Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/6637
Characterization in vitro and in vivo of a pandemic H1N1 influenza virus from a fatal case
Rodriguez, Ariel | Falcon, Ana | Cuevas, Maria Teresa ISCIII | Pozo Sánchez, Francisco ISCIII | Guerra, Susana | Garcia-Barreno, Blanca ISCIII | Martinez-Orellana, Pamela | Pérez-Breña, Pilar ISCIII | Montoya, María CNIC | Melero, Jose Antonio ISCIII | Pizarro, Manuel | Ortin, Juan | Casas, Inmaculada ISCIII | Nieto, Amelia
PLoS One. 2013;8(1):e53515
Pandemic 2009 H1N1 (pH1N1) influenza viruses caused mild symptoms in most infected patients. However, a greater rate of severe disease was observed in healthy young adults and children without co-morbid conditions. Here we tested whether influenza strains displaying differential virulence could be present among circulating pH1N1 viruses. The biological properties and the genotype of viruses isolated from a patient showing mild disease (M) or from a fatal case (F), both without known co-morbid conditions were compared in vitro and in vivo. The F virus presented faster growth kinetics and stronger induction of cytokines than M virus in human alveolar lung epithelial cells. In the murine model in vivo, the F virus showed a stronger morbidity and mortality than M virus. Remarkably, a higher proportion of mice presenting infectious virus in the hearts, was found in F virus-infected animals. Altogether, the data indicate that strains of pH1N1 virus with enhanced pathogenicity circulated during the 2009 pandemic. In addition, examination of chemokine receptor 5 (CCR5) genotype, recently reported as involved in severe influenza virus disease, revealed that the F virus-infected patient was homozygous for the deleted form of CCR5 receptor (CCR5Δ32).
Adult | Alleles | Amino Acids | Animals | Cell Line | Cells, Cultured | Cytokines | Epithelial Cells | Female | Humans | Immunohistochemistry | Influenza A Virus, H1N1 Subtype | Influenza, Human | Mice | Mice, Inbred BALB C | Orthomyxoviridae Infections | Pulmonary Alveoli | Receptors, CCR5 | Viral Load | Virus Replication | Pandemics
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