RSV protects bystander cells against IAV infection by triggering secretion of type I and type III interferons

Czerkies, Maciej; Kochańczyk, Marek; Korwek, Zbigniew; Prus, Wiktor; Lipniacki, Tomasz

doi:10.1101/2021.10.11.463877

Cited by 3 publications

(2 citation statements)

References 75 publications

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“…Interestingly, Czerkies et al (2022) have reported interference between respiratory syncytial virus (RSV) and influenza A virus H1N1 in human alveolar epithelial cells (A549). The authors of the report found that previous infection of cells with RSV does not prevent a subsequent influenza virus infection, whereas RSV indeed protects bystander cells against influenza virus infection by triggering secretion of type I and type III IFNs [83]. A similar effect in PCV2b/SwIV coinfected NPTr cells could be involved and explain the PCV2b impact on the apparent inhibition of SwIV replication.…”

Section: Discussionmentioning

confidence: 95%

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Pulgaron¹,

Provost²,

Pesant³

et al. 2023

Preprint

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The pathogenesis of porcine circovirus type 2b (PCV2b) and swine influenza A virus (SwIV) during co-infection in swine respiratory cells is poorly understood. To elucidate the impact of PCV2b/SwIV co-infection, newborn porcine tracheal epithelial cells (NPTr) and immortalized porcine alveolar macrophages (iPAM 3D4/21) were co-infected with PCV2b and SwIV (H1N1 or H3N2 genotype). Viral replication, cell viability and cytokine mRNA expression were determined and compared between single-infected and co-infected cells. Finally, 3’mRNA sequencing was performed to identify the modulation of gene expression and cellular pathways in co-infected cells. It was found that PCV2b significantly decreased and improved SwIV replication, in co-infected NPTr and iPAM 3D4/21 cells respectively, compared to single infected cells. Interestingly, PCV2b/SwIV co-infection synergistically up-regulated IFN expression in NPTr cells whereas in iPAM 3D4/21 cells, PCV2b impaired the SwIV IFN induced response, both correlating with SwIV replication modulation. RNA-sequencing analyses revealed that the modulation of gene expression and enriched cellular pathways during PCV2b/SwIV H1N1 co-infection is regulated in a cell type-dependent-manner. This study revealed different outcomes of PCV2b/SwIV co-infection in porcine epithelial cells and macrophages and provides new insights on porcine viral co-infections pathogenesis.

show abstract

Section: Discussionmentioning

confidence: 95%

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Pulgaron¹,

Provost²,

Pesant³

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Interestingly, Czerkies et al (2022) have reported interference between respiratory syncytial virus (RSV) and influenza A virus H1N1 in human alveolar epithelial cells (A549). The authors of the report found that previous infection of cells with RSV does not prevent a subsequent influenza virus infection, whereas RSV indeed protects bystander cells against influenza virus infection by triggering secretion of type I and type III IFNs [ 88 ]. A similar effect in PCV2b/SwIV co-infected NPTr cells could be involved and explain the PCV2b impact on the apparent inhibition of SwIV replication.…”

Section: Discussionmentioning

confidence: 99%

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Pulgarón

Provost

Pesant

et al. 2023

Viruses

View full text Add to dashboard Cite

The pathogenesis of porcine circovirus type 2b (PCV2b) and swine influenza A virus (SwIV) during co-infection in swine respiratory cells is poorly understood. To elucidate the impact of PCV2b/SwIV co-infection, newborn porcine tracheal epithelial cells (NPTr) and immortalized porcine alveolar macrophages (iPAM 3D4/21) were co-infected with PCV2b and SwIV (H1N1 or H3N2 genotype). Viral replication, cell viability and cytokine mRNA expression were determined and compared between single-infected and co-infected cells. Finally, 3′mRNA sequencing was performed to identify the modulation of gene expression and cellular pathways in co-infected cells. It was found that PCV2b significantly decreased or improved SwIV replication in co-infected NPTr and iPAM 3D4/21 cells, respectively, compared to single-infected cells. Interestingly, PCV2b/SwIV co-infection synergistically up-regulated IFN expression in NPTr cells, whereas in iPAM 3D4/21 cells, PCV2b impaired the SwIV IFN induced response, both correlating with SwIV replication modulation. RNA-sequencing analyses revealed that the modulation of gene expression and enriched cellular pathways during PCV2b/SwIV H1N1 co-infection is regulated in a cell-type-dependent manner. This study revealed different outcomes of PCV2b/SwIV co-infection in porcine epithelial cells and macrophages and provides new insights on porcine viral co-infections pathogenesis.

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Unraveling the Role of Viral Interference in Disrupting Biennial RSV Epidemics in Northern Stockholm

Li,

Hamrin,

Weinberger

et al. 2024

Preprint

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Respiratory syncytial virus (RSV) primarily impacts infants and older adults, with seasonal winter outbreaks in temperate countries. Biennial cycles of RSV activity have also been identified in Northern Europe and some states in the United States. Delayed RSV activity was reported worldwide during the 2009 influenza pandemic, and a disrupted biennial pattern of RSV activity was observed in northern Stockholm following the pandemic. Biennial patterns shifted to early/large outbreaks in even-numbered years and late/small outbreaks in odd-numbered years. However, the mechanisms underpinning this change in pattern remain unknown. In this work, we constructed an age-stratified mechanistic model to explicitly test three factors that could lead to the change in RSV transmission dynamics: 1) birth rates, 2) temperatures, and 3) viral interference. By fitting the model to weekly RSV admission data over a 20-year period and comparing different models, we found that viral interference from influenza was the only mechanism that explained the shifted biennial pattern. Our work demonstrates the complex interplay between different respiratory viruses, providing evidence that supports the presence of interactions between the H1N1 pandemic influenza virus and RSV at the population level, with implications for future public health interventions.

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RSV protects bystander cells against IAV infection by triggering secretion of type I and type III interferons

Cited by 3 publications

References 75 publications

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Unraveling the Role of Viral Interference in Disrupting Biennial RSV Epidemics in Northern Stockholm

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