Search

Your search keyword '"Coscollá, Mireia"' showing total 159 results
Start Over Author "Coscollá, Mireia"
159 results on '"Coscollá, Mireia"'

2. VIPERA: Viral Intra-Patient Evolution Reporting and Analysis

Author

Ministerio de Ciencia e Innovación (España), European Research Council, Generalitat Valenciana, Ministerio de Economía y Competitividad (España), European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Consejo Superior de Investigaciones Científicas (España), Álvarez-Herrera, Miguel [0000-0002-7922-3180], Sevilla, Jordi [0009-0001-3352-1537], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Vergara, Andrea [0000-0002-5046-4490], Vila, Jordi [0000-0002-8025-3926], Cano-Jiménez, Pablo [0009-0007-4773-3198], González-Candelas, Fernando [0000-0002-0879-5798], Comas, Iñaki [0000-0001-5504-9408], Coscollá, Mireia [0000-0003-0752-0538], Álvarez-Herrera, Miguel, Sevilla, Jordi, Ruiz-Rodríguez, Paula, Vergara, Andrea, Vila, Jordi, Cano-Jiménez, Pablo, González-Candelas, Fernando, Comas, Iñaki, Coscollá, Mireia, Ministerio de Ciencia e Innovación (España), European Research Council, Generalitat Valenciana, Ministerio de Economía y Competitividad (España), European Commission, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Consejo Superior de Investigaciones Científicas (España), Álvarez-Herrera, Miguel [0000-0002-7922-3180], Sevilla, Jordi [0009-0001-3352-1537], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Vergara, Andrea [0000-0002-5046-4490], Vila, Jordi [0000-0002-8025-3926], Cano-Jiménez, Pablo [0009-0007-4773-3198], González-Candelas, Fernando [0000-0002-0879-5798], Comas, Iñaki [0000-0001-5504-9408], Coscollá, Mireia [0000-0003-0752-0538], Álvarez-Herrera, Miguel, Sevilla, Jordi, Ruiz-Rodríguez, Paula, Vergara, Andrea, Vila, Jordi, Cano-Jiménez, Pablo, González-Candelas, Fernando, Comas, Iñaki, and Coscollá, Mireia

Abstract

Viral mutations within patients nurture the adaptive potential of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during chronic infections, which are a potential source of variants of concern. However, there is no integrated framework for the evolutionary analysis of intra-patient SARS-CoV-2 serial samples. Herein, we describe Viral Intra-Patient Evolution Reporting and Analysis (VIPERA), a new software that integrates the evaluation of the intra-patient ancestry of SARS-CoV-2 sequences with the analysis of evolutionary trajectories of serial sequences from the same viral infection. We have validated it using positive and negative control datasets and have successfully applied it to a new case, which revealed population dynamics and evidence of adaptive evolution. VIPERA is available under a free software license at https://github.com/PathoGenOmics-Lab/VIPERA.

Published
2024

5. VIPERA: Viral Intra-Patient Evolution Reporting and Analysis

Author

European Commission, Consejo Superior de Investigaciones Científicas (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia e Innovación (España), Generalitat Valenciana, European Research Council, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía, Industria y Competitividad (España), Álvarez-Herrera, Miguel [0000-0002-7922-3180], Sevilla, Jordi [0009-0001-3352-1537], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Vergara, Andrea [0000-0002-5046-4490], Vila, Jordi [0000-0002-8025-3926], Cano-Jiménez, Pablo [0009-0007-4773-3198], González-Candelas, Fernando [0000-0002-0879-5798], Comas, Iñaki [0000-0001-5504-9408], Coscollá, Mireia [0000-0003-0752-0538], Álvarez-Herrera, Miguel, Sevilla, Jordi, Ruiz-Rodríguez, Paula, Vergara, Andrea, Vila, Jordi, Cano-Jiménez, Pablo, González-Candelas, Fernando, Comas, Iñaki, Coscollá, Mireia, European Commission, Consejo Superior de Investigaciones Científicas (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia e Innovación (España), Generalitat Valenciana, European Research Council, Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Economía, Industria y Competitividad (España), Álvarez-Herrera, Miguel [0000-0002-7922-3180], Sevilla, Jordi [0009-0001-3352-1537], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Vergara, Andrea [0000-0002-5046-4490], Vila, Jordi [0000-0002-8025-3926], Cano-Jiménez, Pablo [0009-0007-4773-3198], González-Candelas, Fernando [0000-0002-0879-5798], Comas, Iñaki [0000-0001-5504-9408], Coscollá, Mireia [0000-0003-0752-0538], Álvarez-Herrera, Miguel, Sevilla, Jordi, Ruiz-Rodríguez, Paula, Vergara, Andrea, Vila, Jordi, Cano-Jiménez, Pablo, González-Candelas, Fernando, Comas, Iñaki, and Coscollá, Mireia

Abstract

Viral mutations within patients nurture the adaptive potential of SARS-CoV-2 during chronic infections, which are a potential source of variants of concern. However, there is no integrated framework for the evolutionary analysis of intra-patient SARS-CoV-2 serial samples. Herein we describe VIPERA (Viral Intra-Patient Evolution Reporting and Analysis), a new software that integrates the evaluation of the intra-patient ancestry of SARS-CoV-2 sequences with the analysis of evolutionary trajectories of serial sequences from the same viral infection. It has been validated using positive and negative control datasets and successfully applied to a novel case, contributing to easy and automatic analysis of intra-patient SARS-CoV-2 sequences.

Published
2023

6. Impact of in vitro evolution on antigenic diversity of Mycobacterium bovis bacillus Calmette-Guerin (BCG)

Author

Copin, Richard, Coscollá, Mireia, Efstathiadis, Efstratios, Gagneux, Sebastien, and Ernst, Joel D

Subjects
Biomedical and Clinical Sciences, Immunology, Prevention, Tuberculosis Vaccine, Infectious Diseases, Rare Diseases, Immunization, Tuberculosis, Biotechnology, Vaccine Related, Infection, Good Health and Well Being, Amino Acid Substitution, Antigenic Variation, BCG Vaccine, DNA Copy Number Variations, Epitopes, T-Lymphocyte, Evolution, Molecular, Genome, Bacterial, Humans, Mycobacterium bovis, Phylogeny, Selection, Genetic, Mycobacterium bovis bacillus, Calmette-Guerin, In vitro evolution, Phylogenetic diversity, T cell epitopes, Mycobacterium bovis bacillus Calmette-Guerin, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Biomedical and clinical sciences, Health sciences
Abstract

Mycobacterium bovis bacillus Calmette-Guerin (BCG), the only vaccine currently used against tuberculosis, is an attenuated derivative of M. bovis that has been propagated in vitro for more than 40 years. We have previously reported that the experimentally-verified human T cell epitopes of the M. tuberculosis complex (MTBC) are the most conserved elements of the genome; whether immune recognition is the force driving the conservation of epitopes in the MTBC is unknown. Therefore, we sequenced the genomes of 12 BCG strains to determine whether T cell epitopes were under selection pressure during BCG in vitro evolution. We constructed a genome-wide phylogeny and refined the previously-determined BCG phylogeny. Notably, we identified a new cluster between BCG Japan and BCG Russia, and repositioned the relationships of several strains within the lineage. We also compared the sequence diversity of 1530 experimentally verified human T cell epitopes in the BCG vaccines with those in the MTBC. We found 23% of the known T cell epitopes are absent, and that the majority (82%) of the absent epitopes in BCG are contained in 6 proteins encoded in 2 regions of difference (RD) unique to BCG strains. We also found that T cell epitope sequences in BCG are more conserved than non-epitope sequences in the same gene. Finally, we find evidence that epitope sequence variation in BCG potentially affects human T cell recognition. These findings provide new insight into sequence variation in a slow-growing bacterium closely related to the MTBC that has been subjected to prolonged passage outside of a mammalian host, and indicate little difference in the extent of variation in vivo and in vitro.

Published
2014

7. Sequence Diversity in the pe_pgrs Genes of Mycobacterium tuberculosis Is Independent of Human T Cell Recognition

Author

Copin, Richard, Coscollá, Mireia, Seiffert, Salome N, Bothamley, Graham, Sutherland, Jayne, Mbayo, Georgetta, Gagneux, Sebastien, and Ernst, Joel D

Subjects
Rare Diseases, Genetics, Human Genome, Tuberculosis, Infectious Diseases, Aetiology, Underpinning research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Good Health and Well Being, Antigens, Bacterial, Bacterial Proteins, Computational Biology, DNA, Bacterial, Epitopes, T-Lymphocyte, Genetic Variation, Genotype, Humans, INDEL Mutation, Membrane Proteins, Molecular Sequence Data, Mycobacterium tuberculosis, Selection, Genetic, Sequence Analysis, DNA, T-Lymphocytes, Microbiology
Abstract

UnlabelledThe Mycobacterium tuberculosis genome includes the large family of pe_pgrs genes, whose functions are unknown. Because of precedents in other pathogens in which gene families showing high sequence variation are involved in antigenic variation, a similar role has been proposed for the pe_pgrs genes. However, the impact of immune selection on pe_pgrs genes has not been examined. Here, we sequenced 27 pe_pgrs genes in 94 clinical strains from five phylogenetic lineages of the M. tuberculosis complex (MTBC). We found that pe_pgrs genes were overall more diverse than the remainder of the MTBC genome, but individual members of the family varied widely in their nucleotide diversity and insertion/deletion (indel) content: some were more, and others were much less, diverse than the genome average. Individual pe_pgrs genes also differed in the ratio of nonsynonymous to synonymous mutations, suggesting that different selection pressures act on individual pe_pgrs genes. Using bioinformatic methods, we tested whether sequence diversity in pe_pgrs genes might be selected by human T cell recognition, the major mechanism of adaptive immunity to MTBC. We found that the large majority of predicted human T cell epitopes were confined to the conserved PE domain and experimentally confirmed the antigenicity of this domain in tuberculosis patients. In contrast, despite being genetically diverse, the PGRS domains harbored few predicted T cell epitopes. These results indicate that human T cell recognition is not a significant force driving sequence diversity in pe_pgrs genes, which is consistent with the previously reported conservation of human T cell epitopes in the MTBC.ImportanceRecognition of Mycobacterium tuberculosis antigens by T lymphocytes is known to be important for immune protection against tuberculosis, but it is unclear whether human T cell recognition drives antigenic variation in M. tuberculosis. We previously discovered that the known human T cell epitopes in the M. tuberculosis complex are highly conserved, but we hypothesized that undiscovered epitopes with naturally occurring sequence variants might exist. To test this hypothesis, we examined the pe_pgrs genes, a large family of genes that has been proposed to function in immune evasion by M. tuberculosis. We found that the pe_pgrs genes exhibit considerable sequence variation, but the regions containing T cell epitopes and the regions of variation are distinct. These findings confirm that the majority of human T cell epitopes of M. tuberculosis are highly conserved and indicate that selection forces other than T cell recognition drive sequence variation in the pe_pgrs genes.

Published
2014

10. Reversion of antibiotic resistance in Mycobacterium tuberculosis by spiroisoxazoline SMARt-420

Author

Blondiaux, Nicolas, Moune, Martin, Desroses, Matthieu, Frita, Rosangela, Flipo, Marion, Mathys, Vanessa, Soetaert, Karine, Kiass, Mehdi, Delorme, Vincent, Djaout, Kamel, Trebosc, Vincent, Kemmer, Christian, Wintjens, René, Wohlkönig, Alexandre, Antoine, Rudy, Huot, Ludovic, Hot, David, Coscolla, Mireia, Feldmann, Julia, Gagneux, Sebastien, Locht, Camille, Brodin, Priscille, Gitzinger, Marc, Déprez, Benoit, Willand, Nicolas, and Baulard, Alain R.

Published
2017

12. Bioinformatics analysis of mutations in SARSCoV- 2 and clinical phenotypes

Author

European Commission, Consejo Superior de Investigaciones Científicas (España), Álvarez-Herrera, Miguel [0000-0002-7922-3180], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Navarro-Domínguez, Beatriz [0000-0003-4077-8696], Rodríguez Santana, Simón [0000-0003-3760-0520], García Rasines, Daniel [0000-0002-1558-5860], Naveiro Flores, Roi [0000-0001-9032-2465], Gil, Carmen [0000-0002-3882-6081], Carazo, José M. [0000-0003-0788-8447], Coscollá, Mireia [0000-0003-0752-0538], Sorzano, Carlos Óscar S. [0000-0002-9473-283X], Campillo, Nuria E. [0000-0002-9948-2665], Ulzurrun, Eugenia, Del Hoyo, Daniel, Álvarez-Herrera, Miguel, Ruiz-Rodríguez, Paula, Navarro-Domínguez, Beatriz, Rodríguez Santana, Simón, García Rasines, Daniel, Naveiro Flores, Roi, Gil, Carmen, Carazo, José M., Coscollá, Mireia, Sorzano, Carlos Óscar S., Campillo, Nuria E., European Commission, Consejo Superior de Investigaciones Científicas (España), Álvarez-Herrera, Miguel [0000-0002-7922-3180], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Navarro-Domínguez, Beatriz [0000-0003-4077-8696], Rodríguez Santana, Simón [0000-0003-3760-0520], García Rasines, Daniel [0000-0002-1558-5860], Naveiro Flores, Roi [0000-0001-9032-2465], Gil, Carmen [0000-0002-3882-6081], Carazo, José M. [0000-0003-0788-8447], Coscollá, Mireia [0000-0003-0752-0538], Sorzano, Carlos Óscar S. [0000-0002-9473-283X], Campillo, Nuria E. [0000-0002-9948-2665], Ulzurrun, Eugenia, Del Hoyo, Daniel, Álvarez-Herrera, Miguel, Ruiz-Rodríguez, Paula, Navarro-Domínguez, Beatriz, Rodríguez Santana, Simón, García Rasines, Daniel, Naveiro Flores, Roi, Gil, Carmen, Carazo, José M., Coscollá, Mireia, Sorzano, Carlos Óscar S., and Campillo, Nuria E.

Abstract

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), initially reported in Wuhan (China) hasspread worldwide. Like other viruses, SARS-CoV-2 accumulates mutations with each cycle of replication by continuously evolving a viral strain with one or more single nucleotide variants (SNVs). However, SNVs that cause severe COVID-19 or lead to immune escape or vaccine failure are not well understood. We aim to identify SNVs associated with severe clinical phenotypes., Methods: In this study, 27429 whole-genome aligned consensus sequences of SARS-CoV-2 were collected from genomic epidemiology of SARS-CoV-2 project in Spain (SeqCOVID) [1]. These samples were obtained from patients who required hospitalization and/or intensive care unit admission (ICU), excluding those registered in the first pandemic wave.Besides, 248 SARS-CoV-2 genomes were isolated from COVID-19 hospitalized patients from Gregorio Marañon General University Hospital (GMH) of which 142 were fully vaccinated. Bioinformatics tools using R and Python programming languages were developed and implemented comparing those to SARS-CoV-2 Wuhan-Hu-1 (reference genome)., Results: Using a selection threshold mutational frequency 10%, 27 SNVs were expected to have association with hospitalization and ICU risk. The reference haplotype differing at the SNV coding for lysine at the residue 203 (N:R203K) was found to have negative association with COVID-19 hospitalization risk (p = 5.37 x 10-04). Similarly, a negative association was observed when the residue at 501 is replaced by tyrosine (S:N501Y) (p = 1.33 x 10-02). The application of a Chi-square test suggested that SNV-haplotypes coding for mutants residues such as (S:A222V, N:A220V, ORF10:V30L) and (ORF1a:T1001I, ORF1a:I2230T, S:N501Y, S:T716S, S:S982A, ORF8:Q27*, N:R203K, N:S235F) have negative associations with COVID-19 hospitalization risk (p = 6.58 x 10-07 and p = 2.27 x 10-16, respectively) and COVID-19 ICU risk (p = 1.15 x 10-02 and p = 2.51 x 10-02, respectively). Focusing on the SNV-haplotype coding the mutations (S:A222V, N:A220V, N:D377Y, ORF10:V30L) were observed to increase the risk of COVID-19 hospitalization (p = 2.71 x 10-04). Results from SARS-CoV-2 genomes analysis from GMH showed 63 coding SNVs which met the established threshold value. Applying a Chi-square test, the SNV-haplotype carrying coding variants for mutant residues in 5 ORF proteins and surface and membrane glycoprotein and nucleocapsid phosphoprotein was significantly associated with vaccine failure in hospitalized COVID-19 patients (p = 7.91 x 10-04)., Conclusions: SNV-haplotypes carrying variants lead to non-synonymous mutations located along SARS-CoV-2 wholeproteome may influence COVID-19 severity and vaccine failure suggesting a functional role in the clinical outcome for COVID-19 patients.

Published
2022

13. The structural role of SARS-CoV-2 genetic background in the emergence and success of spike mutations: The case of the spike A222V mutation

Author

European Commission, Consejo Superior de Investigaciones Científicas (España), Ministerio de Ciencia e Innovación (España), Generalitat Valenciana, Comunidad de Madrid, Banco Santander, Instituto de Salud Carlos III, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Ministerio de Economía y Competitividad (España), Ginex, Tiziana [0000-0002-5739-8713], Marco-Marín, Clara [0000-0002-8813-3515], Wieczor, Milosz [0000-0003-4990-8629], Mata, Carlos P. [0000-0003-3381-7431], Krieger, James [0000-0001-6194-6244], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], López-Redondo, Marisa [0000-0002-3328-6821], Francés-Gómez, Clara [0000-0001-7341-3824], Melero, Roberto [0000-0001-9467-9381], Sorzano, Carlos Óscar S. [0000-0002-9473-283X], Martínez, Marta [0000-0002-8435-5540], Gougeard, Nadine [0000-0001-7338-7267], Forcada-Nadal, Alicia [0000-0003-0179-4044], Zamora-Caballero, Sara [0000-0003-4717-8845], Gozalbo-Rovira, Roberto [0000-0003-3427-3800], Sanz-Frasquet, Carla [0000-0002-6990-3131], Arranz, Rocío [0000-0001-5321-0915], Bravo, Jerónimo [0000-0001-6695-2846], Rubio, Vicente [0000-0001-8124-1196], Marina, Alberto [0000-0002-1334-5273], Geller, Ron [0000-0002-7612-4611], Comas, Iñaki [0000-0001-5504-9408], Gil, Carmen [0000-0002-3882-6081], Coscollá, Mireia [0000-0003-0752-0538], Orozco, Modesto [0000-0002-8608-3278], Llácer, José Luis [0000-0001-5304-1795], Carazo, José M. [0000-0003-0788-8447], Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, Ruiz-Rodríguez, Paula, López-Redondo, Marisa, Francés-Gómez, Clara, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Arranz, Rocío, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, The IBV-Covid19-Pipeline, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, Carazo, José M., European Commission, Consejo Superior de Investigaciones Científicas (España), Ministerio de Ciencia e Innovación (España), Generalitat Valenciana, Comunidad de Madrid, Banco Santander, Instituto de Salud Carlos III, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Ministerio de Economía y Competitividad (España), Ginex, Tiziana [0000-0002-5739-8713], Marco-Marín, Clara [0000-0002-8813-3515], Wieczor, Milosz [0000-0003-4990-8629], Mata, Carlos P. [0000-0003-3381-7431], Krieger, James [0000-0001-6194-6244], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], López-Redondo, Marisa [0000-0002-3328-6821], Francés-Gómez, Clara [0000-0001-7341-3824], Melero, Roberto [0000-0001-9467-9381], Sorzano, Carlos Óscar S. [0000-0002-9473-283X], Martínez, Marta [0000-0002-8435-5540], Gougeard, Nadine [0000-0001-7338-7267], Forcada-Nadal, Alicia [0000-0003-0179-4044], Zamora-Caballero, Sara [0000-0003-4717-8845], Gozalbo-Rovira, Roberto [0000-0003-3427-3800], Sanz-Frasquet, Carla [0000-0002-6990-3131], Arranz, Rocío [0000-0001-5321-0915], Bravo, Jerónimo [0000-0001-6695-2846], Rubio, Vicente [0000-0001-8124-1196], Marina, Alberto [0000-0002-1334-5273], Geller, Ron [0000-0002-7612-4611], Comas, Iñaki [0000-0001-5504-9408], Gil, Carmen [0000-0002-3882-6081], Coscollá, Mireia [0000-0003-0752-0538], Orozco, Modesto [0000-0002-8608-3278], Llácer, José Luis [0000-0001-5304-1795], Carazo, José M. [0000-0003-0788-8447], Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, Ruiz-Rodríguez, Paula, López-Redondo, Marisa, Francés-Gómez, Clara, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Arranz, Rocío, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, The IBV-Covid19-Pipeline, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, and Carazo, José M.

Abstract

The S:A222V point mutation, within the G clade, was characteristic of the 20E (EU1) SARS-CoV-2 variant identified in Spain in early summer 2020. This mutation has since reappeared in the Delta subvariant AY.4.2, raising questions about its specific effect on viral infection. We report combined serological, functional, structural and computational studies characterizing the impact of this mutation. Our results reveal that S:A222V promotes an increased RBD opening and slightly increases ACE2 binding as compared to the parent S:D614G clade. Finally, S:A222V does not reduce sera neutralization capacity, suggesting it does not affect vaccine effectiveness.

Published
2022

14. VIPERA: Viral Intra-Patient Evolution Reporting and Analysis

Author

Sevilla, Jordi, Álvarez-Herrera, Miguel, Cano-Jiménez, Pablo, Vergara, Andrea, Vila, Jordi, González-Candelas, Fernando, Comas, Iñaki, Coscollá, Mireia, Sevilla, Jordi, Álvarez-Herrera, Miguel, Cano-Jiménez, Pablo, Vergara, Andrea, Vila, Jordi, González-Candelas, Fernando, Comas, Iñaki, and Coscollá, Mireia

Abstract

[Background] Viral mutations within patients nurture the adaptive potential of SARS-CoV-2 during chronic infections, which are a potential source of variants of concern. However, there is no integrated framework for the evolutionary analysis of intrapatient SARS-CoV-2 serial samples. Herein we describe VIPERA, a new software that integrates the evaluation of the intrapatient ancestry of SARS-CoV-2 sequences with the analysis of evolutionary trajectories of serial sequences from the same viral infection., [Methods] VIPERA is a pipeline implemented in Snakemake that analyzes a set of SARS-CoV-2 samples serially-collected from the same patient and produces a HTML report with three sections. Firstly, a summary of the samples is reported including lineage designation. Secondly, to ascertain if all samples were collected from the same infection, lineage admixture analyses, phylogenetic analyses and diversity analyses are produced and reported. For the phylogenetic analyses and the diversity analyses, a set of context samples is automatically fetched from GISAID. Thirdly, evolutionary analyses such as dN/dS analysis or the characterization of the nucleotide variants that appear in the studied samples are also carried out and reported. To validate the power to detect serially-sampled infections using VIPERA, we have used it with two validation datasets. The positive control dataset includes 30 sequences collected in Yale from the same patient (Chaguza C et al.,Cell Rep Med, 2023). The negative control dataset includes a mixture of 12 samples collected from one patient in Barcelona in 2020 with 3 other samples from another patient but collected in the same location and dates. Finally, we use VIPERA to carry out the whole intrapatient-evolution analysis with the 12 samples from the same patient that take part in the negative control., [Results] The positive and negative control datasets showed very different lineage composition, with more homogeneous lineage composition in the positive control. Phylogenetic three showed samples from positive control were monophyletic, while sequences from negative control were paraphyletic. Finally, the nucleotide diversity was significantly reduced in the studied sequences compared to the context ones in the positive control, as we expect for sequences derived from the same infection. On the contrary, the nucleotide diversity was not significantly reduced in the studied sequences compared to the context ones in the negative control. Our validation demonstrated that VIPERA has the power to detect serially-sampled infections. Additionally, we analyzed a case study using VIPERA. First we confirmed all sequences derived from a serially-sampled infection because lineage admixture was homogeneous, sequences were monophyletic and the nucleotide diversity was significantly lower than in the context sequences. Intrapatient-evolution analyses reported by VIPERA identified the appearance of mutations that are concerning due to their associated immune scape phenotype. We also detect positive selection along the infection using the dN/dS analysis., [Conclusions] VIPERA provides an aggregate of analysis for detecting whether there is a serially-sampled infection or not, including novel approaches such as genetic diversity and genetic distance at the population level approaches. It also provides a description of the within-host evolution observed in the studied samples.

Published
2023

15. Combinatorial analysis of deletion repair in SARS-CoV-2 variants of concern

Author

Álvarez-Herrera, Miguel, Ruiz-Rodríguez, Paula, Navarro-Domínguez, Beatriz, Zulaica, Joao, Grau, Brayan, Bracho, María Alma, Guerreiro, Manuel, Aguilar-Gallardo, Cristóbal, González-Candelas, Fernando, Comas, Iñaki, Geller, Ron, Coscollá, Mireia, Álvarez-Herrera, Miguel, Ruiz-Rodríguez, Paula, Navarro-Domínguez, Beatriz, Zulaica, Joao, Grau, Brayan, Bracho, María Alma, Guerreiro, Manuel, Aguilar-Gallardo, Cristóbal, González-Candelas, Fernando, Comas, Iñaki, Geller, Ron, and Coscollá, Mireia

Abstract

[Background] The spike protein of SARS-CoV-2 is a key determinant of viral fitness and immune evasion, and its N-terminal domain (NTD) is prone to mutations that may confer fitness advantages to the virus. Most variants of concern (VOCs), including Alpha, Delta, and Omicron, have harbored distinct NTD lineage-defining mutations. However, the relationship between genotype and the impact on viral transmission and viral phenotype is not yet fully understood., [Methods] We analyzed over 10 million SARS-CoV-2 genomes from GISAID to investigate the prevalence and estimate the transmission of different combinations of NTD mutations across the Alpha and the Omicron variants. Additionally, we characterized the viral phenotype of deletion repair events in a surrogate in vitro system, assessing their infectivity, fusogenicity, thermal stability, protein surface expression, and neutralization sensitivity., [Results] Some NTD mutations, such the repair of deleted amino acids at sites S:69/70 and S:144 in Alpha viruses, were associated with an increased transmission rate and higher frequency among older age groups. These deletion repairs were also detected in Omicron, but with different patterns and effects. For instance, the repair of deletion at site S:143/145 in Omicron enhanced viral fusogenicity and neutralization by sera from vaccinated individuals. However, the repair of the deletion at site S:69/70 reduced viral infectivity and did not affect these traits. The co-occurrence of both repairs resulted in reduced fusogenicity., [Conclusions] Our study reveals the complex interplay between NTD mutations, including those that lead to deletion repair, and viral success in SARS-CoV-2. This may have implications for viral transmission, immunity, and vaccine efficacy. Our findings improve our understanding of SARS- CoV-2 evolution, and provide insights for future research and public health interventions.

Published
2023

16. Jornada de Colaboración Científica en Seguridad y Defensa

Author

Martín-González, Marisol, Martell, José María, Calderón, Carlos, Hernández Encinas, Luis, Ríos, David, Fernández Mármol, Verónica, Ramiro Fariñas, Diego, Galindo, Inés, Turiel, Antonio, Trigo-Rodríguez, Josep María, Lozano Fantoba, Manuel, Val, Margarita del, Coscollá, Mireia, Alcamí, Antonio, Marco, María Pilar, Mesas, Mar, Boyero, Maite, Pérez, José María, Armada, Manuel, Pallarés, Jofre, Gamo, Silvia, Cerrato, Sandra, Marí-Klose, Pau, Doña, Alicia, Pino, Eloísa del, Gabinete de Presidencia CSIC, Departamento de Comunicación CSIC, Martín-González, Marisol, Martell, José María, Calderón, Carlos, Hernández Encinas, Luis, Ríos, David, Fernández Mármol, Verónica, Ramiro Fariñas, Diego, Galindo, Inés, Turiel, Antonio, Trigo-Rodríguez, Josep María, Lozano Fantoba, Manuel, Val, Margarita del, Coscollá, Mireia, Alcamí, Antonio, Marco, María Pilar, Mesas, Mar, Boyero, Maite, Pérez, José María, Armada, Manuel, Pallarés, Jofre, Gamo, Silvia, Cerrato, Sandra, Marí-Klose, Pau, Doña, Alicia, Pino, Eloísa del, Gabinete de Presidencia CSIC, and Departamento de Comunicación CSIC

Abstract

El Consejo Superior de Investigaciones Científicas (CSIC) organiza una JORNADA DE COLABORACIÓN CIENTÍFICA EN SEGURIDAD Y DEFENSA el próximo día 31 de mayo. En este evento se buscará potenciar las colaboraciones del CSIC en las áreas de seguridad y defensa con socios y colaboradores externos públicos y privados. La Jornada se dividirá en cuatro cápsulas en las que investigadores presentarán la investigación que se hace en el Consejo en seguridad digital y globalizada; sensores, vigilancia y teledetección para la defensa; riesgos biológicos; y las oportunidades de financiación en proyectos colaborativos competitivos. Finalizará con un coloquio en el que diversos actores debatirán sobre el avance científico en defensa y seguridad y su impacto social.

Published
2023

17. Genomic analysis of Mycobacterium brumae sustains its nonpathogenic and immunogenic phenotype

Author

Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Generalitat de Catalunya, Generalitat Valenciana, Consejo Superior de Investigaciones Científicas (España), Agencia Estatal de Investigación (España), Ministerio de Economía y Competitividad (España), Comas, Iñaki [0000-0001-5504-9408], Torres-Puente, Manuela [0000-0002-8352-180X], Renau-Mínguez, Chantal, Herrero-Abadía, Paula, Ruiz-Rodríguez, Paula, Sentandreu, Vicente, Torrents, Eduard, Chiner-Oms, Álvaro, Torres-Puente, Manuela, Comas, Iñaki, Julián, Esther, Coscollá, Mireia, Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Generalitat de Catalunya, Generalitat Valenciana, Consejo Superior de Investigaciones Científicas (España), Agencia Estatal de Investigación (España), Ministerio de Economía y Competitividad (España), Comas, Iñaki [0000-0001-5504-9408], Torres-Puente, Manuela [0000-0002-8352-180X], Renau-Mínguez, Chantal, Herrero-Abadía, Paula, Ruiz-Rodríguez, Paula, Sentandreu, Vicente, Torrents, Eduard, Chiner-Oms, Álvaro, Torres-Puente, Manuela, Comas, Iñaki, Julián, Esther, and Coscollá, Mireia

Abstract

Mycobacterium brumae is a rapid-growing, non-pathogenic Mycobacterium species, originally isolated from environmental and human samples in Barcelona, Spain. Mycobacterium brumae is not pathogenic and it's in vitro phenotype and immunogenic properties have been well characterized. However, the knowledge of its underlying genetic composition is still incomplete. In this study, we first describe the 4 Mb genome of the M. brumae type strain ATCC 51384T assembling PacBio reads, and second, we assess the low intraspecies variability by comparing the type strain with Illumina reads from three additional strains. Mycobacterium brumae genome is composed of a circular chromosome with a high GC content of 69.2% and containing 3,791 CDSs, 97 pseudogenes, one prophage and no CRISPR loci. Mycobacterium brumae has shown no pathogenic potential in in vivo experiments, and our genomic analysis confirms its phylogenetic position with other non-pathogenic and rapid growing mycobacteria. Accordingly, we determined the absence of virulence-related genes, such as ESX-1 locus and most PE/PPE genes, among others. Although the immunogenic potential of M. brumae was proved to be as high as Mycobacterium bovis BCG, the only mycobacteria licensed to treat cancer, the genomic content of M. tuberculosis T cell and B cell antigens in M. brumae genome is considerably lower than those antigens present in M. bovis BCG genome. Overall, this work provides relevant genomic data on one of the species of the mycobacterial genus with high therapeutic potential.

Published
2023

18. Bioinformatics analysis of mutations in SARSCoV- 2 and clinical phenotypes

Author

Ulzurrun, Eugenia, Del Hoyo, Daniel, Álvarez-Herrera, Miguel, Ruiz-Rodríguez, Paula, Navarro-Domínguez, Beatriz, Rodríguez Santana, Simón, García Rasines, Daniel, Naveiro Flores, Roi, Gil, Carmen, Carazo, José M., Coscollá, Mireia, Sorzano, Carlos Óscar S., Campillo, Nuria E., European Commission, Consejo Superior de Investigaciones Científicas (España), Álvarez-Herrera, Miguel, Ruiz-Rodríguez, Paula, Navarro-Domínguez, Beatriz, Rodríguez Santana, Simón, García Rasines, Daniel, Naveiro Flores, Roi, Gil, Carmen, Carazo, José M., Coscollá, Mireia, Sorzano, Carlos Óscar S., and Campillo, Nuria E.

Abstract

1 p.-1 fig.-8 tab., Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), initially reported in Wuhan (China) hasspread worldwide. Like other viruses, SARS-CoV-2 accumulates mutations with each cycle of replication by continuously evolving a viral strain with one or more single nucleotide variants (SNVs). However, SNVs that cause severe COVID-19 or lead to immune escape or vaccine failure are not well understood. We aim to identify SNVs associated with severe clinical phenotypes., Methods: In this study, 27429 whole-genome aligned consensus sequences of SARS-CoV-2 were collected from genomic epidemiology of SARS-CoV-2 project in Spain (SeqCOVID) [1]. These samples were obtained from patients who required hospitalization and/or intensive care unit admission (ICU), excluding those registered in the first pandemic wave.Besides, 248 SARS-CoV-2 genomes were isolated from COVID-19 hospitalized patients from Gregorio Marañon General University Hospital (GMH) of which 142 were fully vaccinated. Bioinformatics tools using R and Python programming languages were developed and implemented comparing those to SARS-CoV-2 Wuhan-Hu-1 (reference genome)., Results: Using a selection threshold mutational frequency 10%, 27 SNVs were expected to have association with hospitalization and ICU risk. The reference haplotype differing at the SNV coding for lysine at the residue 203 (N:R203K) was found to have negative association with COVID-19 hospitalization risk (p = 5.37 x 10-04). Similarly, a negative association was observed when the residue at 501 is replaced by tyrosine (S:N501Y) (p = 1.33 x 10-02). The application of a Chi-square test suggested that SNV-haplotypes coding for mutants residues such as (S:A222V, N:A220V, ORF10:V30L) and (ORF1a:T1001I, ORF1a:I2230T, S:N501Y, S:T716S, S:S982A, ORF8:Q27*, N:R203K, N:S235F) have negative associations with COVID-19 hospitalization risk (p = 6.58 x 10-07 and p = 2.27 x 10-16, respectively) and COVID-19 ICU risk (p = 1.15 x 10-02 and p = 2.51 x 10-02, respectively). Focusing on the SNV-haplotype coding the mutations (S:A222V, N:A220V, N:D377Y, ORF10:V30L) were observed to increase the risk of COVID-19 hospitalization (p = 2.71 x 10-04). Results from SARS-CoV-2 genomes analysis from GMH showed 63 coding SNVs which met the established threshold value. Applying a Chi-square test, the SNV-haplotype carrying coding variants for mutant residues in 5 ORF proteins and surface and membrane glycoprotein and nucleocapsid phosphoprotein was significantly associated with vaccine failure in hospitalized COVID-19 patients (p = 7.91 x 10-04)., Conclusions: SNV-haplotypes carrying variants lead to non-synonymous mutations located along SARS-CoV-2 wholeproteome may influence COVID-19 severity and vaccine failure suggesting a functional role in the clinical outcome for COVID-19 patients., This research work was funded by the European Commission-NextGenerationEU (Regulation EU 2020/2094), through CSIC’s Global Health Platform (PTI Salud Global)

Published
2022

25. Comparative genomics of Mycobacterium africanum Lineage 5 and Lineage 6 from Ghana suggests distinct ecological niches

Author

Otchere, Isaac Darko, Coscollá, Mireia, Sánchez-Busó, Leonor, Asante-Poku, Adwoa, Brites, Daniela, Loiseau, Chloe, Meehan, Conor, Osei-Wusu, Stephen, Forson, Audrey, Laryea, Clement, Yahayah, Abdallah Iddrisu, Baddoo, Akosua, Ansa, Gloria Akosua, Aboagye, Samuel Yaw, Asare, Prince, Borrell, Sonia, Gehre, Florian, Beckert, Patrick, Kohl, Thomas A., N’dira, Sanoussi, Beisel, Christian, Antonio, Martin, Niemann, Stefan, de Jong, Bouke C., Parkhill, Julian, Harris, Simon R., Gagneux, Sebastien, and Yeboah-Manu, Dorothy

Published
2018
Full Text
View/download PDF

26. The structural role of SARS-CoV-2 genetic background in the emergence and success of spike mutations: the case of the spike A222V mutation

Author

European Commission, Consejo Superior de Investigaciones Científicas (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Comunidad de Madrid, European Research Council, Instituto de Salud Carlos III, Banco Santander, Generalitat Valenciana, Ginex, Tiziana [0000-0002-5739-8713], Marco-Marín, Clara [0000-0002-8813-3515], Wieczor, Milosz [0000-0003-4990-8629], Mata, Carlos P. [0000-0003-3381-7431], Krieger, James [0000-0001-6194-6244], López-Redondo, Marisa [0000-0002-3328-6821], Francés-Gómez, Clara [0000-0001-7341-3824], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Melero, Roberto [0000-0001-9467-9381], Sorzano, Carlos Óscar S. [0000-0002-9473-283X], Martínez, Marta [0000-0002-8435-5540], Gougeard, Nadine [0000-0001-7338-7267], Forcada-Nadal, Alicia [0000-0003-0179-4044], Zamora-Caballero, Sara [0000-0003-4717-8845], Gozalbo-Rovira, Roberto [0000-0003-3427-3800], Sanz-Frasquet, Carla [0000-0002-6990-3131], Bravo, Jerónimo [0000-0001-6695-2846], Rubio, Vicente [0000-0001-8124-1196], Marina, Alberto [0000-0002-1334-5273], Geller, Ron [0000-0002-7612-4611], Comas, Iñaki [0000-0001-5504-9408], Gil, Carmen [0000-0002-3882-6081], Coscollá, Mireia [0000-0003-0752-0538], Orozco, Modesto [0000-0002-8608-3278], Llácer, José Luis [0000-0001-5304-1795], Carazo, José M. [0000-0003-0788-8447], Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, López-Redondo, Marisa, Francés-Gómez, Clara, Ruiz-Rodríguez, Paula, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, Carazo, José M., European Commission, Consejo Superior de Investigaciones Científicas (España), Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Comunidad de Madrid, European Research Council, Instituto de Salud Carlos III, Banco Santander, Generalitat Valenciana, Ginex, Tiziana [0000-0002-5739-8713], Marco-Marín, Clara [0000-0002-8813-3515], Wieczor, Milosz [0000-0003-4990-8629], Mata, Carlos P. [0000-0003-3381-7431], Krieger, James [0000-0001-6194-6244], López-Redondo, Marisa [0000-0002-3328-6821], Francés-Gómez, Clara [0000-0001-7341-3824], Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Melero, Roberto [0000-0001-9467-9381], Sorzano, Carlos Óscar S. [0000-0002-9473-283X], Martínez, Marta [0000-0002-8435-5540], Gougeard, Nadine [0000-0001-7338-7267], Forcada-Nadal, Alicia [0000-0003-0179-4044], Zamora-Caballero, Sara [0000-0003-4717-8845], Gozalbo-Rovira, Roberto [0000-0003-3427-3800], Sanz-Frasquet, Carla [0000-0002-6990-3131], Bravo, Jerónimo [0000-0001-6695-2846], Rubio, Vicente [0000-0001-8124-1196], Marina, Alberto [0000-0002-1334-5273], Geller, Ron [0000-0002-7612-4611], Comas, Iñaki [0000-0001-5504-9408], Gil, Carmen [0000-0002-3882-6081], Coscollá, Mireia [0000-0003-0752-0538], Orozco, Modesto [0000-0002-8608-3278], Llácer, José Luis [0000-0001-5304-1795], Carazo, José M. [0000-0003-0788-8447], Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, López-Redondo, Marisa, Francés-Gómez, Clara, Ruiz-Rodríguez, Paula, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, and Carazo, José M.

Abstract

The S:A222V point mutation, within the G clade, was characteristic of the 20E (EU1) SARS-CoV-2 variant identified in Spain in early summer 2020. This mutation has now reappeared in the Delta subvariant AY.4.2, raising questions about its specific effect on viral infection. We report combined serological, functional, structural and computational studies characterizing the impact of this mutation. Our results reveal that S:A222V promotes an increased RBD opening and slightly increases ACE2 binding as compared to the parent S:D614G clade. Finally, S:A222V does not reduce sera neutralization capacity, suggesting it does not affect vaccine effectiveness.

Published
2021

28. Supplementary Materials: In silico exploration of Mycobacterium tuberculosis metabolic networks shows host-associated convergent fluxomic phenotypes

Author

Santamaria, Guillem, Ruiz-Rodríguez, Paula, Renau-Mínguez, Chantal, Pinto, Francisco R., Coscollá, Mireia, Santamaria, Guillem, Ruiz-Rodríguez, Paula, Renau-Mínguez, Chantal, Pinto, Francisco R., and Coscollá, Mireia

Abstract

Figure S1: Correspondence Analysis of all the potentially deleterious SNPs, Figure S2: Unsupervised analysis of the deletion data of the genes included in iEK1011 2.0 genome-scale metabolic model, Figure S3: Principal Component Analysis of FBA flux distributions of the lineage-specific genome-scale metabolic models, Figure S4: Principal Component Analysis of the sampled solution space of each one of the lineage-specific genome-scale metabolic models, Figure S5: OPLS-DA loadings for the significantly altered subsystems between animal- and human-associated sampled models, Figure S6: Difference of exchange fluxes between sampled models and FBA flux distribution of metabolites in Middlebrock 7H9 OADC + cholesterol for each lineage’s model, Table S1: Illumina genomes information, Table S2: iEK1011 2.0 reaction information, Table S3: Removed reactions per lineage model, Table S4: OPLS-DA variable coefficients, Table S5: Statistically significant reaction fluxes between samples of animal- and human-associated models, File S1: Description of the genes removed from iEK1011 2.0 to generate lineage-specific GEMs, File S2: Lineage-specific genome scale metabolic models.

Published
2022

29. Supplementary Information: The structural role of SARS-CoV-2 genetic background in the emergence and success of spike mutations: The case of the spike A222V mutation

Author

Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, Ruiz-Rodríguez, Paula, López-Redondo, Marisa, Francés-Gómez, Clara, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Arranz, Rocío, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, The IBV-Covid19-Pipeline, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, Carazo, José M., Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, Ruiz-Rodríguez, Paula, López-Redondo, Marisa, Francés-Gómez, Clara, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Arranz, Rocío, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, The IBV-Covid19-Pipeline, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, and Carazo, José M.

Published
2022

30. The role of SARS-CoV-2 genetic background in the emergence and success of spike mutations: the case of the spike A222V mutation

Author

Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, Ruiz-Rodríguez, Paula, López-Redondo, Marisa, Francés-Gómez, Clara, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Arranz, Rocío, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, The IBV-Covid19-Pipeline, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, Carazo, José M., Ginex, Tiziana, Marco-Marín, Clara, Wieczor, Milosz, Mata, Carlos P., Krieger, James, Ruiz-Rodríguez, Paula, López-Redondo, Marisa, Francés-Gómez, Clara, Melero, Roberto, Sorzano, Carlos Óscar S., Martínez, Marta, Gougeard, Nadine, Forcada-Nadal, Alicia, Zamora-Caballero, Sara, Gozalbo-Rovira, Roberto, Sanz-Frasquet, Carla, Arranz, Rocío, Bravo, Jerónimo, Rubio, Vicente, Marina, Alberto, The IBV-Covid19-Pipeline, Geller, Ron, Comas, Iñaki, Gil, Carmen, Coscollá, Mireia, Orozco, Modesto, Llácer, José Luis, and Carazo, José M.

Published
2022

31. Real-time surveillance of SARS-CoV-2: surveying mixtures of lineage- defining markers

Author

Álvarez-Herrera, Miguel, Navarro-Domínguez, Beatriz, Ruiz-Rodríguez, Paula, Bracho, María Alma, Chiner-Oms, Álvaro, González-Candelas, Fernando, Comas, Iñaki, Coscollá, Mireia, Álvarez-Herrera, Miguel, Navarro-Domínguez, Beatriz, Ruiz-Rodríguez, Paula, Bracho, María Alma, Chiner-Oms, Álvaro, González-Candelas, Fernando, Comas, Iñaki, and Coscollá, Mireia

Published
2022

32. Evolutionary genomics of SARS-CoV-2: keys for viral success

Author

Álvarez-Herrera, Miguel, Carazo, José M., Comas, Iñaki, Coscollá, Mireia, Elena, Santiago F., Francés-Gómez, Clara, Franco, María Luisa, García Rasines, Daniel, Geller, Ron, Gil, Carmen, González-Candelas, Fernando, Hillung, Julia, Llácer, José Luis, Marina, Alberto, Marqués, M. Carmen, Naveiro Flores, Roi, Ríos, David, Rodríguez Santana, Simón, Ruiz-Rodríguez, Paula, Sorzano, Carlos Óscar S., Ulzurum, Eugenia, Vilar, Marçal, Álvarez-Herrera, Miguel, Carazo, José M., Comas, Iñaki, Coscollá, Mireia, Elena, Santiago F., Francés-Gómez, Clara, Franco, María Luisa, García Rasines, Daniel, Geller, Ron, Gil, Carmen, González-Candelas, Fernando, Hillung, Julia, Llácer, José Luis, Marina, Alberto, Marqués, M. Carmen, Naveiro Flores, Roi, Ríos, David, Rodríguez Santana, Simón, Ruiz-Rodríguez, Paula, Sorzano, Carlos Óscar S., Ulzurum, Eugenia, and Vilar, Marçal

Published
2022

33. Genomic surveillance and impact of SARS-CoV-2 mutations

Author

Ruiz-Rodríguez, Paula, Álvarez-Herrera, Miguel, Franco, María Luisa, Francés-Gómez, Clara, Marqués, M. Carmen, Hillung, Julia, Ulzurrun, Eugenia, Martínez-Martínez, Francisco José, Rodríguez Santana, Simón, Naveiro Flores, Roi, García Rasines, Daniel, Marina, Alberto, Llácer, José Luis, Vilar, Marçal, Sorzano, Carlos Óscar S., Campillo, Nuria E., Rubio, Vicente, Carazo, José M., Gil, Carmen, González-Candelas, Fernando, Geller, Ron, Comas, Iñaki, Elena, Santiago F., Coscollá, Mireia, Ruiz-Rodríguez, Paula, Álvarez-Herrera, Miguel, Franco, María Luisa, Francés-Gómez, Clara, Marqués, M. Carmen, Hillung, Julia, Ulzurrun, Eugenia, Martínez-Martínez, Francisco José, Rodríguez Santana, Simón, Naveiro Flores, Roi, García Rasines, Daniel, Marina, Alberto, Llácer, José Luis, Vilar, Marçal, Sorzano, Carlos Óscar S., Campillo, Nuria E., Rubio, Vicente, Carazo, José M., Gil, Carmen, González-Candelas, Fernando, Geller, Ron, Comas, Iñaki, Elena, Santiago F., and Coscollá, Mireia

Published
2022

34. In silico exploration of Mycobacterium tuberculosis metabolic networks shows host-associated convergent fluxomic phenotypes

Author

Fundação para a Ciência e a Tecnologia (Portugal), European Commission, Consejo Superior de Investigaciones Científicas (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Generalitat Valenciana, Santamaria, Guillem, Ruiz-Rodríguez, Paula, Renau-Mínguez, Chantal, Pinto, Francisco R., Coscollá, Mireia, Fundação para a Ciência e a Tecnologia (Portugal), European Commission, Consejo Superior de Investigaciones Científicas (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Generalitat Valenciana, Santamaria, Guillem, Ruiz-Rodríguez, Paula, Renau-Mínguez, Chantal, Pinto, Francisco R., and Coscollá, Mireia

Abstract

Mycobacterium tuberculosis, the causative agent of tuberculosis, is composed of several lineages characterized by a genome identity higher than 99%. Although the majority of the lineages are associated with humans, at least four lineages are adapted to other mammals, including different M. tuberculosis ecotypes. Host specificity is associated with higher virulence in its preferred host in ecotypes such as M. bovis. Deciphering what determines the preference of the host can reveal host-specific virulence patterns. However, it is not clear which genomic determinants might be influencing host specificity. In this study, we apply a combination of unsupervised and supervised classification methods on genomic data of ~27,000 M. tuberculosis clinical isolates to decipher host-specific genomic determinants. Host-specific genomic signatures are scarce beyond known lineage-specific mutations. Therefore, we integrated lineage-specific mutations into the iEK1011 2.0 genome-scale metabolic model to obtain lineage-specific versions of it. Flux distributions sampled from the solution spaces of these models can be accurately separated according to host association. This separation correlated with differences in cell wall processes, lipid, amino acid and carbon metabolic subsystems. These differences were observable when more than 95% of the samples had a specific growth rate significantly lower than the maximum achievable by the models. This suggests that these differences might manifest at low growth rate settings, such as the restrictive conditions M. tuberculosis suffers during macrophage infection.

Published
2022

38. Evolution, virulence and immunogenicity of relevant SARS-CoV-2 spike mutants

Author

Coscollá, Mireia, Ruiz-Rodríguez, Paula, Francés-Cuesta, Carlos, Geller, Ron, Chiner-Oms, Álvaro, Jiménez Serrano, Santiago, Marina, Alberto, Martínez-Priego, Llucia, D'Auria, Giuseppe, López, Mariana G., Cancino-Muñoz, Irving, Torres-Puente, Manuela, Bracho, María Alma, Ruiz-Hueso, Paula, González-Candelas, Fernando, Comas, Iñaki, Instituto de Salud Carlos III, Consejo Superior de Investigaciones Científicas (España), Generalitat Valenciana, Ministerio de Ciencia e Innovación (España), Comas, Iñaki, Chiner-Oms, Álvaro, Comas, Iñaki [0000-0001-5504-9408], and Chiner-Oms, Álvaro [0000-0002-0463-0101]

Abstract

SeqCOVm-SPAIN consortium., Trabajo presentado al 31st European Congress of Clinical Microbiology and Infectious Diseases (ECCMID), celebrado online del 9 al 12 de julio de 2021., We have detected two mutations in the Spike protein of SARS-CoV-2 sequences at amino acid positions 1163 and 1167 which appeared independently in multiple transmission clusters and different genetic backgrounds, indicating they may increase viral fitness. Both mutations appeared together in a cluster within clade 20E. This cluster is characterized by 12 additional single nucleotide polymorphisms but no deletions. The available structural information of the S protein in the preand post-fusion conformations we predict that both mutations confer rigidity, that potentially could decrease viral fitness. Despite the multiple and successful appearance of two HR2 mutations during the first year of SARS-CoV-2 evolution, in vi tro stability, infectivi ty, or antibody escape does not seem to play a role., This work was funded by the Instituto de Salud Carlos III project COV2o/o0140 and COV2o/o0437• Spanish National Research Council project CSIC"COV19~021 and CSIC-COVID19-082, and the Generalitat Valenciana (SEJI/2019/011 and Covid 19-SCI).Action co-financed by the European Union through the Operational Program of the European Regional Development Fund (ERDF) ofthe Valencian Community 2014-2020. MC is supported by Ramón y Caja/program from Ministerio de Ciencia, grant RTI2018-094399-A-Joo.

Published
2021

39. Evolutionary and phenotypic characterization of spike mutations in a new SARS-CoV-2 Lineage reveals two Variants of Interest

Author

Ruiz-Rodríguez, Paula, Francés-Gómez, Clara, Chiner-Oms, Álvaro, López, Mariana G., Jiménez Serrano, Santiago, Cancino-Muñoz, Irving, Ruiz-Hueso, Paula, Torres-Puente, Manuela, Bracho, María Alma, D’Auria, Giuseppe, Martínez-Priego, Llucia, Guerreiro, Manuel, Montero-Alonso, Marta, Gómez, María Dolores, Piñana, José Luis, Seqcovid-Spain Consortium, González-Candelas, Fernando, Comas, Iñaki, Marina, Alberto, Geller, Ron, Coscollá, Mireia, Instituto de Salud Carlos III, Consejo Superior de Investigaciones Científicas (España), Generalitat Valenciana, European Commission, Ruiz-Rodríguez, Paula, Frances-Gomez, Clara, Chiner-Oms, Álvaro, López, Mariana G., Jiménez Serrano, Santiago, Cancino-Muñoz, Irving, Ruiz-Hueso, Paula, Torres-Puente, Manuela, D’Auria, Giuseppe, Martínez-Priego, Llucia, González-Candelas, Fernando, Comas, Iñaki, Marina, Alberto, Geller, Ron, Coscolla, Mireia, Ruiz-Rodríguez, Paula [0000-0003-0727-5974], Frances-Gomez, Clara [0000-0001-7341-3824], Chiner-Oms, Álvaro [0000-0002-0463-0101], López, Mariana G. [0000-0002-2216-9232], Jiménez Serrano, Santiago [0000-0003-2917-6053], Cancino-Muñoz, Irving [0000-0002-5261-1634], Ruiz-Hueso, Paula [0000-0003-0217-471X], Torres-Puente, Manuela [0000-0002-8352-180X], D’Auria, Giuseppe [0000-0003-0672-2541], Martínez-Priego, Llucia [0000-0002-1073-269X], González-Candelas, Fernando [0000-0002-0879-5798], Comas, Iñaki [0000-0001-5504-9408], Marina, Alberto [0000-0002-1334-5273], Geller, Ron [0000-0002-7612-4611], and Coscolla, Mireia [0000-0003-0752-0538]

Subjects
2019-20 coronavirus outbreak, Lineage (genetic), Geography, Research council, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), European Regional Development Fund, media_common.cataloged_instance, Spike (database), European union, Valencian community, Genealogy, media_common
Abstract

Molecular epidemiology of SARS-CoV-2 aims to monitor the appearance of new variants with the potential to change the virulence or transmissibility of the virus. During the first year of SARS-CoV-2 evolution, numerous variants with possible public health impact have emerged. We have detected two mutations in the Spike protein at amino acid positions 1163 and 1167 that have appeared independently multiple times in different genetic backgrounds, indicating they may increase viral fitness. Interestingly, the majority of these sequences appear in transmission clusters, with the genotype encoding mutations at both positions increasing in frequency more than single-site mutants. This genetic outcome that we denote as Lineage B.1.177.637, belongs to clade 20E and includes 12 additional single nucleotide polymorphisms but no deletions with respect to the reference genome (first sequence in Wuhan). B.1.177.637 appeared after the first wave of the epidemic in Spain, and subsequently spread to eight additional countries, increasing in frequency among sequences in public databases. Positions 1163 and 1167 of the Spike protein are situated in the HR2 domain, which is implicated in the fusion of the host and viral membranes. To better understand the effect of these mutations on the virus, we examined whether B.1.177.637 altered infectivity, thermal stability, or antibody sensitivity. Unexpectedly, we observed reduced infectivity of this variant relative to the ancestral 20E variant in vitro while the levels of viral RNA in nasopharyngeal swabs did not vary significantly. In addition, we found the mutations do not impact thermal stability or antibody susceptibility in vaccinated individuals but display a moderate reduction in sensitivity to neutralization by convalescent sera from early stages of the pandemic. Altogether, this lineage could be considered a Variant of Interest (VOI), we denote VOI1163.7. Finally, we detected a sub-cluster of sequences within VOI1163.7 that have acquired two additional changes previously associated with antibody escape and it could be identified as VOI1163.7.V2. Overall, we have detected the spread of a new Spike variant that may be advantageous to the virus and whose continuous transmission poses risks by the acquisition of additional mutations that could affect pre-existing immunity., This work was funded by the Instituto de Salud Carlos III project COV20/00140 and COV20/00437, Spanish National Research Council project CSIC-COV19-021 and CSIC-COVID19-082, and the Generalitat Valenciana (SEJI/2019/011 and Covid_19-SCI). Action co-financed by the European Union through the Operational Program of the European Regional Development Fund (ERDF) of the Valencian Community 2014-2020. M.C. and R.G. are supported by Ramon y Cajal program from Ministerio de Ciencia.

Published
2021
Full Text
View/download PDF

40. Integrating genomics and infection biology to decipher differences between human and animal associated M. tuberculosis lineages

Author

Santamaria, Guillem, Renau-Mínguez, Chantal, Gomis, Carlos, Espert, Antonio, Buksa, Nikolina, Ruiz-Rodríguez, Paula, Pinto, Francisco R., Coscollá, Mireia, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Generalitat Valenciana, and European Commission

Abstract

Resumen del póster presentado al XLII Congreso de la Sociedad Española de Genética, celebrado de forma virtual del 14 al 18 de junio de 2021., Mycobacterium tuberculosis, which causes tuberculosis, is of the top 10 causes of death worldwide caused by an infectious disease. The majority of the lineages infect predominantly humans, except four lineages that infect a wide range of other mammals, and we refer to as animal-associated lineages. Because understanding the genetic basis of host specificity can inform about the virulence factors of M. tuberculosis in each host, our objective is to decipher is host specificity correlates with virulence in vitro, and with lineage specific genomic signatures. We combined experiments in macrophage infection model with whole genome sequencing analysis of 35.000 clinical M. tuberculosis strains representing all ecotypes to determine genomic specific signatures of the bacteria during the infectious process. We observed different genomics signatures between human and animal M. tuberculosis associated lineages. A differential signature was observed in three of the four genes that encode for phospholipase C in M. tuberculosis, lost in three out of four animal lineages, and present in the human lineages. Phylogenomic analysis showed that these deletions happened several times during evolution indicating a convergence in the loss of these regions that could be under differential selection pressure in animal and human associated strains. Because phospholipase C has been previously linked to M. tuberculosis virulence, we explored the differential expression of these genes between lineages infecting two different host cells., M.C. is supported by Ramón y Cajal program from Ministerio de Ciencia. This work was funded by Generalitat Valenciana (SEJI/2019/011) and Ministerio de ciencia e innovación (RTI2018-094399-A-I00).

Published
2021

41. The SeqCOVID-Spain consortium: unravelling the dynamics of the COVID-19 first epidemic wave in Spain

Author

Chiner-Oms, Álvaro, López, Mariana G., García de Viedma, Darío, Ruiz-Rodríguez, Paula, Bracho, María Alma, Cancino-Muñoz, Irving, D’Auria, Giuseppe, Marco, Griselda de, García-González, Neris, Goig, Galo A., Gómez-Navarro, Inmaculada, Jiménez Serrano, Santiago, Martínez-Priego, Llucia, Ruiz-Hueso, Paula, Ruiz-Roldán, Lidia, Torres-Puente, Manuela, Coscollá, Mireia, González-Candelas, Fernando, Comas, Iñaki, Seqcovid-Spain Consortium, Instituto de Salud Carlos III, Ministerio de Ciencia e Innovación (España), Consejo Superior de Investigaciones Científicas (España), European Research Council, Comas, Iñaki [0000-0001-5504-9408], and Comas, Iñaki

Abstract

Póster presentado a la Applied Bioinformatics and Public Health Microbiology 2021 Virtual Conference, celebrada del 5 al 7 de mayo de 2021., The COVID-19 pandemic has shaken the world since the beginning of 2020. Spain is among the European countries with the highest incidence of the disease during the first pandemic wave. We established a multidisciplinary consortium to monitor and study the evolution of the epidemic, with the aim of contributing to decision making and stopping rapid spreading across the country. We present the results for 2170 sequences from the first wave of the SARS-Cov-2 epidemic in Spain, representing 12% of diagnosed cases until 14th March. This effort allows us to document at least 500 initialintroductions, between early February-March from multiple international sources. Importantly, we document the early raise of two dominant genetic variants in Spain (Spanish Epidemic Clades), named SEC7 and SEC8, likely amplified by superspreading events. In sharp contrast to other non Asian countries those two variants were closely related to the initial variants of SARS-CoV-2 described in Asia and represented 40% of the genome sequences analyzed. The two dominant SECs were widely spread across the country compared to other genetic variants with SEC8 reaching a 60% prevalence just before the lockdown. Employing Bayesian phylodynamic analysis, we inferred a reduction in the effective reproductive number of these two SECs from around 2.5 to below 0.5 after the implementation of strict public-health interventions in mid-March. The effects of lockdown on the genetic variants of the virus are reflected in the general replacement of pre-existing SECs by a new variant at the beginning of the summer season. Our results reveal a significant difference in the genetic makeup of the epidemic in Spain and support the effectiveness of lockdown measures in controlling virus spread even for the most successful genetic variants., This work was funded by the Instituto de Salud Carlos III project COV20/00140, Spanish National Research Council project CSIC-COV19-021, Ministerio de Ciencia PID2019-104477RB-I00 and ERC StG 638553 to IC, and BFU2017-89594R to FGC. MC is supported by Ramón y Cajal program from Ministerio de Ciencia and grants RTI2018-094399-A-I00 and SEJI/2019/011.

Published
2021

43. Defining antigenic variation in Mycobacterium tuberculosis ecotypes

Author

Ruiz-Rodríguez, Paula and Coscollá, Mireia

Abstract

Resumen del trabajo presentado al 41st Annual Congress of the European Society of Mycobacteriology (ESM), celebrado de forma virtual del 28 al 29 de junio de 2019., Most known pathogens usually adopt the antigenic variation strategy where the host and the microorganism establish an evolutionary arms race, where each of the individuals acquires new improvements to overcome the opponent, setting a balance between them. In the case of Mycobacterium tuberculosis, it is unknown whether the antigenic variation could be behind the ability to evade the immune system. In this study, we identified genomic variation in 3,480 experimentally verified epitopes of T and B cells recognized from 3 different hosts: human, bovine, and murine, over 13,451 non-duplicated genomes from clinical strains representing different M. tuberculosis lineages. We studied how diversity could impact epitope recognition through analysing SNPs, deletions and genetic disruptions. Additionally, we analysed populations by phylogenomics to identify possible evolutionary convergences within ecotypes and host range. We observed that regions harbouring epitopes are more mutated than other regions of the genome. Moreover, we found that human-associated Lineage 4 contained the most diverse T cell epitopes compared with Lineage 2 which showed the most diverse B cell epitopes. In order to verify if highly variable epitopes have immunological consequences, analysis including immunologic experiments in individual epitopes will be conducted.

Published
2021

45. Decyphering Mycobacterium tuberculosis host specificity through the integration of genomics and infection biology

Author

Santamaria, Guillem, Renau-Mínguez, Chantal, Gomis, Carlos, Espert, Antonio, Buksa, Nikolina, Ruiz-Rodríguez, Paula, Pinto, Filipe, and Coscollá, Mireia

Abstract

Resumen del póster presentado al 41st Annual Congress of the European Society of Mycobacteriology (ESM), celebrado de forma virtual del 28 al 29 de junio de 2019., Mycobacterium tuberculosis is the microorganism that produces tuberculosis, which is among the top 10 causes of death worldwide. Most of its lineages infect predominantly humans, except for four, which infect a wide range of other mammals. We will refer to them as animal-associated lineages. As understanding the genetic basis of host specificity can inform about the virulence factors of M. tuberculosis in each host, our objective is to decipher if host specificity correlates with virulence in vitro, and with lineage specific genomic signatures. We combined experiments in macrophage infection model with whole genome sequencing analysis of ~35.000 clinical M. tuberculosis strains to determine genomic specific signatures of the bacteria during the infectious process. We observed different genomic signatures between human and animal M. tuberculosis associated lineages. A differential signature was observed in three of the four genes that encode for phospholipase C in M. tuberculosis (plcABC) and PPE38. These genes are part of a previously described Region of Difference (RD), RD5, which is unevenly distributed between animal- and human-associated lineages. This region is completely lost in two and partially lost in one out of four of the animal lineages, while present in most of the isolates belonging to the human-associated lineages. Phylogenomic analysis showed that these deletions happened several times during evolution indicating the loss of these regions could be under differential selection pressure in animal- and human-associated strains. Because phospholipase C has been previously linked to M. tuberculosis virulence, we explored the differential expression of these genes between lineages infecting macrophages coming from different hosts.

Published
2021

46. Exploring the genome of Mycobacterium brumae, a species of bacterium with therapeutic potential

Author

Renau-Mínguez, Chantal, Herrero-Abadía, Paula, Sentandreu, Vicente, Ruiz-Rodríguez, Paula, Goig, Galo A., Comas, Iñaki, Julián, Esther, Coscollá, Mireia, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Generalitat Valenciana, and Generalitat de Catalunya

Abstract

Resumen del trabajo presentado al XLII Congreso de la Sociedad Española de Genética (SEG), celebrado de forma virtual del 14 al 18 de junio de 2021., This work was supported by RTI2018-094399-A-I00, RTI2018-098777-B-I00 and 2017SGR-229.

Published
2021

47. Genomic determinants associated with SARS-CoV-2 virulence

Author

Ruiz-Rodríguez, Paula, Chaturvedi, N., Bracho, María Alma, Chiner-Oms, Álvaro, Jiménez Serrano, Santiago, López, Mariana G., Cancino-Muñoz, Irving, Ruiz-Hueso, Paula, Torres-Puente, Manuela, D’auria, M., Martínez-Priego, Llucia, González-Candelas, Fernando, Comas, Iñaki, Coscollá, Mireia, Instituto de Salud Carlos III, Consejo Superior de Investigaciones Científicas (España), Generalitat Valenciana, Ministerio de Ciencia e Innovación (España), Comas, Iñaki [0000-0001-5504-9408], Torres-Puente, Manuela [0000-0002-8352-180X], López, Mariana G. [0000-0002-2216-9232], Chiner-Oms, Álvaro [0000-0002-0463-0101], Comas, Iñaki, Torres-Puente, Manuela, López, Mariana G., and Chiner-Oms, Álvaro

Abstract

Trabajo presentado al 31st European Congress of Clinical Microbiology and Infectious Diseases (ECCMID), celebrado online del 9 al 12 de julio de 2021., This work was funded by the Instituto de Salud Carlos III project COV2o/oo140 and COV2o/ o0437,Spanish National Research Council project CSIC­ COV19·0l1 and CSIC-COVID19-082,and the Generalitat Valenciana (SEJI/2019/011 and Covid_19-SCI).Action co-financed by the European Union through the Operatianal Program of the European Regional Development Fund (ERDF) of the Valencian Community 2014-2020.MC is supported by Ramón y Cajal program from Ministerio de Ciencia,grant RTI2018-094399-A-I00.

Published
2021

48. New insights in the genome content of the bacterium Mycobacterium brumae

Author

Renau-Mínguez, Chantal, Herrero-Abadía, Paula, Sentandreu, Vicente, Ruiz-Rodríguez, Paula, Goig, Galo A., Comas, Iñaki, Julián, Esther, and Coscollá, Mireia

Abstract

Resumen del póster presentado al 41st Annual Congress of the European Society of Mycobacteriology (ESM), celebrado de forma virtual del 28 al 29 de junio de 2019., Mycobacterium brumae is a fast-growing, non-pathogenic Mycobacterium species, originally isolated from environmental and human samples in Barcelona, Spain. Previous studies have shown that the implementation of non-pathogenic mycobacteria, such as Mycobacterium bovis BCG can improve the treatment against high-risk non-muscle invasive bladder cancer (BC) by intravesical administration. M. brumae has been shown to be non-pathogenic and its phenotype and immunogenic effect have been well characterized. However, the knowledge of its underlying genetic composition is still incomplete. In this study we have sequenced the genome by means of PACBIO of the M. brumae strain CR-270 obtaining the most complete assembly to date. We describe its genetic content by showing evolutionary relationships between different mycobacteria and we compare its virulence gene content with other virulent mycobacteria such as H37Rv reference strain. Furthermore, we describe the genetic variability of M. brumae by comparative genomics using obtained Illumina sequences. Our results contribute to increase the knowledge about the genetic bases that explain the non-pathogenic phenotype of this bacterium with therapeutic potential.

Published
2021

49. La genética poblacional y evolutiva del SARS-CoV-2

Author

González-Candelas, Fernando, Coscollá, Mireia, and Comas, Iñaki

Abstract

Resumen del trabajo presentado al XLII Congreso de la Sociedad Española de Genética (SEG), celebrado de forma virtual del 14 al 18 de junio de 2021.

Published
2021

50. Lo que nos enseña la epidemiología genómica sobre las olas de COVID-19 en España (y cómo evitar una nueva ola)

Author

Comas, Iñaki [0000-0001-5504-9408], García Marín, Ana María, Chiner-Oms, Álvaro, González-Candelas, Fernando, Comas, Iñaki, López, Mariana G., Coscollá, Mireia, Comas, Iñaki [0000-0001-5504-9408], García Marín, Ana María, Chiner-Oms, Álvaro, González-Candelas, Fernando, Comas, Iñaki, López, Mariana G., and Coscollá, Mireia

Published
2021

Catalog

Books, media, physical & digital resources
See catalog results