sciences-Diagnostic Systems) | HPV16/18: 423 (1.9%) HPV18/45: 208 (0.9%) HPV16/18/45: 538 (2.4%) | HPV 16, 18, 45, and the other 11 genotypes had CIN3 or higher risks of 6.9, 2.6, 1.1, and 2.2%, respectively | Detection of individual HPV 16, 18, or 45 |
| Zhang et al. (26) | China | 16/18+addition | N = 2,665, age ≥ 25 and ≤ 65 y, NILM women positive for HPV | HPV GenoArray test kit (Hybribio Ltd., Hong Kong). | HPV16 (874, 30.2%), HPV58 (452, 15.6%), HPV52 (395, 13.6%), HPV53 (380, 13.1%), HPV18 (224, 7.7%), HPV33 (208, 7.2%) | OR for HSIL+ (95% CI): HPV16/18: 3.26 (2.41–4.40) HPV16/18/31/33: 4.21 (2.99–5.93) HPV16/18/31/33/52/58: 5.73 (3.30–9.97) | Addition of genotyping for HPV31/33 to HPV16/18 |
| Xu et al. (30) | China | Domestic HPV Testing | N = 2,180, age 30–64 years, NILM women | DH3 (a novel domestic high-risk HPV testing based on hybrid capture) | HPV other HPV+: 140 HPV16/18+: 30 HPV16/18& other HPV+: 15 | The cumulative absolute risk for the development of CIN2+ was 37.8% for HPV 16/18 positive women, followed by HR-HPV positive (14.6%), other HR-HPV positive (11.0%) and HPV negative (0.3%) in 3 years | DH3 HPV assay demonstrated excellent clinical performance against CIN2+ detection and utility of risk stratification |
| Song et al. (73) | China | extended genotyping +p16INK immune-staining | N = 2,731, age 30–64 years, NILM women positive for HPV | Seq (BGI Shenzhen, Shenzhen, China) | HPV16 (23.7%), HPV52 (16.7%), HPV58 (14.0%), HPV51 (11.1%), HPV18 (10.5%) | The p16 positivity rates among three genotype strata were 40.2% (HPV16/33), 22.9% (HPV58/31/35), and 18.8% (other 9 types), respectively, increasing with the elevation of hierarchical types (p < 0.0001); three triage strategies were favorable in sensitivity and/or specificity to the ‘HPV16/33+' strategy: p16+; ‘HPV16+ or HPV33/58/31/35 + &p16+'; HPV16/18/31/33/45/52/58 + &p16 + | Genotyping for HPV16/33 could be utilized; p16 immunostaining, either alone or combined with extended genotypes, is more effective than HPV genotypes alone |
| Wright et al. (68) | USA | DS | N = 4,927 HPV-positive women NILM women: 3,090 | Cobas 4,800 and cobas 6,800/8,800 HPV (Roche Molecular Systems, Inc, Pleasanton, CA) | in NILM women: 12 other HPV+ and DS+: 750 (34.2%) 12 other HPV+ and DS-: 1,444 (65.8%) | In 12 “other” HPV-positive women, sensitivity of DS for ≥CIN2 and ≥CIN3 at baseline was 83.0 and 86.0%, respectively, significantly higher as compared to the respective sensitivity estimates of cytology | DS is effective for triage of HPV-positive women, either alone or when combined with partial HPV genotyping |
HPV, human papillomavirus; NILM, negative for intraepithelial lesions or malignancies; CIN, cervical intraepithelial neoplasia; DS, p16/Ki-67 dual-stained cytology.