Human papillomavirus genotype distribution in tonsil cancers.

International audienceBACKGROUND: The incidence of tonsil cancers has increased in several countries. French data on HPV prevalence in tonsil cancers are scarce. The objective of this study was thus to assess the overall and type specific HPV prevalence in tonsil histological samples. METHODS: This French retrospective multicenter study involved 12 centres located throughout the country. Were included 185 histological samples collected from year 2000 to 2009 with a validated diagnosis of tonsil invasive carcinomas. HPV prevalence was studied according to gender, age and histological type of cancer. RESULTS: Overall HPV prevalence was 57% in tonsil cancers. Mean age of diagnosis was comparable in HPV positive tonsils cases (60 ± 11.2) and HPV negative tonsil cases (59 ± 9.6). HPV prevalence was significantly higher in female than in male cases (28/35 versus 78/150 in tonsil cases, respectively, P = 0.003). About 53% of tonsil cases were infected by a single HPV type. Only eight (4%) samples were infected by more than one HPV type. Among HPV positive samples, HPV 16 was found in 89% of tonsil cases. All other HPV types had prevalence below 5%. CONCLUSIONS: Our results indicate that HPV is common in tonsil carcinomas and emphasize the predominant role of HPV 16

Pathogénèse du syndrome sec associé à l'infection par le virus HTLV-1 (variants et syndrome sec ; infection productrice d'une lignée épithéliale d'origine salivaire ; étude de la régulation du promoteur de l'interleukine 6 par la protéine virale Tax)

POITIERS-BU Médecine pharmacie (861942103) / SudocSudocFranceF

Infections à HPV du col utérin (expérience diagnostique au laboratoire de virologie du CHU de Poitiers)

ANGERS-BU Médecine-Pharmacie (490072105) / SudocSudocFranceF

Papillomavirus et cancer de la tonsille (intérêt de la détection des ARNm E6/E7 et de la protéine p16INK4A)

POITIERS-BU Médecine pharmacie (861942103) / SudocSudocFranceF

Etude de la charge virale et de l'intégration du génome d'HPV-16 par PCR en temps-réel dans des prélèvements du col de l'utérus (corrélation avec la cytologie et l'histologie)

POITIERS-BU Médecine pharmacie (861942103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Characterization of a new caseof XMLV (Bxv1) contaminationin the human cell line Hep2 (clone2B)

International audienc

Acanthamoeba castellanii is not be an adequate model to study human adenovirus interactions with macrophagic cells.

Free living amoebae (FLA) including Acanthamoeba castellanii, are protozoa that feed on different microorganisms including viruses. These microorganisms show remarkable similarities with macrophages in cellular structures, physiology or ability to phagocyte preys, and some authors have therefore wondered whether Acanthamoeba and macrophages are evolutionary related. It has been considered that this amoeba may be an in vitro model to investigate relationships between pathogens and macrophagic cells. So, we intended in this study to compare the interactions between a human adenovirus strain and A. castellanii or THP-1 macrophagic cells. The results of molecular and microscopy techniques following co-cultures experiments have shown that the presence of the adenovirus decreased the viability of macrophages, while it has no effect on amoebic viability. On another hand, the viral replication occurred only in macrophages. These results showed that this amoebal model is not relevant to explore the relationships between adenoviruses and macrophages in in vitro experiments

HPV16 E7 expression stimulates UBF1 phosphorylation.

<p>(A), Western blot analysis of H358 WT cells transiently transfected with the pcDNA3.1 (Control), pJ4Ω16E7 (E7) or pcDNA3.1-p14ARF (p14^ARF) expression vector, or both and probed with antibodies to UBF, phosphorylated UBF (P-UBF Ser 388), p14^ARF and actin (as a loading control). (B), Western blot analysis of H358 Cl19 cells cultured with (+Dox) or without (-Dox) 1 mg/ml doxycyclin, transfected with pJ4Ω16E7 (E7), and probed with the indicated antibodies. (C), Western blot analysis of MCF7 cells transduced with LXSN, LXSNE7 (E7), LXSNE6 (E6), and LXSNE6E7 (E6+E7), selected with G418, and probed with the indicated antibodies. Quantification of western blots was done by measuring the relative intensity of the bands compared to internal controls (Actin), the values given are in arbitrary units. Expression of E7 was monitored by quantitative real time RT-PCR. Western blot and qRT-PCR are representative of three experiments at least.</p

Human Papillomavirus 16 Oncoprotein E7 Stimulates UBF1-Mediated rDNA Gene Transcription, Inhibiting a p53-Independent Activity of p14^ARF

<div><p>High-risk human papillomavirus oncoproteins E6 and E7 play a major role in HPV-related cancers. One of the main functions of E7 is the degradation of pRb, while E6 promotes the degradation of p53, inactivating the p14^ARF-p53 pathway. pRb and p14^ARF can repress ribosomal DNA (rDNA) transcription in part by targeting the Upstream Binding Factor 1 (UBF1), a key factor in the activation of RNA polymerase I machinery. We showed, through ectopic expression and siRNA silencing of p14^ARF and/or E7, that E7 stimulates UBF1-mediated rDNA gene transcription, partly because of increased levels of phosphorylated UBF1, preventing the inhibitory function of p14^ARF. Unexpectedly, activation of rDNA gene transcription was higher in cells co-expressing p14^ARF and E7, compared to cells expressing E7 alone. We did not find a difference in P-UBF1 levels that could explain this data. However, p14^ARF expression induced E7 to accumulate into the nucleolus, where rDNA transcription takes place, providing an opportunity for E7 to interact with nucleolar proteins involved in this process. GST-pull down and co-immunoprecipitation assays showed interactions between p14^ARF, UBF1 and E7, although p14^ARF and E7 are not able to directly interact. Co-expression of a pRb-binding-deficient mutant (E7C24G) and p14^ARF resulted in EC24G nucleolar accumulation, but not in a significant higher activation of rDNA transcription, suggesting that the inactivation of pRb is involved in this phenomenon. Thus, p14^ARF fails to prevent E7-mediated UBF1 phosphorylation, but could facilitate nucleolar pRb inactivation by targeting E7 to the nucleolus. While others have reported that p19^ARF, the mouse homologue of p14^ARF, inhibits some functions of E7, we showed that E7 inhibits a p53-independent function of p14^ARF. These results point to a mutually functional interaction between p14^ARF and E7 that might partly explain why the sustained p14^ARF expression observed in most cervical pre-malignant lesions and malignancies may be ineffective.</p></div