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Browsing by Author "Dias-Neto, E"

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    Publication
    Gene content, phage cycle regulation model and prophage inactivation disclosed by prophage genomics in the Helicobacter pylori Genome Project
    (Taylor and Francis Ltd., 2024) Vale, FF; Roberts, RJ; Kobayashi, I; Camargo, MC; Rabkin, CS; Wang, D; Hicks, B; Zhu, B; Yeager, M; Hutchinson, A; Teshome, K; Jones, K; Luo, W; Goldstein, AM; Hu, N; Taylor, PR; Song, M; Gutiérrez-Escobar, AJ; Yu, K; Abnet, CC; Chanock, SJ; Romero-Gallo, J; Krishna, U; Peek, RM; Piazuelo, MB; Wilson, KT; Loh, JT; Cover, TL; Raaf, N; Aftab, H; Akada, J; Matsumoto, T; Yamaoka, Y; Haesebrouck, F; Bartelli, TF; Nunes, DN; Pelosof, A; Sztokfisz, CZ; Dias-Neto, E; Assumpção, PP; Tishkov, I; Goodman, KJ; Geary, J; Cromarty, TJ; Price, NL; Quilty, D; Corvalan, AH; Serrano, CA; Gonzalez, R; Riquelme, A; García-Cancino, A; Parra-Sepúlveda, C; Castillo, F; Bravo, MM; Pazos, A; Bravo, LE; Fox, JG; Ramírez-Mayorga, V; Molina-Castro, S; Durán-Bermúdez, S; Campos-Núñez, C; Chaves-Cervantes, M; Tshibangu-Kabamba, E; Tumba, GD; Tshimpi-Wola, A; de Jesus Ngoma-Kisoko, P; Ngoyi, DM; Cruz, M; Hosking, C; Abreu, JJ; Varon, C; Benejat, L; Jehanne, Q; Lehours, P; Megraud, F; Secka, O; Link, A; Malfertheiner, P; Adinortey, MB; Bockarie, AS; Adinortey, CA; Ofori, EG; Sgouras, DN; Martinez-Gonzalez, B; Michopoulos, S; Georgopoulos, S; Hernandez, E; Dominguez, RL; Morgan, DR; Harðardóttir, H; Gunnarsdóttir, AI; Guðjónsson, H; Jónasson, JG; Björnsson, ES; Ballal, M; Shetty, V; Miftahussurur, M; Sugihartono, T; Alfaray, RI; Waskito, LA; Fauzia, KA; Syam, AF; Maulahela, H; Malekzadeh, R; Sotoudeh, M; Peretz, A; Azrad, M; On, A; De, Re, V; Zanussi, S; Cannizzaro, R; Canzonieri, V; Shimura, T; Tokunaga, K; Osaki, T; Kamiya, S; Jadallah, K; Matalka, I; Sagynbekuly, IN; Moldobaeva, MS; Rakhat, A; Choi, IJ; Kim, JG; Kim, N; Leja, M; Vangravs, R; Šķenders, Ģ; Rūdule, A; Kikuste, I; Vanags, A; Rudzīte, D; Kupcinskas, J; Skieceviciene, J; Jonaitis, L; Kiudelis, G; Jonaitis, P; Kiudelis, V; Varkalaite, G; Vadivelu, J; Loke, MF; Vellasamy, KM; Herrera-Goepfert, R; Alonso-Larraga, JO; Yee, TT; Htet, K; Matsuhisa, T; Shrestha, PK; Ansari, S; Abiodun, O; Jemilohun, C; Akande, KO; Olu-Abiodun, O; Magaji, FA; Omotoso, A; Okonkwo, U; Osuagwu, CC; Owoseni, OO; Castaneda, C; Castillo, M; Velapatino, B; Gilman, RH; Krzyżek, P; Gościniak, G; Pawełka, D; Korona-Glowniak, I; Cichoz-Lach, H; Oleastro, M; Figueiredo, C; Machado, JC; Ferreira, RM; Bordin, DS; Livzan, MA; Tsukanov, VV; Tan, P; Yeoh, KG; Zhu, F; Ally, R; Haas, R; Fischer, W; Montes, M; Fernández-Reyes, M; Tamayo, E; Lizasoain, J; Bujanda, L; Lario, S; Ramírez-Lázaro, MJ; Calvet, X; Brunet-Mas, E; Domper-Arnal, MJ; García-Mateo, S; Abad-Baroja, D; Delgado-Guillena, P; Moreira, L; Botargues, J; Pérez-Martínez, I; Barreiro-Alonso, E; Flores, V; Gisbert, JP; Muro, EA; Linares, P; Alcoba, L; Martin, V; Fleitas-Kanonnikoff, T; Altayeb, HN; Engstrand, L; Enroth, H; Keller, PM; Wagner, K; Pohl, D; Lee, Y-C; Liou, J-M; Wu, M-S; Kocazeybek, B; Sarıbas, S; Tasçı, İ; Demiryas, S; Kepil, N; Quiel, L; Villagra, M; Norton, M; Johnson, D; Huang, RJ; Hwang, JH; Szymczak, W; Rajagopalan, S; Asare, E; Jacobs, WR; In, H; Bollag, R; Lopez, A; Kruse, EJ; White, J; Graham, DY; Lane, C; Gao, Y; Gold, BD; Cruz-Correa, M; González-Pons, M; Rodriguez, LM; Tuan, VP; Dung, HDQ; Binh, TT; Trang, TTH; Van, Khien, V; Chen, X; Zhao, Y; Raley, C; Kessing, B; Tran, B; Katsura, Y; Gonzalez-Hormazabal, P; Didelot, X; Sheppard, S; Tarazona-Santos, E; Zamudio, R; Mariño-Ramírez, L; Backert, S; Naumann, M; Smet, A; Berg, DE; Chiner-Oms, Á; Comas, I; Martínez-Martínez, FJ; Yahara, K; Blaser, MJ; Vincze, T; Morgan, RD; Dekker, JP; Torres, J; Noureen, M; Cherry, JL; Osada, N; Fukuyo, M; Arita, M; Sandoval-Motta, S; Agostini, RB; Ghirotto, S; Muñoz-Ramírez, ZY; Torres, RC; Falush, D; Thorell, K; Uchiyama, I
    Prophages can have major clinical implications through their ability to change pathogenic bacterial traits. There is limited understanding of the prophage role in ecological, evolutionary, adaptive processes and pathogenicity of Helicobacter pylori, a widespread bacterium causally associated with gastric cancer. Inferring the exact prophage genomic location and completeness requires complete genomes. The international Helicobacter pylori Genome Project (HpGP) dataset comprises 1011 H. pylori complete clinical genomes enriched with epigenetic data. We thoroughly evaluated the H. pylori prophage genomic content in the HpGP dataset. We investigated population evolutionary dynamics through phylogenetic and pangenome analyses. Additionally, we identified genome rearrangements and assessed the impact of prophage presence on bacterial gene disruption and methylome. We found that 29.5% (298) of the HpGP genomes contain prophages, of which only 32.2% (96) were complete, minimizing the burden of prophage carriage. The prevalence of H. pylori prophage sequences was variable by geography and ancestry, but not by disease status of the human host. Prophage insertion occasionally results in gene disruption that can change the global bacterial epigenome. Gene function prediction allowed the development of the first model for lysogenic-lytic cycle regulation in H. pylori. We have disclosed new prophage inactivation mechanisms that appear to occur by genome rearrangement, merger with other mobile elements, and pseudogene accumulation. Our analysis provides a comprehensive framework for H. pylori prophage biological and genomics, offering insights into lysogeny regulation and bacterial adaptation to prophages. © 2024 The Author(s). Published with license by Taylor & Francis Group, LLC.
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    Publication
    Prevalence of Helicobacter pylori Infection, Its Virulent Genotypes, and Epstein-Barr Virus in Peruvian Patients With Chronic Gastritis and Gastric Cancer
    (American Society of Clinical Oncology, 2019) Castaneda, Carlos; Castillo, Miluska; Chavez, I; Barreda, F; Suarez, N; Nieves, J; Bernabe, LA; Valdivia, D; Ruiz, E; Dias-Neto, E; Landa-Baella, MP; Bazan, Y; Rengifo, CA; Montenegro, P
    Purpose: Helicobacter pylori (HP) and Epstein Barr virus (EBV) infections induce chronic gastritis (CG) and are accepted carcinogenics of gastric cancer (GC). Our objective for this study was to determine the prevalence of these agents and clinicopathological features of GC and CG associated with the infection. Patients and methods: A single-center cohort of 375 Peruvian patients with GC and 165 control subjects with CG were analyzed. Evaluation of HP and EBV genes was performed through quantitative polymerase chain reaction. Results: Prevalence of HP was 62.9% in the whole population and 60.8% in the GC subset. The cagA gene was detected in 79.9%; vacAs1 and vacAm1 alleles in 41.6% and 60.7%, respectively; and concurrent expression of vacAs1 and vacAm1 in 30.4% of infected patients in the whole series. The prevalence of EBV was 14.1% in the whole population and was higher in GC (P < .001). Coinfection of HP and EBV was found in 7.8% and was also higher in GC in univariate (P < .001) and multivariate (P = .011) analyses. Infection rates of HP and EBV were not associated with a geographic location in the whole series. Few clinicopathological features have been associated with infectious status. Conclusion: Prevalence of HP infection and virulent strains are high in the Peruvian population. Infection by EBV was more frequent in patients with GC.

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