Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add filters

Language
Document Type
Year range
1.
medrxiv; 2024.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2024.02.01.24302052

ABSTRACT

The HIPRA-HH-2 was a multicentre, randomized, active-controlled, double-blind, non-inferiority phase IIb clinical trial to compare the immunogenicity and safety of a heterologous booster with PHH-1V adjuvanted recombinant vaccine versus a homologous booster with mRNA vaccine. Interim results showed a strong humoral and cellular immune response against the SARS-CoV-2 Wuhan-Hu-1 strain and the Beta, Delta, and Omicron BA.1 variants up to day 98 after dosing. Here we report that these humoral and cellular responses after PHH-1V dosing are sustained up to 6 months. These results are observed both when including or not participants who reported SARS-CoV-2 infection and in a high-risk population ([≥]65 years). Additional analysis revealed a non-inferiority of PHH-1V booster in eliciting neutralizing antibodies also for SARS-CoV-2 Omicron XBB.1.5 when compared to mRNA vaccine after 6 months. The PHH-1V vaccine provides long-lasting protection against a wide variety of SARS-CoV-2 emerging variants to prevent severe COVID-19. ClinicalTrials.gov Identifier: NCT05142553


Subject(s)
COVID-19
2.
medrxiv; 2022.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2022.07.05.22277210

ABSTRACT

Summary Background A SARS-CoV-2 protein-based heterodimer vaccine, PHH-1V, has been shown to be safe and well-tolerated in healthy young adults in a first-in-human, Phase I/IIa study dose-escalation trial. Here, we report the interim results of the Phase IIb HH-2, where the immunogenicity and safety of a heterologous booster with PHH-1V is assessed versus a homologous booster with BNT162b2 at 14 and 98 days after vaccine administration. Methods The HH-2 study is an ongoing multicentre, randomised, active-controlled, double-blind, non-inferiority Phase IIb trial, where participants 18 years or older who had received two doses of BNT162b2 were randomly assigned in a 2:1 ratio to receive a booster dose of vaccine – either heterologous (PHH-1V group) or homologous (BNT162b2 group) – in 10 centres in Spain. Eligible subjects were allocated to treatment stratified by age group (18-64 versus ≥65 years) with approximately 10% of the sample enrolled in the older age group. The endpoints were humoral immunogenicity measured by changes in levels of neutralizing antibodies against the ancestral Wuhan-Hu-1 strain and different variants of SARS-CoV-2 after the PHH-1V or the BNT162b2 boost, the T-cell responses towards the SARS-CoV-2 spike glycoprotein peptides and the safety and tolerability of PHH-1V as a boost. This study is ongoing and is registered with ClinicalTrials.gov, NCT05142553 . Findings From 15 November 2021, 782 adults were randomly assigned to PHH-1V (n=522) or BNT162b2 (n=260) boost vaccine groups. The geometric mean titre (GMT) ratio of neutralizing antibodies on days 14 and 98, shown as BNT162b2 active control versus PHH-1V, was, respectively, 1·68 (p<0·0001) and 0·87 (p=0·43) for the ancestral Wuhan-Hu-1 strain; 0·61 (p<0·0001) and 0·57 (p=0·0064) for the beta variant; 1·01 (p=0·89) and 0·52 (p=0·0003) for the delta variant; and 0·59 (p=<0·0001) and 0·56 (p=0·0026) for the omicron variant. Additionally, PHH-1V as a booster dose induced a significant increase of CD4 + and CD8 + T-cells expressing IFN-γ on day 14. There were 458 participants who experienced at least one adverse event (89·3%) in the PHH-1V and 238 (94·4%) in the BNT162b2 group. The most frequent adverse events were injection site pain (79·7% and 89·3%), fatigue (27·5% and 42·1%) and headache (31·2 and 40·1%) for the PHH-1V and the BNT162b2 groups, respectively. A total of 52 COVID-19 cases occurred from day 14 post-vaccination (10·14%) for the PHH-1V group and 30 (11·90%) for the BNT162b2 group (p=0·45), and none of the subjects developed severe COVID-19. Interpretation Our interim results from the Phase IIb HH-2 trial show that PHH-1V as a heterologous booster vaccine, when compared to BNT162b2, elicits a strong and sustained neutralizing antibody response against Wuhan-Hu-1 strain, and a superior one concerning the previous circulating beta and delta SARS-CoV-2 variants, as well as the currently circulating omicron. Moreover, the PHH-1V boost also induces a strong and balanced T-cell response. Concerning the safety profile, subjects in the PHH-1V group report significantly fewer adverse events than those in the BNT162b2 group, most of mild intensity, and both vaccine groups present comparable COVID-19 breakthrough cases, none of them severe. Funding HIPRA SCIENTIFIC, S.L.U.


Subject(s)
COVID-19
3.
Frauke Degenhardt; David Ellinghaus; Simonas Juzenas; Jon Lerga-Jaso; Mareike Wendorff; Douglas Maya-Miles; Florian Uellendahl-Werth; Hesham ElAbd; Malte C. Ruehlemann; Jatin Arora; Onur oezer; Ole Bernt Lenning; Ronny Myhre; May Sissel Vadla; Eike Matthias Wacker; Lars Wienbrandt; Aaron Blandino Ortiz; Adolfo de Salazar; Adolfo Garrido Chercoles; Adriana Palom; Agustin Ruiz; Alberto Mantovani; Alberto Zanella; Aleksander Rygh Holten; Alena Mayer; Alessandra Bandera; Alessandro Cherubini; Alessandro Protti; Alessio Aghemo; Alessio Gerussi; Alexander Popov; Alfredo Ramirez; Alice Braun; Almut Nebel; Ana Barreira; Ana Lleo; Ana Teles; Anders Benjamin Kildal; Andrea Biondi; Andrea Ganna; Andrea Gori; Andreas Glueck; Andreas Lind; Anke Hinney; Anna Carreras Nolla; Anna Ludovica Fracanzani; Annalisa Cavallero; Anne Ma Dyrhol-Riise; Antonella Ruello; Antonio Julia; Antonio Muscatello; Antonio Pesenti; Antonio Voza; Ariadna Rando-Segura; Aurora Solier; Beatriz Cortes; Beatriz Mateos; Beatriz Nafria-Jimenez; Benedikt Schaefer; Bjoern Jensen; Carla Bellinghausen; Carlo Maj; Carlos Ferrando; Carmen de la Horrra; Carmen Quereda; Carsten Skurk; Charlotte Thibeault; Chiara Scollo; Christian Herr; Christoph D. Spinner; Christoph Lange; Cinzia Hu; Clara Lehmann; Claudio Cappadona; Clinton Azuure; - COVICAT study group; - Covid-19 Aachen Study (COVAS); Cristiana Bianco; Cristina Sancho; Dag Arne Lihaug Hoff; Daniela Galimberti; Daniele Prati; David Haschka; David Jimenez; David Pestana; David Toapanta; Elena Azzolini; Elio Scarpini; Elisa T. Helbig; Eloisa Urrechaga; Elvezia Maria Paraboschi; Emanuele Pontali; Enric Reverter; Enrique J. Calderon; Enrique Navas; Erik Solligard; Ernesto Contro; Eunate Arana; Federico Garcia; Felix Garcia Sanchez; Ferruccio Ceriotti; Filippo Martinelli-Boneschi; Flora Peyvandi; Florian Kurth; Francesco Blasi; Francesco Malvestiti; Francisco J. Medrano; Francisco Mesonero; Francisco Rodriguez-Frias; Frank Hanses; Fredrik Mueller; Giacomo Bellani; Giacomo Grasselli; Gianni Pezzoli; Giorgio Costantino; Giovanni Albano; Giuseppe Bellelli; Giuseppe Citerio; Giuseppe Foti; Giuseppe Lamorte; Holger Neb; Ilaria My; Ingo Kurth; Isabel Hernandez; Isabell Pink; Itziar de Rojas; Ivan Galvan-Femenia; Jan C. Holter; Jan Egil Egil Afset; Jan Heyckendorf; Jan Damas; Jan Kristian Rybniker; Janine Altmueller; Javier Ampuero; Jesus M. Banales; Joan Ramon Badia; Joaquin Dopazo; Jochen Schneider; Jonas Bergan; Jordi Barretina; Joern Walter; Jose Hernandez Quero; Josune Goikoetxea; Juan Delgado; Juan M. Guerrero; Julia Fazaal; Julia Kraft; Julia Schroeder; Kari Risnes; Karina Banasik; Karl Erik Mueller; Karoline I. Gaede; Koldo Garcia-Etxebarria; Kristian Tonby; Lars Heggelund; Laura Izquierdo-Sanchez; Laura Rachele Bettini; Lauro Sumoy; Leif Erik Sander; Lena J. Lippert; Leonardo Terranova; Lindokuhle Nkambule; Lisa Knopp; Lise Tuset Gustad; Lucia Garbarino; Luigi Santoro; Luis Tellez; Luisa Roade; Mahnoosh Ostadreza; Maider Intxausti; Manolis Kogevinas; Mar Riveiro-Barciela; Marc M. Berger; Mari E.K. Niemi; Maria A. Gutierrez-Stampa; Maria Grazia Valsecchi; Maria Hernandez-Tejero; Maria J.G.T. Vehreschild; Maria Manunta; Mariella D'Angio; Marina Cazzaniga; Marit M. Grimsrud; Markus Cornberg; Markus M. Noethen; Marta Marquie; Massimo Castoldi; Mattia Cordioli; Maurizio Cecconi; Mauro D'Amato; Max Augustin; Melissa Tomasi; Merce Boada; Michael Dreher; Michael J. Seilmaier; Michael Joannidis; Michael Wittig; Michela Mazzocco; Miguel Rodriguez-Gandia; Natale Imaz Ayo; Natalia Blay; Natalia Chueca; Nicola Montano; Nicole Ludwig; Nikolaus Marx; Nilda Martinez; - Norwegian SARS-CoV-2 Study group; Oliver A. Cornely; Oliver Witzke; Orazio Palmieri; - Pa COVID-19 Study Group; Paola Faverio; Paolo Bonfanti; Paolo Tentorio; Pedro Castro; Pedro M. Rodrigues; Pedro Pablo Espana; Per Hoffmann; Philip Rosenstiel; Philipp Schommers; Phillip Suwalski; Raul de Pablo; Ricard Ferrer; Robert Bals; Roberta Gualtierotti; Rocio Gallego-Duran; Rosa Nieto; Rossana Carpani; Ruben Morilla; Salvatore Badalamenti; Sammra Haider; Sandra Ciesek; Sandra May; Sara Bombace; Sara Marsal; Sara Pigazzini; Sebastian Klein; Selina Rolker; Serena Pelusi; Sibylle Wilfling; Silvano Bosari; Soren Brunak; Soumya Raychaudhuri; Stefan Schreiber; Stefanie Heilmann-Heimbach; Stefano Aliberti; Stephan Ripke; Susanne Dudman; - The Humanitas COVID-19 Task Forse; - The Humanitas Gavazzeni COVID-19 Task Force; Thomas Bahmer; Thomas Eggermann; Thomas Illig; Thorsten Brenner; Torsten Feldt; Trine Folseraas; Trinidad Gonzalez Cejudo; Ulf Landmesser; Ulrike Protzer; Ute Hehr; Valeria Rimoldi; Vegard Skogen; Verena Keitel; Verena Kopfnagel; Vicente Friaza; Victor Andrade; Victor Moreno; Wolfgang Poller; Xavier Farre; Xiaomin Wang; Yascha Khodamoradi; Zehra Karadeniz; Anna Latiano; Siegfried Goerg; Petra Bacher; Philipp Koehler; Florian Tran; Heinz Zoller; Eva C. Schulte; Bettina Heidecker; Kerstin U. Ludwig; Javier Fernandez; Manuel Romero-Gomez; Agustin Albillos; Pietro Invernizzi; Maria Buti; Stefano Duga; Luis Bujanda; Johannes R. Hov; Tobias L. Lenz; Rosanna Asselta; Rafael de Cid; Luca Valenti; Tom H. Karlsen; Mario Caceres; Andre Franke.
medrxiv; 2021.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2021.07.21.21260624

ABSTRACT

Due to the highly variable clinical phenotype of Coronavirus disease 2019 (COVID-19), deepening the host genetic contribution to severe COVID-19 may further improve our understanding about underlying disease mechanisms. Here, we describe an extended GWAS meta-analysis of 3,260 COVID-19 patients with respiratory failure and 12,483 population controls from Italy, Spain, Norway and Germany, as well as hypothesis-driven targeted analysis of the human leukocyte antigen (HLA) region and chromosome Y haplotypes. We include detailed stratified analyses based on age, sex and disease severity. In addition to already established risk loci, our data identify and replicate two genome-wide significant loci at 17q21.31 and 19q13.33 associated with severe COVID-19 with respiratory failure. These associations implicate a highly pleiotropic ~0.9-Mb 17q21.31 inversion polymorphism, which affects lung function and immune and blood cell counts, and the NAPSA gene, involved in lung surfactant protein production, in COVID-19 pathogenesis.


Subject(s)
COVID-19 , Respiratory Insufficiency
4.
biorxiv; 2020.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2020.12.22.423917

ABSTRACT

COVID-19 manifests with a wide diversity of clinical phenotypes characterized by dysfunctional and exaggerated host immune responses. Many results have been described on the status of the immune system of patients infected with SARS-CoV-2, but there are still aspects that have not been fully characterized. In this study, we have analyzed a cohort of patients with mild, moderate and severe disease. We performed flow cytometric studies and correlated the data with the clinical features and clinical laboratory values of patients. Both conventional and unsupervised data analyses concluded that patients with severe disease are characterized, among others, by a higher state of activation in all T cell subsets, higher expression of perforin and granzyme B in cytotoxic cells, expansion of adaptive NK cells and the accumulation of activated and immature dysfunctional monocytes which are identified by a low expression of HLA-DR and an intriguing abrupt change in the expression pattern of CD300 receptors. More importantly, correlation analysis showed a strong association between the alterations in the immune cells and the clinical signs of severity. These results indicate that patients with severe COVID-19 have a broad perturbation of their immune system, and they will help to understand the immunopathogenesis of severe COVID-19 as well as could be of special value for physicians to decide which specific therapeutic options are most effective for their patients.


Subject(s)
von Willebrand Disease, Type 3 , Sexual Dysfunction, Physiological , COVID-19 , Teratoma
SELECTION OF CITATIONS
SEARCH DETAIL