Browsing by Author "van Bakel, Harm"

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    Cross-species and mammal-to-mammal transmission of clade 2.3.4.4b highly pathogenic avian influenza A/H5N1 with PB2 adaptations
    (2025) Pardo Roa, Catalina; Nelson, Martha I.; Ariyama, Naomi; Aguayo, Carolina; Almonacid Cárdenas, Leonardo Iván; Gonzalez-Reiche, Ana S.; Muñoz, Gabriela; Ulloa, Mauricio; Avila, Claudia; Navarro, Carlos; Reyes, Rodolfo; Castillo Torres, Pablo Nicolás; Mathieu, Christian; Vergara, Ricardo; Gonzalez, Alvaro; Gonzalez, Carmen Gloria; Araya, Hugo; Castillo, Andres; Torres, Juan Carlos; Covarrubias, Paulo; Bustos, Patricia; van Bakel, Harm; Fernandez, Jorge; Fasce, Rodrigo A.; Johow, Magdalena; Neira, Victor; Medina, Rafael
    Highly pathogenic H5N1 avian influenza viruses (HPAIV) belonging to lineage 2.3.4.4b emerged in Chile in December 2022, leading to mass mortality events in wild birds, poultry, and marine mammals and one human case. We detected HPAIV in 7,33% (714/9745) of cases between December 2022-April 2023 and sequenced 177 H5N1 virus genomes from poultry, marine mammals, a human, and wild birds spanning >3800 km of Chilean coastline. Chilean viruses were closely related to Peru's H5N1 outbreak, consistent with north-to-south spread down the Pacific coastline. One human virus and nine marine mammal viruses in Chile had the rare PB2 D701N mammalian-adaptation mutation and clustered phylogenetically despite being sampled 5 weeks and hundreds of kilometers apart. These viruses shared additional genetic signatures, including another mammalian PB2 adaptation (Q591K, n = 6), synonymous mutations, and minor variants. Several mutations were detected months later in sealions in the Atlantic coast, indicating that the pinniped outbreaks on the west and east coasts of South America are genetically linked. These data support sustained mammal-to-mammal transmission of HPAIV in marine mammals over thousands of kilometers of Chile's Pacific coastline, which subsequently continued through the Atlantic coastline.
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    Cross-species and mammal-to-mammal transmission of clade 2.3.4.4b highly pathogenic avian influenza A/H5N1 with PB2 adaptations
    (2025) Pardo Roa, Catalina; Nelson, Martha I.; Ariyama, Naomi; Aguayo, Carolina; Almonacid Cárdenas, Leonardo Iván; Gonzalez-Reiche, Ana S.; Muñoz, Gabriela; Ulloa, Mauricio; Avila, Claudia; Navarro, Carlos; Reyes, Rodolfo; Castillo Torres, Pablo Nicolás; Mathieu, Christian; Vergara, Ricardo; Gonzalez, Alvaro; Gonzalez, Carmen Gloria; Araya, Hugo; Castillo, Andres; Torres, Juan Carlos; Covarrubias, Paulo; Bustos, Patricia; van Bakel, Harm; Fernandez, Jorge; Fasce, Rodrigo A.; Johow, Magdalena; Neira, Victor; Medina, Rafael
    Highly pathogenic H5N1 avian influenza viruses (HPAIV) belonging to lineage 2.3.4.4b emerged in Chile in December 2022, leading to mass mortality events in wild birds, poultry, and marine mammals and one human case. We detected HPAIV in 7,33% (714/9745) of cases between December 2022-April 2023 and sequenced 177 H5N1 virus genomes from poultry, marine mammals, a human, and wild birds spanning >3800 km of Chilean coastline. Chilean viruses were closely related to Peru's H5N1 outbreak, consistent with north-to-south spread down the Pacific coastline. One human virus and nine marine mammal viruses in Chile had the rare PB2 D701N mammalian-adaptation mutation and clustered phylogenetically despite being sampled 5 weeks and hundreds of kilometers apart. These viruses shared additional genetic signatures, including another mammalian PB2 adaptation (Q591K, n = 6), synonymous mutations, and minor variants. Several mutations were detected months later in sealions in the Atlantic coast, indicating that the pinniped outbreaks on the west and east coasts of South America are genetically linked. These data support sustained mammal-to-mammal transmission of HPAIV in marine mammals over thousands of kilometers of Chile's Pacific coastline, which subsequently continued through the Atlantic coastline.
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    Genome-Wide Characterization of Light-Regulated Gene Expression in Botrytis cinerea Reveals Underlying Complex Photobiology
    (2023) Perez-Lara, Gabriel; Olivares-Yanez, Consuelo; van Bakel, Harm; Larrondo, Luis F.; Canessa, Paulo
    Botrytis cinerea is a necrotrophic fungus characterized mainly by its wide host range of infected plants. The deletion of the white-collar-1 gene (bcwcl1), which encodes for a blue-light receptor/transcription factor, causes a decrease in virulence, particularly when assays are conducted in the presence of light or photocycles. However, despite ample characterization, the extent of the light-modulated transcriptional responses regulated by BcWCL1 remains unknown. In this study, pathogen and pathogen:host RNA-seq analyses, conducted during non-infective in vitro plate growth and when infecting Arabidopsis thaliana leaves, respectively, informed on the global gene expression patterns after a 60 min light pulse on the wild-type B05.10 or increment bcwcl1 B. cinerea strains. The results revealed a complex fungal photobiology, where the mutant did not react to the light pulse during its interaction with the plant. Indeed, when infecting Arabidopsis, no photoreceptor-encoding genes were upregulated upon the light pulse in the increment bcwcl1 mutant. Differentially expressed genes (DEGs) in B. cinerea under non-infecting conditions were predominantly related to decreased energy production in response to the light pulse. In contrast, DEGs during infection significantly differ in the B05.10 strain and the? bcwcl1 mutant. Upon illumination at 24 h post-infection in planta, a decrease in the B. cinerea virulence-associated transcripts was observed. Accordingly, after a light pulse, biological functions associated with plant defense appear enriched among light-repressed genes in fungus-infected plants. Taken together, our results show the main transcriptomic differences between wild-type B. cinerea B05.10 and ? bcwcl1 after a 60 min light pulse when growing saprophytically on a Petri dish and necrotrophically over A. thaliana.