scholarly journals Replication Efficiency of Influenza A Virus H9N2: A Comparative Analysis Between Different Origin Cell Types

2013 ◽  
Vol 6 (9) ◽  
Author(s):  
Nima Zarrin Lebas ◽  
Shahla Shahsavandi ◽  
Ashraf Mohammadi ◽  
Mohammad Majid Ebrahimi ◽  
Mehran Bakhshesh
Keyword(s):  
Comparative Analysis ◽  
Influenza A Virus ◽  
Influenza A ◽  
Cell Types ◽  
Replication Efficiency ◽  
Different Origin

scholarly journals Infection of Human Airway Epithelium by Human and Avian Strains of Influenza A Virus

2006 ◽  
Vol 80 (16) ◽  
pp. 8060-8068 ◽  
Author(s):  
Catherine I. Thompson ◽  
Wendy S. Barclay ◽  
Maria C. Zambon ◽  
Raymond J. Pickles
Keyword(s):  
Sialic Acid ◽  
Avian Influenza ◽  
Influenza A Virus ◽  
Airway Epithelium ◽  
Influenza A ◽  
Cell Types ◽  
Influenza Viruses ◽  
Apical Surface ◽  
Ciliated Cells ◽  
Human Viruses

ABSTRACT We describe the characterization of influenza A virus infection of an established in vitro model of human pseudostratified mucociliary airway epithelium (HAE). Sialic acid receptors for both human and avian viruses, α-2,6- and α-2,3-linked sialic acids, respectively, were detected on the HAE cell surface, and their distribution accurately reflected that in human tracheobronchial tissue. Nonciliated cells present a higher proportion of α-2,6-linked sialic acid, while ciliated cells possess both sialic acid linkages. Although we found that human influenza viruses infected both ciliated and nonciliated cell types in the first round of infection, recent human H3N2 viruses infected a higher proportion of nonciliated cells in HAE than a 1968 pandemic-era human virus, which infected proportionally more ciliated cells. In contrast, avian influenza viruses exclusively infected ciliated cells. Although a broad-range neuraminidase abolished infection of HAE by human parainfluenza virus type 3, this treatment did not significantly affect infection by influenza viruses. All human viruses replicated efficiently in HAE, leading to accumulation of nascent virus released from the apical surface between 6 and 24 h postinfection with a low multiplicity of infection. Avian influenza A viruses also infected HAE, but spread was limited compared to that of human viruses. The nonciliated cell tropism of recent human H3N2 viruses reflects a preference for the sialic acid linkages displayed on these cell types and suggests a drift in the receptor binding phenotype of the H3 hemagglutinin protein as it evolves in humans away from its avian virus precursor.

scholarly journals Comprehensive Transcriptomic Analysis Identifies Novel Antiviral Factors Against Influenza A Virus Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Ao Zhou ◽  
Xia Dong ◽  
Mengyun Liu ◽  
Bin Tang
Keyword(s):  
Epithelial Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Broad Spectrum ◽  
Influenza A ◽  
Cell Types ◽  
Immune Defense ◽  
Host Responses ◽  
Different Cell Types ◽  
Host Genes

Influenza A virus (IAV) has a higher genetic variation, leading to the poor efficiency of traditional vaccine and antiviral strategies targeting viral proteins. Therefore, developing broad-spectrum antiviral treatments is particularly important. Host responses to IAV infection provide a promising approach to identify antiviral factors involved in virus infection as potential molecular drug targets. In this study, in order to better illustrate the molecular mechanism of host responses to IAV and develop broad-spectrum antiviral drugs, we systematically analyzed mRNA expression profiles of host genes in a variety of human cells, including transformed and primary epithelial cells infected with different subtypes of IAV by mining 35 microarray datasets from the GEO database. The transcriptomic results showed that IAV infection resulted in the difference in expression of amounts of host genes in all cell types, especially those genes participating in immune defense and antiviral response. In addition, following the criteria of P<0.05 and |logFC|≥1.5, we found that some difference expression genes were overlapped in different cell types under IAV infection via integrative gene network analysis. IFI6, IFIT2, ISG15, HERC5, RSAD2, GBP1, IFIT3, IFITM1, LAMP3, USP18, and CXCL10 might act as key antiviral factors in alveolar basal epithelial cells against IAV infection, while BATF2, CXCL10, IFI44L, IL6, and OAS2 played important roles in airway epithelial cells in response to different subtypes of IAV infection. Additionally, we also revealed that some overlaps (BATF2, IFI44L, IFI44, HERC5, CXCL10, OAS2, IFIT3, USP18, OAS1, IFIT2) were commonly upregulated in human primary epithelial cells infected with high or low pathogenicity IAV. Moreover, there were similar defense responses activated by IAV infection, including the interferon-regulated signaling pathway in different phagocyte types, although the differentially expressed genes in different phagocyte types showed a great difference. Taken together, our findings will help better understand the fundamental patterns of molecular responses induced by highly or lowly pathogenic IAV, and the overlapped genes upregulated by IAV in different cell types may act as early detection markers or broad-spectrum antiviral targets.

scholarly journals Unique Transcriptional Architecture in Airway Epithelial Cells and Macrophages Shapes Distinct Responses following Influenza Virus Infection Ex Vivo

2019 ◽  
Vol 93 (6) ◽  
Author(s):  
Joel Z. Ma ◽  
Wy Ching Ng ◽  
Luke Zappia ◽  
Linden J. Gearing ◽  
Moshe Olshansky ◽  
...  
Keyword(s):  
Steady State ◽  
Epithelial Cells ◽  
Rna Sequencing ◽  
Influenza A Virus ◽  
Influenza A ◽  
Cell Types ◽  
Airway Epithelial Cells ◽  
Type I ◽  
Airway Epithelial ◽  
Transcriptional Responses

ABSTRACT Airway epithelial cells and macrophages differ markedly in their responses to influenza A virus (IAV) infection. To investigate transcriptional responses underlying these differences, purified subsets of type II airway epithelial cells (ATII) and alveolar macrophages (AM) recovered from the lungs of mock- or IAV-infected mice at 9 h postinfection were subjected to RNA sequencing. This time point was chosen to allow for characterization of cell types first infected with the virus inoculum, prior to multicycle virus replication and the infiltration of inflammatory cells into the airways. In the absence of infection, AM predominantly expressed genes related to immunity, whereas ATII expressed genes consistent with their physiological roles in the lung. Following IAV infection, AM almost exclusively activated cell-intrinsic antiviral pathways that were dependent on interferon (IFN) regulatory factor 3/7 (IRF3/7) and/or type I IFN signaling. In contrast, IAV-infected ATII activated a broader range of physiological responses, including cell-intrinsic antiviral pathways, which were both independent of and dependent on IRF3/7 and/or type I IFN. These data suggest that transcriptional profiles hardwired during development are a major determinant underlying the different responses of ATII and AM to IAV infection. IMPORTANCE Airway epithelial cells (AEC) and airway macrophages (AM) represent major targets of influenza A virus (IAV) infection in the lung, yet the two cell types respond very differently to IAV infection. We have used RNA sequencing to define the host transcriptional responses in each cell type under steady-state conditions as well as following IAV infection. To do this, different cell subsets isolated from the lungs of mock- and IAV-infected mice were subjected to RNA sequencing. Under steady-state conditions, AM and AEC express distinct transcriptional activities, consistent with distinct physiological roles in the airways. Not surprisingly, these cells also exhibited major differences in transcriptional responses following IAV infection. These studies shed light on how the different transcriptional architectures of airway cells from two different lineages drive transcriptional responses to IAV infection.

scholarly journals Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity

2016 ◽  
Vol 113 (14) ◽  
pp. 3861-3866 ◽  
Author(s):  
Jennifer R. Hamilton ◽  
David Sachs ◽  
Jean K. Lim ◽  
Ryan A. Langlois ◽  
Peter Palese ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Cell Types ◽  
Innate Immune ◽  
Viral Immunity ◽  
Club Cells ◽  
Response Phenotype ◽  
Infected Cells ◽  
Induced Immunity ◽  
Nonspecific Inflammation

A brief window of antigen-nonspecific protection has been observed after influenza A virus (IAV) infection. Although this temporary immunity has been assumed to be the result of residual nonspecific inflammation, this period of induced immunity has not been fully studied. Because IAV has long been characterized as a cytopathic virus (based on its ability to rapidly lyse most cell types in culture), it has been a forgone conclusion that directly infected cells could not be contributing to this effect. Using a Cre recombinase-expressing IAV, we have previously shown that club cells can survive direct viral infection. We show here not only that these cells can eliminate all traces of the virus and survive but also that they acquire a heightened antiviral response phenotype after surviving. Moreover, we experimentally demonstrate temporary nonspecific viral immunity after IAV infection and show that surviving cells are required for this phenotype. This work characterizes a virally induced modulation of the innate immune response that may represent a new mechanism to prevent viral diseases.

scholarly journals Mutations in the M-Gene Segment Can Substantially Increase Replication Efficiency of NS1 Deletion Influenza A Virus in MDCK Cells

2012 ◽  
Vol 86 (22) ◽  
pp. 12341-12350 ◽  
Author(s):  
R. van Wielink ◽  
M. M. Harmsen ◽  
D. E. Martens ◽  
B. P. H. Peeters ◽  
R. H. Wijffels ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Mdck Cells ◽  
Gene Segment ◽  
M Gene ◽  
Replication Efficiency

scholarly journals Co-infection of influenza A virus enhances SARS-CoV-2 infectivity

2020 ◽  
Author(s):  
Lei Bai ◽  
Yongliang Zhao ◽  
Jiazhen Dong ◽  
Simeng Liang ◽  
Ming Guo ◽  
...  
Keyword(s):  
Public Health ◽  
Viral Load ◽  
Influenza A Virus ◽  
Northern Hemisphere ◽  
Influenza A ◽  
Cell Types ◽  
Lung Damage ◽  
Live Virus ◽  
Severe Lung

AbstractThe upcoming flu season in the northern hemisphere merging with the current COVID-19 pandemic raises a potentially severe threat to public health. Through experimental co-infection of IAV with either pseudotyped or SARS-CoV-2 live virus, we found that IAV pre-infection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Remarkably, increased SARS-CoV-2 viral load and more severe lung damage were observed in mice co-infected with IAV in vivo. Moreover, such enhancement of SARS-CoV-2 infectivity was not seen with several other viruses probably due to a unique IAV segment as an inducer to elevate ACE2 expression. This study illustrates that IAV has a special nature to aggravate SARS-CoV-2 infection, and prevention of IAV is of great significance during the COVID-19 pandemic.

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