In order to determine geographically related intratypic variation in human papillomavirus (HPV) type 16 and 18 isolates that could be associated with lesion development, data were analysed from an ongoing cohort study of the natural course of infection of HPVs and cervical neoplasia. Testing for HPVs was carried out by PCR and molecular variants of these HPVs were characterized by sequence analysis of the long control region and by dot blot hybridization of the E6 and L1 genes. Tests for HPV were done in multiple first-year specimens from 1690 women enrolled in a cancer screening program from 1993 to 1997. Subjects were followed-up by cytology and cervicography for detection of cervical lesions. Seven variants of HPV-16 and four of HPV-18 were detected in one or more specimens from 65 subjects. The same variant was found in specimens taken on different visits from each case of persistent infection. Overall, non-European variants tended to persist more frequently [odds ratio (OR)=4·5; 95% confidence interval (CI), 1·6–12·4] than European (E) variants (OR=2·5; 95% CI, 1·3–4·9), relative to the risk of persistence for non-oncogenic HPVs. In addition, non-E variants were more strongly associated with risk of both prevalent (age- and race-adjusted OR=172·2; 95% CI, 47·1–630·1) and incident [relative risk (RR)=22·5; 95% CI, 6·0–83·9] high-grade lesions than E variants (prevalent lesions OR=46·3; 95% CI, 15·5–138·0 and incident lesons RR=6·1; 95% CI, 1·3–27·4), relative to the risk for HPV-negative women. Although consistent, the latter differences were not statistically significant. If confirmed in other populations, measurement of intratypic variation of HPV-16 and -18 has the potential to serve as an ancillary tool in cervical cancer screening.

The intratypic variability of HPVs 16 and 18 has been extensively studied and has been used as an important tool in epidemiological studies of viral transmission, persistence and progression to clinically relevant cervical lesions. Infections by non‐European variants of HPVs 16 and 18 are associated with an increased risk for the development of high grade squamous intraepithelial lesions (HSIL). Our aim was to correlate the intratypic molecular variability of both HPV types and risk of persistent infection and lesion outcome in a cohort study conducted in Brazil. We characterized molecular variants of HPV types 16 and 18 by sequencing a fragment of the LCR, and of the E6 and L1 genes, for HPV‐16 variants only. For both types, European variants composed the most prevalent and diverse group. Persistent infections with HPV‐18 were associated with continuous detection of European variants. However, risk for simultaneous detection of HSIL and HPV DNA was higher in women harboring non‐European variants of HPV‐16. The same trend was observed with HSIL detected during follow‐up. Our study confirms the association between non‐European variants and risk of cervical neoplasia, and highlights the importance of their geographic distribution for cervical cancer risk assessment.

Human papillomavirus (HPV) infection is linked to the development of cervical cancer, and several cofactors contribute to the risk of disease. Research on the intratypic variability of HPVs has defined variants that are associated with persistent infections and are potentially more oncogenic, translating to a higher risk of malignant disease. The genetic variability of the host also plays a role in the risk of cervical cancer, especially genes controlling the immune response, such as HLA class I and II. These highly polymorphic genes are important risk determinants of HPV persistence and disease progression. The interaction between host and viral factors is complex and needs to be further investigated, paving the way to better define the patients at the highest risk of developing malignant diseases linked to HPV infection.

Human papillomavirus (HPV)-related head and neck squamous cell carcinoma (HNSCC) is considered to be a distinct clinical entity with better prognosis than the classical tobacco- and alcohol-associated tumors. The increasing incidence of this neoplasia during the last decades highlights the need to better understand the role of HPV in the development of these cancers. Although the proportion of HNSCC attributed to HPV varies considerably according to anatomical site, overall approximately 25% of all HNSCC are HPV-DNA positive, and HPV-16 is by far the most prevalent type. In this review we discuss the existing evidence for a causal association between HPV infection and HNSCC at diverse anatomical head and neck subsites.