“…Notably, the influenza virus can modulate the dynamics of different cytoskeletal filaments by promoting their remodeling to support viral replication [ 95 ]. In this regard, the IAV can subvert the structural organization of cytokeratin 8, enhancing its phosphorylation state and thereby promoting its replicative efficiency [ 96 ]. Moreover, it has been assessed that the influenza virus stimulated the phosphorylation of cytoskeletal ezrin, radixin, and moesin, inducing structural cytoskeletal changes and permeability increases in pulmonary microvascular endothelial cells that favor its replication [ 97 ].…”
Section: The Involvement Of the Cellular Cytoskeleton In Influenza Vi...mentioning
Influenza is one of the most prevalent causes of death worldwide. Influenza A viruses (IAVs) naturally infect various avian and mammalian hosts, causing seasonal epidemics and periodic pandemics with high morbidity and mortality. The recent SARS-CoV-2 pandemic showed how an animal virus strain could unpredictably acquire the ability to infect humans with high infection transmissibility. Importantly, highly pathogenic avian influenza A viruses (AIVs) may cause human infections with exceptionally high mortality. Because these latter infections pose a pandemic potential, analyzing the ecology and evolution features of host expansion helps to identify new broad-range therapeutic strategies. Although IAVs are the prototypic example of molecular strategies that capitalize on their coding potential, the outcome of infection depends strictly on the complex interactions between viral and host cell factors. Most of the studies have focused on the influenza virus, while the contribution of host factors remains largely unknown. Therefore, a comprehensive understanding of mammals’ host response to AIV infection is crucial. This review sheds light on the involvement of the cellular cytoskeleton during the highly pathogenic AIV infection of mammalian hosts, allowing a better understanding of its modulatory role, which may be relevant to therapeutic interventions for fatal disease prevention and pandemic management.
“…Notably, the influenza virus can modulate the dynamics of different cytoskeletal filaments by promoting their remodeling to support viral replication [ 95 ]. In this regard, the IAV can subvert the structural organization of cytokeratin 8, enhancing its phosphorylation state and thereby promoting its replicative efficiency [ 96 ]. Moreover, it has been assessed that the influenza virus stimulated the phosphorylation of cytoskeletal ezrin, radixin, and moesin, inducing structural cytoskeletal changes and permeability increases in pulmonary microvascular endothelial cells that favor its replication [ 97 ].…”
Section: The Involvement Of the Cellular Cytoskeleton In Influenza Vi...mentioning
Influenza is one of the most prevalent causes of death worldwide. Influenza A viruses (IAVs) naturally infect various avian and mammalian hosts, causing seasonal epidemics and periodic pandemics with high morbidity and mortality. The recent SARS-CoV-2 pandemic showed how an animal virus strain could unpredictably acquire the ability to infect humans with high infection transmissibility. Importantly, highly pathogenic avian influenza A viruses (AIVs) may cause human infections with exceptionally high mortality. Because these latter infections pose a pandemic potential, analyzing the ecology and evolution features of host expansion helps to identify new broad-range therapeutic strategies. Although IAVs are the prototypic example of molecular strategies that capitalize on their coding potential, the outcome of infection depends strictly on the complex interactions between viral and host cell factors. Most of the studies have focused on the influenza virus, while the contribution of host factors remains largely unknown. Therefore, a comprehensive understanding of mammals’ host response to AIV infection is crucial. This review sheds light on the involvement of the cellular cytoskeleton during the highly pathogenic AIV infection of mammalian hosts, allowing a better understanding of its modulatory role, which may be relevant to therapeutic interventions for fatal disease prevention and pandemic management.
“…Concerning cell culture methods, the nasal swab was tested by: (i) immunofluorescence assay in exfoliated cells directly derived from the sample, to detect Respiratory Syncytial virus and Influenza antigens (monoclonal antibodies to Respiratory Syncytial Virus and Influenza A and B species; IMAGEN TM Respiratory Syncytial Virus kit and Influenza Virus A and B kit, OXOID), that was positive for Influenza virus; (ii) the same immunofluorescence technique after a 24-hours incubation of inoculated cell monolayers grown on a chamber-slide to detect influenza (A and B), parainfluenza (1–3), RSV-specific antigens (rapid cell culture method) performed as previously described [ 3 , 11 , 12 ]; it resulted positive for Influenza A virus ( Figure 1 A); (iii) conventional cell culture method by sample inoculation in different cell type monolayers to detect cytopathogenic respiratory viral agents by daily microscopic observation, according to previously described methods [ 3 , 11 , 12 ]. Figure 1 (Panels A): Immunofluorescence analysis of Influenza A (FLU A) antigen expression in MDCK SIAT-1 cell monolayers at 24h p.i.…”
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