Volume 82, Issue 7 pp. 1168-1178
Research Article
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Polymorphism of the capsid L1 gene of human papillomavirus types 31, 33, and 35

Gilbert Cornut

Gilbert Cornut

Laboratoire de Virologie Moléculaire, Centre de Recherche and Département de Microbiologie-Infectiologie, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada

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Simon Gagnon

Simon Gagnon

Laboratoire de Virologie Moléculaire, Centre de Recherche and Département de Microbiologie-Infectiologie, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada

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Catherine Hankins

Catherine Hankins

Département de Médecine Sociale et Préventive, Université de Montréal, Montréal, Québec, Canada

Direction de la Santé Publique de Montréal-Centre, Institut National de Santé Publique du Québec, Montréal, Québec, Canada

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Deborah Money

Deborah Money

Department of Obstetrics and Gynecology, University of British Columbia, Vancouver, British Columbia, Canada

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Karina Pourreaux

Karina Pourreaux

Département de Médecine Sociale et Préventive, Université de Montréal, Montréal, Québec, Canada

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Eduardo L. Franco

Eduardo L. Franco

Division of Cancer Epidemiology, Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Québec, Canada

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François Coutlée

Corresponding Author

François Coutlée

Laboratoire de Virologie Moléculaire, Centre de Recherche and Département de Microbiologie-Infectiologie, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada

Division of Cancer Epidemiology, Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Québec, Canada

Département de Microbiologie et Immunologie, Université de Montréal, Montréal, Québec, Canada

Département de Microbiologie et Infectiologie, Hôpital Notre-Dame du Centre Hospitalier de l'Université de Montréal, 1560 Sherbrooke est, Montréal, Québec, Canada H2L 4M1.===Search for more papers by this author
for The Canadian Women's HIV Study Group

for The Canadian Women's HIV Study Group

The Canadian Women's HIV Study Group includes the following investigators from across Canada: Halifax: Janet Conners, Rob Grimshaw, David Haase, Lynn Johnston, Wally Schlech, Arlo Yuzicappi-Fayant. Hamilton: Stephen Landis, Fiona Smaill. London: Tom Austin, Ole Hammerberg, Ted Ralph. Montréal: François Coutlée, Julian Falutz, Alex Ferenczy, Catherine Hankins, Marina Klein, Louise Labrecque, Normand Lapointe, Richard Lalonde, John Macleod, Grégoire Noël, Chantal Perron, Jean-Pierre Routy, and Emil Toma. Ottawa: Claire Touchie, Garry Victor. Québec: Louise Coté, Hélène Senay, Sylvie Trottier. Saskatoon: Kurt Williams. Sherbrooke: Alain Piché. Sudbury: Roger Sandre. Toronto: Louise Binder, Donna Keystone, Anne Phillips, Anita Rachlis, Irving Salit, Cheryl Wagner, Sharon Walmsley. Vancouver: Paula Braitstein, David Burdge, Marianne Harris, Deborah Money, Julio Montaner.

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First published: 25 May 2010
Citations: 19

There was no conflict of interest by any of the authors of this paper related to the subject of the article.

Abstract

The L1 gene encodes for the major capsid protein of human papillomaviruses (HPV). There is limited information on the polymorphism of L1 for types related to HPV-16. This report explores the polymorphism of L1 in phylogenetically related types 31, 33, and 35 compared to HPV-16. Genital specimens collected from 732 HIV-seropositive and 323 HIV-seronegative women were screened for HPV DNA with consensus L1 PCR. Cervical samples positive for HPV-16 (n = 74), HPV-31 (n = 78), HPV-33 (n = 37), and HPV-35 (n = 58) were further characterized by PCR-sequencing of the complete L1 gene. The number of nucleotide substitutions within L1 ranged from 19 for HPV-33 to 52 for HPV-31. The ratio of the number of variants/number of isolates tested was higher for HPV-31 (56.4%, P = 0.05) and HPV-35 (60.3%, P = 0.04) compared to HPV-16 (40.5%), while this ratio was lower for HPV-33 (24.3%), although not significantly (P = 0.14). The maximal distance between HPV variants was greater in the five putative surface-exposed loops of L1 than in sequences outside the loops (P < 0.01). Synonymous variations were encountered in 1.7% (95% CI 1.1–2.3) of nucleotides inside the L1 loops and 2.4% (95% CI1.2–3.7) of nucleotides outside the L1 loops. Non-synonymous variations were encountered in 1.8% (95% CI 1.1–2.5) of nucleotides within the L1 loops and 0.2% (95% CI 0–0.4) of nucleotides outside the loops. dN/dS ratios were below 1.0 in extra-loop and intra-loop regions, but they were lower in extra-loop regions. These results suggest that sequences within and outside the hypervariable loops of L1 were under selective constraint. J. Med. Virol. 82: 1168–1178, 2010. © 2010 Wiley-Liss, Inc.

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