Purification of sialoglycoproteins from bovine milk using serotonin-functionalized magnetic particles and their application against influenza A virus

2020 ◽  
Vol 11 (8) ◽  
pp. 6911-6920
Author(s):  
Xilong Wang ◽  
Tianran Ma ◽  
Hanjie Yu ◽  
Zhuo Chen ◽  
Bojing Zhu ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Magnetic Particles ◽  
Mdck Cells ◽  
Bovine Milk ◽  
Functionalized Particles

Serotonin-functionalized particles were used to isolate sialoglycoproteins, which have the ability to inhibit the attachment of IAV mimics to MDCK cells.

scholarly journals Comprehensive N ‐glycosylation analysis of the influenza A virus proteins HA and NA from adherent and suspension MDCK cells

FEBS Journal ◽  
2021 ◽  
Author(s):  
Alexander Pralow ◽  
Marcus Hoffmann ◽  
Terry Nguyen‐Khuong ◽  
Markus Pioch ◽  
René Hennig ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Mdck Cells ◽  
Virus Proteins

A human cell polarity protein Lgl2 regulates influenza A virus nucleoprotein exportation from nucleus in MDCK cells

2020 ◽  
Vol 45 (1) ◽  
Author(s):  
Jing Liu ◽  
Haiying Wang ◽  
Mengdan Fang ◽  
Xuexin Chen ◽  
Xiaobo Zeng
Keyword(s):  
Cell Polarity ◽  
Influenza A Virus ◽  
Human Cell ◽  
Influenza A ◽  
Mdck Cells

Characterization of proteins with Siaα2-3/6Gal-linked glycans from bovine milk and role of their glycans against influenza A virus

2018 ◽  
Vol 9 (10) ◽  
pp. 5198-5208 ◽  
Author(s):  
Hanjie Yu ◽  
Yaogang Zhong ◽  
Zhiwei Zhang ◽  
Xiawei Liu ◽  
Kun Zhang ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Bovine Milk ◽  
Milk Proteins ◽  
Biological Functions ◽  
Wide Range ◽  
Range Of Functions ◽  
Bovine Milk Proteins

The bovine milk proteins have a wide range of functions, but the role of the attached glycans in their biological functions has not been fully understood yet.

scholarly journals Lack of Bax Prevents Influenza A Virus-Induced Apoptosis and Causes Diminished Viral Replication

2009 ◽  
Vol 83 (16) ◽  
pp. 8233-8246 ◽  
Author(s):  
Jeffrey E. McLean ◽  
Emmanuel Datan ◽  
Demetrius Matassov ◽  
Zahra F. Zakeri
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Mdck Cells ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Induction Of Apoptosis ◽  
Influenza A Virus Infection ◽  
Induced Apoptosis

ABSTRACT The ectopic overexpression of Bcl-2 restricts both influenza A virus-induced apoptosis and influenza A virus replication in MDCK cells, thus suggesting a role for Bcl-2 family members during infection. Here we report that influenza A virus cannot establish an apoptotic response without functional Bax, a downstream target of Bcl-2, and that both Bax and Bak are directly involved in influenza A virus replication and virus-induced cell death. Bak is substantially downregulated during influenza A virus infection in MDCK cells, and the knockout of Bak in mouse embryonic fibroblasts yields a dramatic rise in the rate of apoptotic death and a corresponding increase in levels of virus replication, suggesting that Bak suppresses both apoptosis and the replication of virus and that the virus suppresses Bak. Bax, however, is activated and translocates from the cytosol to the mitochondria; this activation is required for the efficient induction of apoptosis and virus replication. The knockout of Bax in mouse embryonic fibroblasts blocks the induction of apoptosis, restricts the infection-mediated activation of executioner caspases, and inhibits virus propagation. Bax knockout cells still die but by an alternative death pathway displaying characteristics of autophagy, similarly to our previous observation that influenza A virus infection in the presence of a pancaspase inhibitor leads to an increase in levels of autophagy. The knockout of Bax causes a retention of influenza A virus NP within the nucleus. We conclude that the cell and virus struggle to control apoptosis and autophagy, as appropriately timed apoptosis is important for the replication of influenza A virus.

scholarly journals Effects of Host-Dependent Glycosylation of Hemagglutinin on Receptor-Binding Properties of H1N1 Human Influenza A Virus Grown in MDCK Cells and in Embryonated Eggs

Virology ◽  
1998 ◽  
Vol 247 (2) ◽  
pp. 170-177 ◽  
Author(s):  
A.S. Gambaryan ◽  
V.P. Marinina ◽  
A.B. Tuzikov ◽  
N.V. Bovin ◽  
I.A. Rudneva ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Receptor Binding ◽  
Influenza A ◽  
Mdck Cells ◽  
Human Influenza ◽  
Binding Properties

scholarly journals Extending the Cytoplasmic Tail of the Influenza A Virus M2 Protein Leads to Reduced Virus Replication In Vivo but Not In Vitro

2007 ◽  
Vol 82 (2) ◽  
pp. 1059-1063 ◽  
Author(s):  
Wai-Hong Wu ◽  
Andrew Pekosz
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Mdck Cells ◽  
Cytoplasmic Tail ◽  
M2 Protein ◽  
Coding Region ◽  
Epitope Tag ◽  
Carboxy Terminal

ABSTRACT A carboxy-terminal epitope tag introduced into the coding region of the A/WSN/33 M2 protein resulted in a recombinant virus (rWSN M2myc) which replicated to titers similar to those of the parental virus (rWSN) in MDCK cells. The rWSN M2myc virus was attenuated in its ability to induce mortality and weight loss after the intranasal inoculation of BALB/c mice, indicating that the M2 cytoplasmic tail plays a role in virus virulence. Mice infected with rWSN M2myc were completely protected from subsequent challenge with rWSN, suggesting that epitope tagging of the M2 protein may be a useful way of attenuating influenza A virus strains.

scholarly journals Cellular co-infection can modulate the efficiency of influenza A virus production and shape the interferon response

2019 ◽  
Author(s):  
Brigitte E. Martin ◽  
Jeremy D. Harris ◽  
Jiayi Sun ◽  
Katia Koelle ◽  
Christopher B. Brooke
Keyword(s):  
Influenza A Virus ◽  
Cell Lines ◽  
Influenza A ◽  
Mdck Cells ◽  
A549 Cells ◽  
Virus Production ◽  
Innate Immune ◽  
Type I ◽  
Functional Forms ◽  
A Cell

ABSTRACTDuring viral infection, the numbers of virions infecting individual cells can vary significantly over time and space. The functional consequences of this variation in cellular multiplicity of infection (MOI) remain poorly understood. Here, we rigorously quantify the phenotypic consequences of cellular MOI during influenza A virus (IAV) infection over a single round of replication in terms of cell death rates, viral output kinetics, interferon and antiviral effector gene transcription, and superinfection potential. By statistically fitting mathematical models to our data, we precisely define specific functional forms that quantitatively describe the modulation of these phenotypes by MOI at the single cell level. To determine the generality of these functional forms, we compare two distinct cell lines (MDCK cells and A549 cells), both infected with the H1N1 strain A/Puerto Rico/8/1934 (PR8). We find that a model assuming that infected cell death rates are independent of cellular MOI best fits the experimental data in both cell lines. We further observe that a model in which the rate and efficiency of virus production increase with cellular co-infection best fits our observations in MDCK cells, but not in A549 cells. In A549 cells, we also find that induction of type III interferon, but not type I interferon, is highly dependent on cellular MOI, especially at early timepoints. This finding identifies a role for cellular co-infection in shaping the innate immune response to IAV infection. Finally, we show that higher cellular MOI is associated with more potent superinfection exclusion, thus limiting the total number of virions capable of infecting a cell. Overall, this study suggests that the extent of cellular co-infection by influenza viruses may be a critical determinant of both viral production kinetics and cellular infection outcomes in a host cell type-dependent manner.AUTHOR SUMMARYDuring influenza A virus (IAV) infection, the number of virions to enter individual cells can be highly variable. Cellular co-infection appears to be common and plays an essential role in facilitating reassortment for IAV, yet little is known about how cellular co-infection influences infection outcomes at the cellular level. Here, we combine quantitative in vitro infection experiments with statistical model fitting to precisely define the phenotypic consequences of cellular co-infection in two cell lines. We reveal that cellular co-infection can increase and accelerate the efficiency of IAV production in a cell line-dependent fashion, identifying it as a potential determinant of viral replication kinetics. We also show that induction of type III, but not type I, interferon is highly dependent upon the number of virions that infect a given cell, implicating cellular co-infection as an important determinant of the host innate immune response to infection. Altogether, our findings show that cellular co-infection plays a crucial role in determining infection outcome. The integration of experimental and statistical modeling approaches detailed here represents a significant advance in the quantitative study of influenza virus infection and should aid ongoing efforts focused on the construction of mathematical models of IAV infection.

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