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Human papillomavirus type-16 variants in Quechua aboriginals from Argentina

✍ Scribed by María Alejandra Picconi; Lidia Virginia Alonio; Laura Sichero; Viviana Mbayed; Luisa Lina Villa; Jorge Gronda; Rodolfo Campos; Angélica Teyssié


Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
94 KB
Volume
69
Category
Article
ISSN
0146-6615

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✦ Synopsis


Abstract

Cervical carcinoma is the leading cause of cancer death in Quechua indians from Jujuy (northwestern Argentina). To determine the prevalence of HPV‐16 variants, 106 HPV‐16 positive cervical samples were studied, including 33 low‐grade squamous intraepithelial lesions (LSIL), 28 high‐grade squamous intraepithelial lesions (HSIL), 9 invasive cervical cancer (ICC), and 36 samples from women with normal colposcopy and cytology. HPV genome variability was examined in the L1 and E6 genes by PCR‐hybridization. In a subset of 20 samples, a LCR fragment was also analyzed by PCR‐sequencing. Most variants belonged to the European branch with subtle differences that depended on the viral gene fragment studied. Only about 10% of the specimens had non‐European variants, including eight Asian‐American, two Asian, and one North‐American‐1. E6 gene analysis revealed that 43% of the samples were identical to HPV‐16 prototype, while 57% corresponded to variants. Interestingly, the majority (87%) of normal smears had HPV‐16 prototype, whereas variants were detected mainly in SIL and ICC. LCR sequencing yielded 80% of variants, including 69% of European, 19% Asian‐American, and 12% Asian. We identified a new variant, the Argentine Quechua‐51 (AQ‐51), similar to B‐14 plus two additional changes: G7842→A and A7837→C; phylogenetic inference allocated it in the Asian‐American branch. The high proportion of European variants may reflect Spanish colonial influence on these native Inca descendants. The predominance of HPV‐16 variants in pathologic samples when compared to normal controls could have implications for the natural history of cervical lesions. J. Med. Virol. 69:546–552, 2003. © 2003 Wiley‐Liss, Inc.


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