Human Papillomavirus Type 16 Variants and Risk of Cervical Cancer

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Abstract
There are substantial data demonstrating that human papillomaviruses (HPVs) are the sexually transmitted etiologic agents of cervical cancer (1). HPV type 16 (HPV16) is the most common HPV type detected in tumors, accounting for 50% of cancers and their precursors, called high-grade squamous intraepithelial lesions (HSILs) (2). Preliminary studies (3–16) have suggested that variants of HPV16 may show varying degrees of association with cervical neoplasia. This may partially explain why some HPV16 infections progress to HSIL or cancer, while others do not. If causal, these associations may be explained by differences in the transcriptional regulation of the virus by different variants, in the biologic activities of the proteins encoded by HPV16 variants (e.g., enhanced transforming abilities of E6/E7), or in the ability of the host to respond immunologically to specific viral epitopes encoded by variants. This last effect is likely to be mediated through human leukocyte antigen (HLA) presentation of viral antigens (17–21). Previous studies of viral variants and cervical neoplasia have relied on convenience samples, limiting their interpretation, while others have had small sample size.

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