>> P-609: Molecular characterization of Human Papillomavirus type 16, -18, -31, -33 and -52 variants in HIV1-positive and -negative men who have sex with men
19:00 PM - 19:00 PM
1Unidad de Retrovirus y Papilomavirus, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain; 2Centro Sanitario Sandoval, Madrid, Spain.
Objective: The objective of the present study is to analyse the genomic polymorphisms in E6, E7 and LCR regions of Human Papillomavirus (HPV) types 16, -18, -31, -33 and -52 among HIV-positive and -negative men who had sex with men (MSM).
Methods: Subjects were selected from participants in a cross-sectional study of a convenience sample of 401 HIV1-positive and -negative MSM recruited from a Sexually Transmitted Infections (STI) clinic in Madrid. High-risk HPV prevalence obtained by Hybrid Capture was 74.8% and 43.3% in HIV1-positive and -negative MSM, respectively. The HPV type specific prevalence was 21.9% (88/401) for HPV-16, 12.1% (48/401) for HPV-18, 7.3% (29/401) for HPV-31, 5.6% (22/401) for HPV-33 and 6.3% (25/401) for HPV-52. A type specific set of primers were used for PCR and sequencing. Multiple sequence alignments were performed with MegAling program (DNASTAR, Madison USA) using reference sequences from Genbank.
Results: In 83 HPV-16, 46 HPV-18, 29 HPV-31, 22 HPV-33 and 22 HPV-52 anal samples enough DNA was available for polymorphisms characterization. For HPV-16, 72 sequences (86.7%) were classified as European (E) variants, eight samples (9.6%) as Asian-American (AA) variants and three as African-2 (Af) variants. For HPV-18 samples, 78.3% of the variants were assigned to E lineage, 6.5% to Asian-American (AsAi) branch, 8.7% to Af lineage and 6.5% were classified as recombinant sequences of variants (two E/AsAi and one E/Af). For HPV-31, HVP-33, HPV-52, of the total of samples analysed 17.2%, 36.4% and 36.4% were classified as prototype.
Discussion: European intra-type variants were the most frequently detected for HPV-16 and -18. Recombinant sequences were identified only in HPV-18 variants and could be formed probably because of homologous recombination or a concurrent infection with different intra-types variants; this event could be favoured by the high prevalence of HR-HPV infections in this population.