T cell responses, dendritic cells, vaccines, HIV-1
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Scopus Publications
Scopus Publications
Dolutegravir restores gut microbiota in late-stage HIV-1 unlike darunavir: an open-label, randomized clinical trial Francesc Català-Moll, Carlos Blázquez-Bondia, Judit Farré-Badia, Ferran Torres, Christian Manzardo, Eva Bonfill, Adrià Curran, Pere Domingo, Daniel Podzamczer, Lluís Force, Vicenç Falcó, Mariona Parera, Maria Casadellà, José Maria Miró, Marc Noguera-Julian, Roger Paredes, , , Alessandra Borgognone, Nel Marín, Oriol Careta, Valentina Triviño, , Anna Cruceta, Nuria Climent, Francisco Lozano, Montserrat Plana, Juan Ambrosioni, Cristina Rovira, Carmen Hurtado, Maria José Maleno, Alexy Inciarte, Anna Castelli, Emma Fernández, Carmen Ligero, Sandra Serrano, Maria Ángeles Marcos, Elisa Rubio, Jordi Vila, Elisa de Lazzari, Jose M. Gatell, Daniela Marlano-Barletta, , Paula Suanzes, Esteve Ribera, Ariadna Torrella, Bibiana Planas, , Mar Gutierrez, Gracia Mateo, Jèssica Muñoz, Ana García, Kanura Lamarca, Lucía Millan, Judit Fernández, Isabel Mur, Noemí Corbacho, M. Ema Molas, , Maria Saumoy, Laura Acerete, Nerea Rozas, Elena Ferrer, Benito Garcia, Maria Silvana Diyacovo, Josefa Torres, Ana Silva, Juan Manuel Tiraboschi, Arkaitz Imaz, Cristina Padilla, , Pilar Barrufet, Xavier Boquet, Gloria Sempere Nature Communications, 2026 Late presentation of HIV-1 infection is linked to gut dysbiosis, impaired immune reconstitution, excess inflammation, immune activation, and increased morbidity and mortality. It is unclear if antiretroviral therapy initiation can reverse HIV-associated gut dysbiosis at all, or if specific antiretroviral regimens are more effective in restoring the gut microbiota than others. This has important implications for the long-term health of individuals with HIV. In this multicenter, open-label, randomized clinical trial (NCT02337322), 88 antiretroviral-naïve individuals with advanced HIV-1 infection (median CD4+ T cells of 34 cells/mm3) were randomized (1:1) to initiate lamivudine/abacavir plus either dolutegravir or ritonavir-boosted darunavir, and were followed for 2 years. Both groups had similar HIV-1 suppression rates and recovery of CD4+ T cells. However, treatment with dolutegravir led to increased gut microbial richness and diversity and enrichment of specific microbial taxa and metabolic pathways. These changes were associated with reduced inflammation and lower immune activation, outcomes that did not occur with darunavir/ritonavir. After two years, participants on dolutegravir-based therapy had gut microbiota profiles more closely resembling those of people without HIV, compared to individuals taking darunavir/ritonavir. In summary, dolutegravir-based therapy restores the gut microbiota more effectively than darunavir/ritonavir in patients who present late with HIV. Advanced HIV-1 infection is associated with gut dysbiosis, and it’s not known whether this is reversed with antiviral therapy. The ADVANZ-4 MISTRAL trial shows that dolutegravir restores gut microbiota in late-stage HIV1 patients better than darunavir, and that recovery is linked to improved immune reconstitution.
Author Correction: Dolutegravir restores gut microbiota in late-stage HIV-1 unlike darunavir: an open-label, randomized clinical trial (Nature Communications, (2026), 17, 1, (2022), 10.1038/s41467-026-69846-7) Francesc Català-Moll, Carlos Blázquez-Bondia, Judit Farré-Badia, Ferran Torres, Christian Manzardo, Eva Bonfill, Adrià Curran, Pere Domingo, Daniel Podzamczer, Lluís Force, Vicenç Falcó, Mariona Parera, Maria Casadellà, José Maria Miró, Marc Noguera-Julian, Roger Paredes, , , Alessandra Borgognone, Nel Marín, Oriol Careta, Valentina Triviño, , Anna Cruceta, Nuria Climent, Francisco Lozano, Montserrat Plana, Juan Ambrosioni, Cristina Rovira, Carmen Hurtado, Maria José Maleno, Alexy Inciarte, Anna Castelli, Emma Fernández, Carmen Ligero, Sandra Serrano, Maria Ángeles Marcos, Elisa Rubio, Jordi Vila, Elisa de Lazzari, Jose M. Gatell, Daniela Malano-Barletta, , Paula Suanzes, Esteve Ribera, Ariadna Torrella, Bibiana Planas, , Mar Gutierrez, Gracia Mateo, Jèssica Muñoz, Ana García, Kanura Lamarca, Lucía Millan, Judit Fernández, Isabel Mur, Noemí Corbacho, M. Ema Molas, , Maria Saumoy, Laura Acerete, Nerea Rozas, Elena Ferrer, Benito Garcia, Maria Silvana Diyacovo, Josefa Torres, Ana Silva, Juan Manuel Tiraboschi, Arkaitz Imaz, Cristina Padilla, , Pilar Barrufet, Xavier Boquet, Gloria Sempere Nature Communications, 2026
Fingolimod increases cellular resistance to HIV-1 infection and limits viral reservoir size in peripheral CD4+ T-cells Elisa Moraga, Núria Climent, Alejandro Sánchez-Molina, Sònia Vicens-Artés, María José Maleno, Gabriel Valero López, Carlos Galera Peñaranda, Juan Ambrosioni, José M. Miró, Josep Mallolas, Helena Albendín-Iglesias, José Alcamí, Sonsoles Sánchez-Palomino Plos Pathogens, 2026 Background Fingolimod, a treatment for multiple sclerosis (MS), decreases autoreactive lymphocytes by lymph node sequestration. In vitro , fingolimod decreases HIV-1 infection and viral reservoir (VR) through SAMHD1 phosphorylation inhibition and reducing lymphocyte activation and CD4 expression. We identified an exceptional MS patient infected with HIV-1 (HIV+ MS+) while on fingolimod therapy and we have analyzed its impact on HIV-1 infection in vivo and ex vivo . Methods The case was the HIV+ MS+ patient. Controls were 20 PWH (HIV+ MS-), five HIV-negative donors (HIV-MS) and three HIV-negative MS patients treated with fingolimod (HIV-MS+), as the case reported. VR was quantified by IPDA and HIV-1 intracellular RNAs (icRNAs) by ddPCR in peripheral blood CD4 + T-cells. CD4 + T-cells were infected in vitro with an NL4.3-Renilla strain. Immunophenotype, activation markers and phosphorylated SAMHD1 levels were determined by flow cytometry. Findings At diagnosis, HIV+ MS+ viral load was nine-fold lower than HIV+ MS- treated at similar Fiebig stage. One year after ART, HIV+ MS+ showed lower intact and defective VR than the HIV+ MS- control group (28-and six-fold decrease respectively). After three years on ART no intact proviruses were detected in HIV+ MS+ . HIV-1 in vitro infection was decreased in HIV+ MS+ and HIV- MS + vs HIV+ MS- and HIV-MS-. CD4 + T-cells levels from fingolimod treated patients were lower and showed decreased CD4 expression, lymphocyte activation and SAMHD1 phosphorylation vs HIV- MS-. icRNAs were significantly increased after T-cell activation in the HIV+ MS-, while they were barely detected at resting and activated HIV+ MS+ CD4 + T-cells. Conclusions We describe a strong restriction to HIV-1 infection and replication in vivo and ex vivo leading to indetectable intact VR in HIV+ MS+ after three years of ART. Potential mechanisms of restriction are CD4 downregulation, T-cell activation inhibition, and SAMHD1 activity enhancement.
Immune reconstitution in very advanced HIV patients treated with dolutegravir vs. darunavir-based triple antiretroviral therapy: the Advanz-4 randomized clinical trial Jose M. Miro, Ferran Torres, Christian Manzardo, Eva Bonfill, Adrià Curran, Pere Domingo, Daniel Podzamczer, Roger Paredes, Lluis Force, Vicenç Falco, Mar Gutierrez, Maria Saumoy, Anna Castelli, Alexy Inciarte, Cristina Rovira, Anna Cruceta, Carmen Hurtado, Núria Climent, Francisco Lozano, Montserrat Plana, Jose M. Miro, Ferran Torres, Christian Manzardo, Eva Bonfill, Anna Cruceta, Núria Climent, Francisco Lozano, Montserrat Plana, Juan Ambrosioni, Cristina Rovira, Carmen Hurtado, Maria José Maleno, Alexy Inciarte, Anna Castelli, Emma Fernández, Carmen Ligero, Sandra Serrano, Maria Ángeles Marcos, Elisa Rubio, Jordi Vila, Elisa de Lazzari, Jose M. Gatell, Esteve Ribera, Adrià Curran, Paula Suanzes, Ariadna Torrella, Bibiana Planas, Vicenç Falcó, Pere Domingo, Mar Gutierrez, Gracia Mateo, Jèssica Muñoz, Ana García, Kanura Lamarca, Lucía Millan, Judit Fernández, Isabel Mur, Noemí Corbacho, M. Ema Molas, Daniel Podzamczer, Maria Saumoy, Laura Acerete, Nerea Rozas, Elena Ferrer, Antonia Vila, Benito Garcia, Maria Silvana Diyacovo, Josefa Torres, Ana Silva, Juan Manuel Tiraboschi, Arkaitz Imaz, Cristina Padilla, Antonio Moreno, Roger Paredes, Guillem Sirera, Boris Revollo, Beatriz Mothe, José Ramón Santos, Anna Chamorro, Lluis Force, Pilar Barrufet, Xavier Boquet, Gloria Sempere, Hernando Knobel, Judith Villar, Francesc Vidal, Jose R. Arribas Clinical Microbiology and Infection, 2026
Hodgkin and non-Hodgkin lymphomas in the post-antiretroviral therapy era according to HIV virological suppression Teresa Aldámiz‐Echevarria, Francisco Tejerina, Chiara Fanciulli, Cristina Diez, Leire Perez, José Maria Bellón, Nuria Espinosa, Santiago Moreno Guillén, Maria del Mar Arcos‐Rueda, Marta Montero‐Alonso, Lucio García‐Fraile, Victor Asensi, Marian Fernández López, Diana Corona‐Mata, Alfonso Cabello‐Úbeda, Meritxell Gavaldà Manso, Jose Antonio Iribarren, Laura Pérez‐Martínez, María Remedios Alemán Valls, Irene Portilla‐Tamarit, Joaquim Peraire, Inés Suárez‐García, Mar Masiá, María José Núñez Orantos, Ángela Gutiérrez Liarte, Arkaitz Imaz, Cristina Hernández Gutiérrez, Maria Tasias Pitarch, Marta Rava, CoRIS Cohort HIV Medicine, 2026 Objectives Lymphomas remain among the most frequent HIV‐associated malignancies, with risk persisting despite effective virological control. This study describes the clinical, epidemiological and prognostic characteristics of lymphomas (both Hodgkin [HL] and non‐Hodgkin [NHL]) in people living with HIV (PLWH), according to virological suppression at diagnosis and assesses lymphoma‐related mortality at 1 year and overall survival at 5 years. Methods We conducted a multicentre retrospective study including PLWH from the Spanish CoRIS cohort, who were diagnosed with lymphoma between 2004 and 2022 and had HIV viral load data at diagnosis. Virological suppression was defined as HIV‐1 RNA <100 copies/mL within the 6 months prior to and 1 month following lymphoma diagnosis. Results Among 18 573 PLWH included in CoRIS, 291 developed lymphoma, with virological data available for 245 individuals, of whom 49 (20%) had virological suppression. People with detectable HIV viral load had lower CD4 counts (median 180 cells/mm 3 [IQR 80–330] vs. 371 cells/mm 3 [IQR 202–583], p < 0.001) and more advanced Ann Arbor stage (stage III–IV: 82.0% vs. 64.1%, p = 0.027) compared with those with virological suppression. Despite this, they showed similar treatment response (complete remission: 67.1% vs. 76.2%) and relapse rates (16.3% vs. 18.4%, p = 0.779). Furthermore, virological suppression was not independently associated with 1‐year lymphoma‐specific or 5‐year overall survival. Conclusions In PLWH diagnosed with lymphoma, prognosis is independent of HIV virological status at diagnosis. These findings support that lymphoma management in PLWH should be guided by standard oncological criteria, alongside antiretroviral therapy, regardless of HIV viral suppression status.
Cellular senescence meets infection: highlights from the 10th annual International Cell Senescence Association (ICSA) conference, Rome 2025 Stefanie Deinhardt-Emmer, François Trottein, Federico Armando, Rocío M. Tolosa, Andrea Rodríguez-Agustín, Victor Casanova, Núria Climent, Pamela Martinez-Orellana, Edoardo Scarpa, Marisa Gariglio, Marco De Andrea Aging, 2025 , p21, and NF-κB pathways. Evidence across immune, epithelial, and neuronal systems have revealed that senescence contributes to impaired regeneration, persistent inflammation, and altered host-pathogen dynamics. Emerging therapeutic data suggest that senolytic or senomorphic strategies may alleviate infection-associated tissue damage. Collectively, the conference highlighted IDS as an expanding frontier that bridges infection biology and aging research, emphasizing its potential relevance for prevention and therapy of chronic age-related disease.
Intracellular HIV-1 Tat regulator induces epigenetic changes in the DNA methylation landscape Andrea Rodríguez-Agustín, Rubén Ayala-Suárez, Francisco Díez-Fuertes, María José Maleno, Izar de Villasante, Angelika Merkel, Mayte Coiras, Víctor Casanova, José Alcamí, Núria Climent Frontiers in Immunology, 2025 IntroductionThe HIV regulatory protein Tat enhances viral transcription and also modifies host gene expression, affecting cell functions like cell cycle and apoptosis. Residual expression of Tat protein is detected in blood and other tissues even under antiretroviral treatment. Cohort studies have indicated that, despite virologic suppression, people with HIV (PWH) are at increased risk of comorbidities linked to chronic inflammation, accelerated immune ageing, and cellular senescence, sometimes associated with abnormal genomic methylation patterns. We analysed whether Tat influences DNA methylation and subsequently impacts the transcriptional signature, contributing to inflammation and accelerated ageing.MethodsWe transfected Jurkat cells with full-length Tat (Tat101), Tat’s first exon (Tat72), or an empty vector (TetOFF). We assessed DNA methylation modifications via the Infinium MethylationEPIC array, and we evaluated transcriptomic alterations through RNA-Seq. Methylation levels in gene promoters or body regions were correlated to their expression data, and subsequently, we performed an overrepresentation analysis to identify the biological terms containing differentially methylated and expressed genes.ResultsTat101 expression caused significant hyper- and hypomethylation changes at individual CpG sites, resulting in slightly global DNA hypermethylation. Methylation changes at gene promoters and bodies resulted in altered gene expression, specifically regulating gene transcription in 5.1% of differentially expressed genes (DEGs) in Tat101- expressing cells. In contrast, Tat72 had a minimal impact on this epigenetic process. The observed differentially methylated and expressed genes were involved in inflammatory responses, lipid antigen presentation, and apoptosis.DiscussionTat expression in HIV infection may constitute a key epigenetic modelling actor that contributes to HIV pathogenesis and chronic inflammation. Clinical interventions targeting Tat blockade may reduce chronic inflammation and cellular senescence related to HIV infection comorbidities.
HIV-Tat upregulates the expression of senescence biomarkers in CD4+ T-cells Víctor Casanova, Andrea Rodríguez-Agustín, Rubén Ayala-Suárez, Elisa Moraga, María José Maleno, Josep Mallolas, Esteban Martínez, Sonsoles Sánchez-Palomino, José M. Miró, José Alcamí, Núria Climent Frontiers in Immunology, 2025 IntroductionCurrent antiretroviral therapy (ART) for HIV infection reduces plasma viral loads to undetectable levels and has increased the life expectancy of people with HIV (PWH). However, this increased lifespan is accompanied by signs of accelerated aging and a higher prevalence of age-related comorbidities. Tat (Trans-Activator of Transcription) is a key protein for viral replication and pathogenesis. Tat is encoded by 2 exons, with the full-length Tat ranging from 86 to 101 aa (Tat101). Introducing a stop codon in position 73 generates a 1 exon, synthetic 72aa Tat (Tat72). Intracellular, full-length Tat activates the NF-κB pro-inflammatory pathway and increases antiapoptotic signals and ROS generation. These effects may initiate a cellular senescence program, characterized by cell cycle arrest, altered cell metabolism, and increased senescence-associated secretory phenotype (SASP) mediator release However, the precise role of HIV-Tat in inducing a cellular senescence program in CD4+ T-cells is currently unknown.MethodsJurkat Tetoff cell lines stably transfected with Tat72, Tat101, or an empty vector were used. Flow cytometry and RT-qPCR were used to address senescence biomarkers, and 105 mediators were assessed in cell supernatants with an antibody-based membrane array. Key results obtained in Jurkat-Tat cells were addressed in primary, resting CD4+ T-cells by transient electroporation of HIV-Tat-FLAG plasmid DNA.ResultsIn the Jurkat cell model, expression of Tat101 increased the levels of the senescence biomarkers BCL-2, CD87, and p21, and increased the release of sCD30, PDGF-AA, and sCD31, among other factors. Tat101 upregulated CD30 and CD31 co-expression in the Jurkat cell surface, distinguishing these cells from Tat72 and Tetoff Jurkats. The percentage of p21+, p16+, and γ-H2AX+ cells were higher in Tat-expressing CD4+ T-cells, detected as a FLAG+ population compared to their FLAG- (Tat negative) counterparts. Increased levels of sCD31 and sCD26 were also detected in electroporated CD4+ T-cell supernatants.DiscussionIntracellular, full-length HIV-Tat expression increases several senescence biomarkers in Jurkat and CD4+ T-cells, and SASP/Aging mediators in cell supernatants. Intracellular HIV-Tat may initiate a cellular senescence program, contributing to the premature aging phenotype observed in PWH.
Pharmacokinetics, the Immunological Impact, and the Effect on HIV Ex-Vivo Infectivity of Maraviroc, Raltegravir, and Lopinavir in Men Who Have Sex with Men Using Postexposure Prophylaxis Lorna Leal, Alberto C. Guardo, Luis M. Bedoya, Cristina Rodríguez de Miguel, Núria Climent, Cristina Rovira, Manuela Beltrán, Josep Llach, Jose Alcamí, Angela D.M. Kashuba, Jose M. Gatell, Montserrat Plana, Felipe García AIDS Research and Human Retroviruses, 2023 Most of the studies using the colorectal tissue explants challenge model have been conducted after one single-dose and before reaching a steady-state. We consider that longer exposure as in 28-day post-exposure prophylaxis (PEP) course and in an at-risk setting, such as after a sexual risk exposure to HIV could give us valuable information about these drugs. In a substudy we assessed pharmacokinetics, changes on immune system and ex-vivo rectal mucosal susceptibility to HIV-1 infection after taking maraviroc (MVC), raltegravir (RAL) and ritonavir-boosted lopinavir (LPV/r) PEP-based regimens in 30 men who have sex with men. Participants received 28 days of twice-daily MVC (n=11), RAL (n=10) or LPV/r (n=9) all with tenofovir/emtricitabine backbone. Blood, rectal fluid (RF) and rectal tissue (RT) samples were collected at day 7, 28 and 90 after starting PEP. The samples obtained at day 90 were considered baseline. All studied antiretrovirals were quantifiable at 7 and 28 days in all tissues. Activation markers were increased in CD4 mucosal mononuclear cells (MMC) after 28 days of MVC: CD38+ 68.5 vs 85.1, p=0.008 and CD38+DR+ 16.1 vs 26.7, p=0.008. Exposure to MVC at both end-points (7 and 28 days) was associated with significant suppression of HIV-1BAL (p=0.005 and p=0.028) but we did not observe this effect with RAL or LPV/r. Merging together changes in MMC in all arms, we found a positive correlation in the CD8 T-cell lineage between the infectivity at day 7 and activation (CD38+ r=0.43, p=0.025, DR+ r=0.547, p=0.003 and 38+DR+ r=0.526, p=0.05), senescence (CD57+CD28- r=0.479, p=0.012), naïve cells (RA+CCR7+ r=0.484, p=0.01) and CCR5 expression (r=0.593, p=0.001). We conclude that maraviroc in combination with tenofovir/emtricitabine was associated with viral suppression in rectal explants and that overall ex-vivo HIV infectivity correlated with activation and senescence in CD8 mucosal mononuclear cells.
Immunomodulatory Activity of the Tyrosine Kinase Inhibitor Dasatinib to Elicit NK Cytotoxicity against Cancer, HIV Infection and Aging Andrea Rodríguez-Agustín, Víctor Casanova, Judith Grau-Expósito, Sonsoles Sánchez-Palomino, José Alcamí, Núria Climent Pharmaceutics, 2023 Tyrosine kinase inhibitors (TKIs) have been extensively used as a treatment for chronic myeloid leukemia (CML). Dasatinib is a broad-spectrum TKI with off-target effects that give it an immunomodulatory capacity resulting in increased innate immune responses against cancerous cells and viral infected cells. Several studies reported that dasatinib expanded memory-like natural killer (NK) cells and γδ T cells that have been related with increased control of CML after treatment withdrawal. In the HIV infection setting, these innate cells are associated with virus control and protection, suggesting that dasatinib could have a potential role in improving both the CML and HIV outcomes. Moreover, dasatinib could also directly induce apoptosis of senescence cells, being a new potential senolytic drug. Here, we review in depth the current knowledge of virological and immunogenetic factors associated with the development of powerful cytotoxic responses associated with this drug. Besides, we will discuss the potential therapeutic role against CML, HIV infection and aging.
Immunological and virological findings in a patient with exceptional post-treatment control: a case report Núria Climent, Juan Ambrosioni, Tània González, Cristina Xufré, Maria Casadellà, Marc Noguera-Julian, Roger Paredes, Montserrat Plana, Judith Grau-Expósito, Josep Mallolas, José Alcamí, Sonsoles Sánchez-Palomino, José M Miró, David Nicolás, Cristina Xufré, Carmen Hurtado, Cristina Rovira, Omar Sued, Mercé Brunet, María López-Diéguez, Christian Manzardo, Fernando Agüero, Montserrat Tuset, Alberto C Guardo, Maria A. Marcos, María del Mar Mosquera, M. Ángeles Muñoz-Fernández, Miguel Caballero, Carmen Ligero, Emma Fernández, M. Ángeles Marcos, José M Gatell, Elisa de Lazzari, Teresa Gallart, Ana Fernandez-Tenreiro, Begoña Gomez, Leire Berrocal, David Nicolás, Cristina Xufré, Carmen Hurtado, Cristina Rovira, Omar Sued, Mercé Brunet, María López-Diéguez, Christian Manzardo, Fernando Agüero, Montserrat Tuset, Alberto C Guardo, Maria A. Marcos, María del Mar Mosquera, M. Ángeles Muñoz-Fernández, Miguel Caballero, Carmen Ligero, Emma Fernández, M. Ángeles Marcos, José M Gatell, Elisa de Lazzari, Teresa Gallart, Ana Fernandez-Tenreiro, Begoña Gomez, Leire Berrocal Lancet HIV, 2023
Natural killer cells act as an extrinsic barrier for in vivo reprogramming Elena Melendez, Dafni Chondronasiou, Lluc Mosteiro, Jaime Martínez de Villarreal, Marcos Fernández-Alfara, Cian J. Lynch, Dirk Grimm, Francisco X. Real, José Alcamí, Núria Climent, Federico Pietrocola, Manuel Serrano Development Cambridge, 2022
APOBEC3G rescues cells from the deleterious effects of DNA damage Alexander Botvinnik, Pushkar Shivam, Yoav Smith, Gunjan Sharma, Udy Olshevsky, Ofra Moshel, Zakhariya Manevitch, Nuria Climent, Harold Oliva, Elena Britan‐Rosich, Moshe Kotler FEBS Journal, 2021
Lower expression of plasma-derived exosome miR-21 levels in HIV-1 elite controllers with decreasing CD4 T cell count María J. Ruiz-de-León, María A. Jiménez-Sousa, Santiago Moreno, Marcial García, Mónica Gutiérrez-Rivas, Agathe León, Marta Montero-Alonso, Juan González-García, Salvador Resino, Norma Rallón, José M. Benito, Alejandro Vallejo, J.M. Benito, N. Rallón, C. Restrepo, N. Rodríguez, M. García, A. Cabello, M. Gorgolas, S. Resino, V. Briz, M.A. Jiménez, M.S. Vázquez, A. Fernández, P. García, M.A. Muñoz, J. Sánchez, J.L. Jiménez, D. Sepúlveda, I. García, I. Consuegra, A. León, M. Arnedo, M. Plana, N. Climent, F. García, E. Ruiz-Mateos, B. Domínguez, L. Tarancón, M. Rafii-El-Idrissi, M.J. Polaino, M. Genebat, P. Viciana, M. Leal, F. Vidal, E. Rodríguez, C. Viladés, J. Peraire, J. Romero, C Rodríguez, M. Vera, J. Esté, E. Ballana, M.A. Martínez, S. Franco, M. Nevot, A. Vallejo, S. Moreno, M. Pernas, C. Casado, C. López, L. Capa, M. Pérez, J. Alcami, R. Sanjuán, J.M. Cueva, R. Delgado, O. Sierra, A. Valenzuela Journal of Microbiology Immunology and Infection, 2019
Safety and immunogenicity of a modified vaccinia Ankara-based HIV-1 vaccine (MVA-B) in HIV-1-infected patients alone or in combination with a drug to reactivate latent HIV-1 B. Mothe, N. Climent, M. Plana, M. Rosas, J. L. Jimenez, M. A. Munoz-Fernandez, M. C. Puertas, J. Carrillo, N. Gonzalez, A. Leon, J. Pich, J. A. Arnaiz, J. M. Gatell, B. Clotet, J. Blanco, J. Alcami, J. Martinez-Picado, C. Alvarez-Fernandez, S. Sanchez-Palomino, A. C. Guardo, J. Pena, J. M. Benito, N. Rallon, C. E. Gomez, B. Perdiguero, J. Garcia-Arriaza, M. Esteban, J. C. Lopez Bernaldo de Quiros, C. Brander, F. Garcia, on behalf of the RISVAC Study Group, B. Mothe, P. Cobarsi, M. Rosas, M. C. Puertas, J. Carrillo, J. Blanco, J. Martinez-Picado, B. Clotet, C. Brander, N. Climent, M. Plana, C. Alvarez, S. Sanchez, A. Leon, J. Pich, J. A. Arnaiz, L. Leal, B. Torres, C. Lucero, A. C. Guardo, J. M. Gatell, F. Garcia, J. L. Jimenez, M. A. Munoz-Fernandez, J. C. Lopez Bernaldo de Quiros, M. Esteban, C. E. Gomez, B. Perdiguero, J. Garcia-Arriaza, V. Cepeda, C. O. Sanchez-Sorzano, N. Gonzalez, J. Alcami, L. Jimenez, J. M. Benito, N. Rallon, J. Pena, and Journal of Antimicrobial Chemotherapy, 2014
Ex vivo production of autologous whole inactivated HIV-1 for clinical use in therapeutic vaccines Cristina Gil, Núria Climent, Felipe García, Carmen Hurtado, Sara Nieto-Márquez, Agathe León, M Teresa García, Cristina Rovira, Laia Miralles, Judith Dalmau, Tomás Pumarola, Manel Almela, Javier Martinez-Picado, Jeffrey D. Lifson, Laura Zamora, José M. Miró, Christian Brander, Bonaventura Clotet, Teresa Gallart, José M. Gatell Vaccine, 2011
A therapeutic dendritic cell-based vaccine for HIV-1 infection Felipe García, Núria Climent, Lambert Assoumou, Cristina Gil, Nuria González, José Alcamí, Agathe León, Joan Romeu, Judith Dalmau, Javier Martínez-Picado, Jeff Lifson, Brigitte Autran, Dominique Costagliola, Bonaventura Clotet, Josep M Gatell, Montserrat Plana, Teresa Gallart, and Journal of Infectious Diseases, 2011
Therapeutic immunization with dendritic cells loaded with heat-inactivated autologous HIV-1 in patients with chronic HIV-1 infection Felipe García, Merylene Lejeune, Nuria Climent, Cristina Gil, José Alcamí, Vanessa Morente, Llucia Alós, Alba Ruiz, Javier Setoain, Emilio Fumero, Pedro Castro, Anna López, Anna Cruceta, Carlos Piera, Eric Florence, Arturo Pereira, Agnes Libois, Nuria González, Meritxell Guilá, Miguel Caballero, Francisco Lomeña, Joan Joseph, José M Miró, Tomás Pumarola, Montserrat Plana, José M Gatell, Teresa Gallart Journal of Infectious Diseases, 2005
Generation of human monoclonal antibodies from HIV-infected individuals Inmunologia, 2004
