Highly replicating hepatitis C virus variants emerge in immunosuppressed patients causing severe disease Paul Rothhaar, Tomke Arand, Ha Gyu-Thomas Seong, Christian Heuss, Margaret Tulessin, Zhiqing Wang, Colin Förster, Alina C. Schneider, Jocelyn Quistrebert, Haiting Chai, Marvin Reineke, Louise Benning, Jonathan Honegger, Maike Hofmann, Robert Thimme, Jörg Timm, , Graham S. Cooke, Sarah Pett, Leanne McCabe, Chris Jones, Richard Gilson, Sumita Verma, Stephen D. Ryder, Jane D. Collier, Stephen T. Barclay, Aftab Ala, Sanjay Bhagani, Mark Nelson, Chin Lye Ch’ng, Ben Stone, Martin Wiselka, Daniel Forton, Stuart McPherson, Rachel Halford, Dung Nguyen, David Smith, Emily Dennis, Fleur Hudson, Eleanor J. Barnes, Ann Sarah Walker, Paul Schnitzler, Uta Merle, Naglaa H. Shoukry, Julie Bruneau, Chaturaka Rodrigo, Andrew Lloyd, Rowena A. Bull, M. Azim Ansari, Carolin Mogler, John McLauchlan, Xavier Forns, Sofía Pérez-del-Pulgar, Volker Lohmann Nature Communications, 2025 Hepatitis C virus (HCV) exists as a heterogenous quasispecies, but the phenotypic consequences of viral variability are widely unexplored. Here we identify a replication enhancing domain (ReED) in non-structural protein 5A conferring high replication fitness to clinical isolates. Accumulation of mutations in the ReED mediates high genome replication capacity. In a cohort of liver transplant patients, high replicator variants are exclusively found in individuals with severe disease outcome, suggesting that high viral replication fitness is associated with increased viral pathogenesis. Analysis of large sequence cohorts reveals that overall only 10% of viral genomes show genetic signatures of high replicators, which are enriched in recipients of liver transplantations, patients developing hepatocellular carcinoma and in HIV coinfected individuals. Overall, our data suggests that low replication fitness is a hallmark of HCV, contributing to establishment of persistence, whereas high replicators appear to have an advantage under conditions of immune suppression, thereby enforcing pathogenesis.
HBV Suppression by Nucleos(t)ide Analogues Reduces PD-1 Expression on Liver-Resident T Cells Mireia García‐López, Sabela Lens, Laura J. Pallett, Anna Pocurull, Thais Leonel, Ernest Belmonte, Ester García‐Pras, Sergio Rodríguez‐Tajes, Zoe Mariño, Maria Sàez‐Palma, Concepción Bartres, Ariadna Rando‐Segura, Francisco Rodríguez‐Frías, Jonah Lin, Adam J. Gehring, Mala K. Maini, Xavier Forns, Sofía Pérez‐del‐Pulgar Liver International, 2025 Background and AimPD‐1‐expressing T cells within the HBV‐infected liver constitute a target of novel immunotherapeutics. Our aim was to investigate the impact of viral suppression on PD‐1 expression on intrahepatic versus circulating lymphocyte populations from chronic hepatitis B (CHB) patients.MethodsTwenty‐two CHB patients, nine of them on nucleos(t)ide analogues (NUCs), had paired blood, liver fine needle aspirations (FNAs) and biopsies. A subset had a follow‐up FNA after treatment initiation (n = 4) or discontinuation (n = 4). Intrahepatic (iHBV‐DNA and cccDNA) and serum (HBV‐DNA, HBsAg, HBcrAg and cirB‐RNA) viral markers were quantified. Flow cytometry was used for immunophenotyping PBMCs and intrahepatic lymphocytes. An independent liver FNA scRNAseq dataset was used to consolidate our results.ResultsPD‐1 expression on tissue‐resident memory CD8 T cells (TRM) correlated with both iHBV‐DNA and cccDNA, as well as surrogate markers of cccDNA transcriptional activity (cirB‐RNA and HBcrAg) in CHB patients with mild hepatitis. These associations were not reflected in circulating T cells. PD‐1 expression intensity on CD8 TRM was lower in NUC‐treated than in naive patients, changes that were again not detectable in the circulation. Longitudinal analysis showed that viral load rebound induced by NUC discontinuation had the potential to drive re‐expression of high levels of PD‐1 on CD8 TRM. Conversely, therapy initiation and subsequent viral suppression reversed these changes. scRNAseq results further extended the profiling of these PD‐1 + CD8 TRM, showing a phenotype consistent with bystander activation in response to subclinical liver damage.ConclusionsIntrahepatic viral markers correlate with PD‐1 expression on global liver‐resident T cells of CHB patients with mild hepatitis, with a reduction after prolonged NUC therapy and re‐expression following treatment withdrawal.
Differential HBV RNA and HBcrAg patterns in untreated patients with chronic hepatitis delta Elisabetta Degasperi, Caroline Scholtes, Barbara Testoni, Sara Uceda Renteria, Maria Paola Anolli, Caroline Charre, Floriana Facchetti, Marie-Laure Plissonnier, Dana Sambarino, Riccardo Perbellini, Sara Monico, Annapaola Callegaro, Ester García-Pras, Sabela Lens, Maria Francesca Cortese, Xavier Forns, Sofía Pérez-del-Pulgar, Marintha Heil, Massimo Levrero, Fabien Zoulim, Pietro Lampertico Journal of Hepatology, 2025
HBcrAg and cirB-RNA Do Not Predict Clinical and Virological Outcomes in Patients With HBeAg-Negative Chronic Infection Sara Battistella, Thais Leonel, Anna Pocurull, Sergio Rodrìguez‐Tajes, Maria Saez‐Palma, Ariadna Rando‐Segura, Zoe Mariño, David Tabernero, Juan Carlos Hurtado, Maria Francesca Cortese, Sofía Pérez‐del‐Pulgar, Sabela Lens, Xavier Forns Liver International, 2025 Background & AimsPredicting clinical and virological outcomes in HBeAg‐negative (HBeAg‐neg) chronic infection often requires long‐term monitoring. Our study explored whether a single measurement of quantitative HBsAg (qHBsAg), HBV core‐related antigen (HBcrAg), and circulating HBV RNA (cirB‐RNA) can define the natural course of untreated HBeAg‐neg chronic infection patients.MethodsTo this aim, we included 128 naïve HBeAg‐neg chronic infection patients, stratified according to qHBsAg levels in: (1) 10–1000 IU/mL, (2) 1000–10 000 IU/mL, and (3) > 10 000 IU/mL.ResultsHBcrAg and cirB‐RNA were detected in 27% and 19% of patients with qHBsAg > 1000 IU/mL but rarely detected in patients with qHBsAg < 1000 IU/mL. After a median follow‐up of 5.1 years, 9.4% of patients lost HBsAg, and 8.5% experienced an increase in HBV DNA > 2000 IU/mL. qHBsAg < 1000 IU/mL was the only factor independently associated with functional cure.ConclusionsIn untreated HBeAg‐neg chronic infection patients, single‐point cirB‐RNA and HBcrAg do not offer additional predictive value over qHBsAg < 1000 IU/mL for spontaneous HBsAg loss.
Tracking B cell immunity during perturbation of hepatitis B infection induced by treatment withdrawal Sabela Lens, Alice R Burton, Jessica Davies, Maelle Locatelli, Mireia García-López, Anna Pocurull, Anna Jeffery-Smith, Nikolai Novikov, Simon P Fletcher, Xavier Forns, Sofía Pérez-del-Pulgar, Mala K Maini Gut, 2025 Background Withdrawal of prolonged nucleos(t)ide analogue (NA) treatment results in hepatitis B surface antigen (HBsAg) loss in some subjects with chronic hepatitis B (CHB), potentially revealing immune correlates of functional cure. Objective We investigated whether baseline or longitudinal changes in humoral immunity correlated with outcome of discontinuing prolonged NA treatment. Design Global memory B cells (MBC) and T follicular helper cells (Tfh) were analysed by flow cytometry. HBs (small surface)/HBc (core)-MBC were quantified by ex-vivo bait staining and function assessed by cultured ELISpots (enzyme-linked immunosorbent spots). Immune parameters assessed at end-of-treatment (EOT), 12 and 48 weeks after treatment withdrawal (and at 4–8 years in a subset) were correlated with intrahepatic and longitudinal serum viral markers and alanine transaminase (ALT). Results Individuals on prolonged NA had comparable frequencies of HBc-MBC and HBs-MBC, although the latter were PD-1 hi and functionally defective. Following treatment withdrawal, increases in class-switched HBc-MBC were frequently temporally linked with hepatic flares. Subjects achieving HBsAg loss had an increase in activated global MBC detectable at EOT that become more marked by week 48, accompanied by significant increases in plasmablasts. HBs-MBC in those with HBsAg loss showed significant reductions in PD-1, trends to increased activation (CD71) and function and a more robust correlation with Tfh, compared with HBsAg persistence. MBC changes were maintained 4–8 years after HBsAg seroconversion. Conclusion Differences in global and HBs-specific B cell immunity associate with HBsAg loss, whereas HBc-MBC temporally associates with flares, following withdrawal of prolonged NA treatment. Our results underscore the need to further explore the potential of B cell targets for monitoring and enhancing HBV functional cure in larger cohorts.
Detection of Hepatitis C Virus Infection from Patient Sera in Cell Culture Using Semi-Automated Image Analysis Noemi Schäfer, Paul Rothhaar, Christian Heuss, Christoph Neumann-Haefelin, Robert Thimme, Julia Dietz, Christoph Sarrazin, Paul Schnitzler, Uta Merle, Sofía Pérez-del-Pulgar, Vibor Laketa, Volker Lohmann Viruses, 2024 The study of hepatitis C virus (HCV) replication in cell culture is mainly based on cloned viral isolates requiring adaptation for efficient replication in Huh7 hepatoma cells. The analysis of wild-type (WT) isolates was enabled by the expression of SEC14L2 and by inhibitors targeting deleterious host factors. Here, we aimed to optimize cell culture models to allow infection with HCV from patient sera. We used Huh7-Lunet cells ectopically expressing SEC14L2, CD81, and a GFP reporter with nuclear translocation upon cleavage by the HCV protease to study HCV replication, combined with a drug-based regimen for stimulation of non-modified wild-type isolates. RT-qPCR-based quantification of HCV infections using patient sera suffered from a high background in the daclatasvir-treated controls. We therefore established an automated image analysis pipeline based on imaging of whole wells and iterative training of a machine learning tool, using nuclear GFP localization as a readout for HCV infection. Upon visual validation of hits assigned by the automated image analysis, the method revealed no background in daclatasvir-treated samples. Thereby, infection events were found for 15 of 34 high titer HCV genotype (gt) 1b sera, revealing a significant correlation between serum titer and successful infection. We further show that transfection of viral RNA extracted from sera can be used in this model as well, albeit with so far limited efficiency. Overall, we generated a robust serum infection assay for gt1b isolates using semi-automated image analysis, which was superior to conventional RT-qPCR-based quantification of viral genomes.
Hepatitis C virus-induced differential transcriptional traits in host cells after persistent infection elimination by direct-acting antivirals in cell culture Victoria Castro, Gema Calvo, Juan Carlos Oliveros, Sofía Pérez‐del‐Pulgar, Pablo Gastaminza Journal of Medical Virology, 2024 Chronic hepatitis C virus infection (HCV) causes liver inflammation and fibrosis, leading to the development of severe liver disease, such as cirrhosis or hepatocellular carcinoma (HCC). Approval of direct‐acting antiviral drug combinations has revolutionized chronic HCV therapy, with virus eradication in >98% of the treated patients. The efficacy of these treatments is such that it is formally possible for cured patients to carry formerly infected cells that display irreversible transcriptional alterations directly caused by chronic HCV Infection. Combining differential transcriptomes from two different persistent infection models, we observed a major reversion of infection‐related transcripts after complete infection elimination. However, a small number of transcripts were abnormally expressed in formerly infected cells. Comparison of the results obtained in proliferating and growth‐arrested cell culture models suggest that permanent transcriptional alterations may be established by several mechanisms. Interestingly, some of these alterations were also observed in the liver biopsies of virologically cured patients. Overall, our data suggest a direct and permanent impact of persistent HCV infection on the host cell transcriptome even after virus elimination, possibly contributing to the development of HCC.
miRNA Expression and HCC Occurrence in HCV Cirrhotic Patients Treated with Direct Acting Antivirals Antonietta Romano, Alessandra Brocca, Zoe Mariño, Sofía Pérez-del-Pulgar, Sabela Lens, Loreto Boix, María Reig, Jordi Bruix, Giulio Ceolotto, Valeria Calvino, Gianluca Zilio, Paula Piñero Romero, Ranka Vukotic, Valeria Guarneri, Pietro Andreone, Saverio Giuseppe Parisi, Francesco Paolo Russo, Salvatore Piano, Umberto Cillo, Paolo Angeli Livers, 2024 Background: The risk of hepatocarcinoma in HCV cirrhotic patient responders after treatment with DAAs decrease, but HCC still occurs. A correlation between specific miRNAs and the development of hepatocarcinoma have been highlighted. Aim: To investigate miRNA expression in HCV-infected cirrhotic patients treated with DAAs, regarding whether or not they developed HCC at follow-up. Methods: A total of 73 outpatients with HCV-related cirrhosis treated with DAAs were enrolled, 28 of which had HCC. Samples were collected at the start and at the end of treatment. In the screening phase, 172 miRNAs were analyzed at baseline. Differentially expressed miRNAs were validated in the entire cohort. Results: In the validation phase, at baseline and in patients treated for 12 weeks, miR-28-5p was confirmed to be more highly expressed in the HCC group compared to the non-HCC group. In all of the patients treated for 12 weeks, at end of the treatment we found a significant downregulation in miR-132-3p, miR-133b-3p, miR-221-3p and miR-324-3p. In the HCC group, miR-28-5p was significantly downregulated after DAA therapy as well as in HCC patients treated for 24 weeks. Conclusion: In the HCC group, miR28-5p was differently expressed both at baseline and at the end of therapy with DAAs. This difference in expression should suggest its involvement in HCC development.
Tissue CD14+CD8+ T cells reprogrammed by myeloid cells and modulated by LPS Laura J. Pallett, Leo Swadling, Mariana Diniz, Alexander A. Maini, Marius Schwabenland, Adrià Dalmau Gasull, Jessica Davies, Stephanie Kucykowicz, Jessica K. Skelton, Niclas Thomas, Nathalie M. Schmidt, Oliver E. Amin, Upkar S. Gill, Kerstin A. Stegmann, Alice R. Burton, Emily Stephenson, Gary Reynolds, Matt Whelan, Jenifer Sanchez, Roel de Maeyer, Clare Thakker, Kornelija Suveizdyte, Imran Uddin, Ana M. Ortega-Prieto, Charlotte Grant, Farid Froghi, Giuseppe Fusai, Sabela Lens, Sofia Pérez-del-Pulgar, Walid Al-Akkad, Giuseppe Mazza, Mahdad Noursadeghi, Arne Akbar, Patrick T. F. Kennedy, Brian R. Davidson, Marco Prinz, Benjamin M. Chain, Muzlifah Haniffa, Derek W. Gilroy, Marcus Dorner, Bertram Bengsch, Anna Schurich, Mala K. Maini Nature, 2023
Control of occult hepatitis B virus infection Marta Lalana Garcés, Oihana Ortiz Pastor, Gemma Solé Enrech, Armando R. Guerra-Ruiz, Gregori Casals Mercadal, Alejandro Almería Lafuente, María Antonieta Ballesteros Vizoso, Pablo Gabriel Medina, Sergio Salgüero Fernández, Angielys Zamora Trillo, Isabel Aured de la Serna, Juan Carlos Hurtado, Sofía Pérez-Del-Pulgar, Xavier Forns, Manuel Morales Ruiz Advances in Laboratory Medicine, 2022
Control of occult hepatitis B virus infection Marta Lalana Garcés, Oihana Ortiz Pastor, Gemma Solé Enrech, Armando Raul Guerra-Ruiz, Gregori Casals Mercadal, Alejandro Almería Lafuente, María Antonieta Ballesteros Vizoso, Pablo Gabriel Medina, Sergio Salgüero Fernández, Angielys Zamora Trillo, Isabel Aured de la Serna, Juan Carlos Hurtado, Sofía Pérez-Del-Pulgar, Xavier Forns, Manuel Morales Ruiz Advances in Laboratory Medicine, 2022
Hepatocellular Carcinoma in Mongolia Delineates Unique Molecular Traits and a Mutational Signature Associated with Environmental Agents Laura Torrens, Marc Puigvehí, Miguel Torres-Martín, Huan Wang, Miho Maeda, Philipp K. Haber, Thais Leonel, Mireia García-López, Roger Esteban-Fabró, Wei Qiang Leow, Carla Montironi, Sara Torrecilla, Ajay Ramakrishnan Varadarajan, Patricia Taik, Genís Campreciós, Chinbold Enkhbold, Erdenebileg Taivanbaatar, Amankyeldi Yerbolat, Augusto Villanueva, Sofía Pérez-del-Pulgar, Swan Thung, Jigjidsuren Chinburen, Eric Letouzé, Jessica Zucman-Rossi, Andrew Uzilov, Jaclyn Neely, Xavier Forns, Sasan Roayaie, Daniela Sia, Josep M. Llovet Clinical Cancer Research, 2022
Epigenetic priming in chronic liver disease impacts the transcriptional and genetic landscapes of hepatocellular carcinoma John Gallon, Mairene Coto‐Llerena, Caner Ercan, Gaia Bianco, Viola Paradiso, Sandro Nuciforo, Stephanie Taha‐Melitz, Marie‐Anne Meier, Tujana Boldanova, Sofía Pérez‐del‐Pulgar, Sergio Rodríguez‐Tajes, Markus Flüe, Savas D. Soysal, Otto Kollmar, Josep M. Llovet, Augusto Villanueva, Luigi M. Terracciano, Markus H. Heim, Charlotte K. Y. Ng, Salvatore Piscuoglio Molecular Oncology, 2022
Aberrant integration of Hepatitis B virus DNA promotes major restructuring of human hepatocellular carcinoma genome architecture Eva G. Álvarez, Jonas Demeulemeester, Paula Otero, Clemency Jolly, Daniel García-Souto, Ana Pequeño-Valtierra, Jorge Zamora, Marta Tojo, Javier Temes, Adrian Baez-Ortega, Bernardo Rodriguez-Martin, Ana Oitaben, Alicia L. Bruzos, Mónica Martínez-Fernández, Kerstin Haase, Sonia Zumalave, Rosanna Abal, Jorge Rodríguez-Castro, Aitor Rodriguez-Casanova, Angel Diaz-Lagares, Yilong Li, Keiran M. Raine, Adam P. Butler, Iago Otero, Atsushi Ono, Hiroshi Aikata, Kazuaki Chayama, Masaki Ueno, Shinya Hayami, Hiroki Yamaue, Kazuhiro Maejima, Miguel G. Blanco, Xavier Forns, Carmen Rivas, Juan Ruiz-Bañobre, Sofía Pérez-del-Pulgar, Raúl Torres-Ruiz, Sandra Rodriguez-Perales, Urtzi Garaigorta, Peter J. Campbell, Hidewaki Nakagawa, Peter Van Loo, Jose M. C. Tubio Nature Communications, 2021
Deep-sequencing reveals broad subtype-specific HCV resistance mutations associated with treatment failure Qian Chen, Celia Perales, María Eugenia Soria, Damir García-Cehic, Josep Gregori, Francisco Rodríguez-Frías, María Buti, Javier Crespo, José Luis Calleja, David Tabernero, Marta Vila, Fernando Lázaro, Ariadna Rando-Segura, Leonardo Nieto-Aponte, Meritxell Llorens-Revull, Maria Francesca Cortese, Irati Fernandez-Alonso, José Castellote, Jordi Niubó, Arkaitz Imaz, Xavier Xiol, Lluís Castells, Mar Riveiro-Barciela, Jordi Llaneras, Jordi Navarro, Víctor Vargas-Blasco, Salvador Augustin, Isabel Conde, Ángel Rubín, Martín Prieto, Xavier Torras, Nuria Margall, Xavier Forns, Zoe Mariño, Sabela Lens, Martin Bonacci, Sofía Pérez-del-Pulgar, Maria Carlota Londoño, María Luisa García-Buey, Paloma Sanz-Cameno, Rosa Morillas, Elisa Martró, Verónica Saludes, Helena Masnou-Ridaura, Javier Salmerón, Rosa Quíles, José Antonio Carrión, Montserrat Forné, Mercè Rosinach, Inmaculada Fernández, Javier García-Samaniego, Antonio Madejón, Pilar Castillo-Grau, Carme López-Núñez, María José Ferri, Rosa Durández, Federico Sáez-Royuela, Moisés Diago, Concepción Gimeno, Rafael Medina, Juan Buenestado, Albert Bernet, Juan Turnes, Matilde Trigo-Daporta, Manuel Hernández-Guerra, Manuel Delgado-Blanco, Angelina Cañizares, Juan Ignacio Arenas, Maria Juana Gomez-Alonso, Manuel Rodríguez, Elisabet Deig, Gemma Olivé, Oscar del Río, Joaquín Cabezas, Ildefonso Quiñones, Mercè Roget, Silvia Montoliu, Juan García-Costa, Lluís Force, Silvia Blanch, Miguel Miralbés, María José López-de-Goicoechea, Angels García-Flores, María Saumoy, Teresa Casanovas, Carme Baliellas, Pau Gilabert, Albert Martin-Cardona, Rosa Roca, Mercè Barenys, Joana Villaverde, Silvia Salord, Blau Camps, María Silvan di Yacovo, Imma Ocaña, Silvia Sauleda, Marta Bes, Judit Carbonell, Elena Vargas-Accarino, Sofía P. Ruzo, Mercedes Guerrero-Murillo, Georg Von Massow, María Isabel Costafreda, Rosa Maria López, Leticia González-Moreno, Yolanda Real, Doroteo Acero-Fernández, Silvia Viroles, Xavier Pamplona, Mireia Cairó, María Dolores Ocete, José Francisco Macías-Sánchez, Angel Estébanez, Joan Carles Quer, Álvaro Mena-de-Cea, Alejandra Otero, Ángeles Castro-Iglesias, Francisco Suárez, Ángeles Vázquez, David Vieito, Soledad López-Calvo, Pilar Vázquez-Rodríguez, Francisco José Martínez-Cerezo, Raúl Rodríguez, Ramiro Macenlle, Alba Cachero, Gasshan Mereish, Carme Mora-Moruny, Silvia Fábregas, Begoña Sacristán, Agustín Albillos, Juan José Sánchez-Ruano, Raquel Baluja-Pino, Javier Fernández-Fernández, Carlos González-Portela, Carmen García-Martin, Gloria Sánchez-Antolín, Raúl Jesús Andrade, Miguel Angel Simón, Juan Manuel Pascasio, Manolo Romero-Gómez, José Antonio del-Campo, Esteban Domingo, Rafael Esteban, Juan Ignacio Esteban, Josep Quer Antiviral Research, 2020
Tuning a cellular lipid kinase activity adapts hepatitis C virus to replication in cell culture Christian Harak, Max Meyrath, Inés Romero-Brey, Christian Schenk, Claire Gondeau, Philipp Schult, Katharina Esser-Nobis, Mohsan Saeed, Petra Neddermann, Paul Schnitzler, Daniel Gotthardt, Sofia Perez-del-Pulgar, Christoph Neumann-Haefelin, Robert Thimme, Philip Meuleman, Florian W. R. Vondran, Raffaele De Francesco, Charles M. Rice, Ralf Bartenschlager, Volker Lohmann Nature Microbiology, 2016
High-resolution hepatitis C virus subtyping using NS5B deep sequencing and phylogeny, an alternative to current methods Josep Quer, Josep Gregori, Francisco Rodríguez-Frias, Maria Buti, Antonio Madejon, Sofia Perez-del-Pulgar, Damir Garcia-Cehic, Rosario Casillas, Maria Blasi, Maria Homs, David Tabernero, Miguel Alvarez-Tejado, Jose Manuel Muñoz, Maria Cubero, Andrea Caballero, Jose Antonio delCampo, Esteban Domingo, Irene Belmonte, Leonardo Nieto, Sabela Lens, Paloma Muñoz-de-Rueda, Paloma Sanz-Cameno, Silvia Sauleda, Marta Bes, Jordi Gomez, Carlos Briones, Celia Perales, Julie Sheldon, Lluis Castells, Lluis Viladomiu, Javier Salmeron, Angela Ruiz-Extremera, Rosa Quiles-Pérez, Ricardo Moreno-Otero, Rosario López-Rodríguez, Helena Allende, Manuel Romero-Gómez, Jaume Guardia, Rafael Esteban, Javier Garcia-Samaniego, Xavier Forns, Juan Ignacio Esteban Journal of Clinical Microbiology, 2015
Analysis of serine codon conservation reveals diverse phenotypic constraints on hepatitis C virus glycoprotein evolution Richard J. P. Brown, George Koutsoudakis, Richard A. Urbanowicz, Deeman Mirza, Corinne Ginkel, Nina Riebesehl, Noémie Calland, Anna Albecka, Louisa Price, Natalia Hudson, Véronique Descamps, Matthijs Backx, C. Patrick McClure, Gilles Duverlie, Eve-Isabelle Pecheur, Jean Dubuisson, Sofia Perez-del-Pulgar, Xavier Forns, Eike Steinmann, Alexander W. Tarr, Thomas Pietschmann, Jonathan K. Ball Journal of Virology, 2014
CD14 modulates inflammation-driven insulin resistance José Manuel Fernández-Real, Sofia Pérez del Pulgar, Elodie Luche, José Maria Moreno-Navarrete, Aurelie Waget, Matteo Serino, Eleonora Sorianello, Alex Sánchez-Pla, Francesc Carmona Pontaque, Joan Vendrell, Matilde R. Chacón, Wifredo Ricart, Remy Burcelin, Antonio Zorzano Diabetes, 2011
Possible alternative to European Pharmacopoeia's method of analysis Test for Fc Function of Immunoglobulin (2.7.9) by using tetanus toxoid as antigen. Pharmeuropa Scientific Notes, 2006
