scholarly journals Interferon induction and not replication interference mainly determines anti-influenza virus activity of defective interfering particles

2021 ◽  
Author(s):  
Prerna Arora ◽  
Najat Bdeir ◽  
Sabine Gärtner ◽  
Stefanie Reiter ◽  
Lars Pelz ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Antiviral Activity ◽  
Innate Immune ◽  
Molecular Signatures ◽  
Defective Interfering Particles ◽  
Effector Functions ◽  
Virus Activity ◽  
Interferon Induction ◽  
Influenza Virus Replication

Defective interfering (DI) RNAs arise during influenza virus replication, can be packaged into particles (DIPs) and suppress spread of wildtype (WT) virus. However, the molecular signatures of DI RNAs and the mechanism underlying antiviral activity are incompletely understood. Here, we show that any central deletion is sufficient to convert a viral RNA into a DI RNA and that antiviral activity of DIPs is inversely correlated with DI RNA length when induction of the interferon (IFN) system is disfavored. When induction of the IFN system was allowed, it was found to be the major contributor to DIP antiviral activity. Finally, while both DIPs and influenza virus triggered expression of IFN-stimulated genes (ISG) only virus stimulated robust expression of IFN. These results suggest a key role of innate immune activation in DIP antiviral activity and point towards previously unappreciated differences in DIP- and influenza virus-mediated activation of the effector functions of the IFN system.

scholarly journals Role of the viral hemagglutinin in the anti-influenza virus activity of newly synthesized polycyclic amine compounds

2013 ◽  
Vol 99 (3) ◽  
pp. 281-291 ◽  
Author(s):  
Eva Torres ◽  
María D. Duque ◽  
Evelien Vanderlinden ◽  
Chunlong Ma ◽  
Lawrence H. Pinto ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Activity ◽  
Viral Hemagglutinin ◽  
Amine Compounds

Dynamic phospho-modification of viral proteins as a crucial regulatory layer of influenza A virus replication and innate immune responses

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Yvonne Boergeling ◽  
Linda Brunotte ◽  
Stephan Ludwig
Keyword(s):  
Influenza Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Current Knowledge ◽  
Viral Proteins ◽  
Transport Processes ◽  
Influenza Viruses ◽  
Innate Immune ◽  
A Genome ◽  
Influenza Virus Replication

Abstract Influenza viruses are small RNA viruses with a genome of about 13 kb. Because of this limited coding capacity, viral proteins have evolved to fulfil multiple functions in the infected cell. This implies that there must be mechanisms allowing to dynamically direct protein action to a distinct activity in a spatio-temporal manner. Furthermore, viruses exploit many cellular processes, which also have to be dynamically regulated during the viral replication cycle. Phosphorylation and dephosphorylation of proteins are fundamental for the control of many cellular responses. There is accumulating evidence that this mechanism represents a so far underestimated level of regulation in influenza virus replication. Here, we focus on the current knowledge of dynamics of phospho-modifications in influenza virus replication and show recent examples of findings underlining the crucial role of phosphorylation in viral transport processes as well as activation and counteraction of the innate immune response.

scholarly journals Phagocytosis, Degranulation and Extracellular Traps Release by Neutrophils—The Current Knowledge, Pharmacological Modulation and Future Prospects

2021 ◽  
Vol 12 ◽  
Author(s):  
Barbara Gierlikowska ◽  
Albert Stachura ◽  
Wojciech Gierlikowski ◽  
Urszula Demkow
Keyword(s):  
Molecular Mechanisms ◽  
Viral Infections ◽  
Current Knowledge ◽  
Innate Immune ◽  
Therapeutic Approaches ◽  
Effector Functions ◽  
Pharmacological Modulation ◽  
Synthetic Drugs ◽  
Extracellular Traps

Neutrophils are crucial elements of innate immune system, which assure host defense via a range of effector functions, such as phagocytosis, degranulation, and NET formation. The latest literature clearly indicates that modulation of effector functions of neutrophils may affect the treatment efficacy. Pharmacological modulation may affect molecular mechanisms activating or suppressing phagocytosis, degranulation or NET formation. In this review, we describe the role of neutrophils in physiology and in the course of bacterial and viral infections, illustrating the versatility and plasticity of those cells. This review also focus on the action of plant extracts, plant-derived compounds and synthetic drugs on effector functions of neutrophils. These recent advances in the knowledge can help to devise novel therapeutic approaches via pharmacological modulation of the described processes.

scholarly journals Antiviral activity of baicalin against influenza virus H1N1-pdm09 is due to modulation of NS1-mediated cellular innate immune responses

2014 ◽  
Vol 69 (5) ◽  
pp. 1298-1310 ◽  
Author(s):  
M. K. Nayak ◽  
A. S. Agrawal ◽  
S. Bose ◽  
S. Naskar ◽  
R. Bhowmick ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Antiviral Activity ◽  
Immune Responses ◽  
Innate Immune ◽  
Virus H1n1 ◽  
Innate Immune Responses

scholarly journals Metabolite Transporters as Regulators of Immunity

Metabolites ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 418
Author(s):  
Hauke J. Weiss ◽  
Stefano Angiari
Keyword(s):  
Intracellular Signaling ◽  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Signaling Cascades ◽  
Effector Functions ◽  
Immunological Responses ◽  
The Face ◽  
Specific Receptors

In the past decade, the rise of immunometabolism has fundamentally reshaped the face of immunology. As the functions and properties of many (immuno)metabolites have now been well described, their exchange among cells and their environment have only recently sparked the interest of immunologists. While many metabolites bind specific receptors to induce signaling cascades, some are actively exchanged between cells to communicate, or induce metabolic reprograming. In this review, we give an overview about how active metabolite transport impacts immune cell function and shapes immunological responses. We present some examples of how specific transporters feed into metabolic pathways and initiate intracellular signaling events in immune cells. In particular, we focus on the role of metabolite transporters in the activation and effector functions of T cells and macrophages, as prototype adaptive and innate immune cell populations.

scholarly journals Innate Immune Sensing of Influenza A Virus

Viruses ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 755
Author(s):  
Gaurav Malik ◽  
Yan Zhou
Keyword(s):  
Influenza Virus ◽  
Immune Responses ◽  
Influenza A ◽  
Influenza Virus Infection ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Pyrin Domain ◽  
Immune Sensing ◽  
Influenza Viral Infection

Influenza virus infection triggers host innate immune response by stimulating various pattern recognition receptors (PRRs). Activation of these PRRs leads to the activation of a plethora of signaling pathways, resulting in the production of interferon (IFN) and proinflammatory cytokines, followed by the expression of interferon-stimulated genes (ISGs), the recruitment of innate immune cells, or the activation of programmed cell death. All these antiviral approaches collectively restrict viral replication inside the host. However, influenza virus also engages in multiple mechanisms to subvert the innate immune responses. In this review, we discuss the role of PRRs such as Toll-like receptors (TLRs), Retinoic acid-inducible gene I (RIG-I), NOD-, LRR-, pyrin domain-containing protein 3 (NLRP3), and Z-DNA binding protein 1 (ZBP1) in sensing and restricting influenza viral infection. Further, we also discuss the mechanisms influenza virus utilizes, especially the role of viral non-structure proteins NS1, PB1-F2, and PA-X, to evade the host innate immune responses.

scholarly journals Dynamics of Biologically Active Subpopulations of Influenza Virus: Plaque-Forming, Noninfectious Cell-Killing, and Defective Interfering Particles

2009 ◽  
Vol 83 (16) ◽  
pp. 8122-8130 ◽  
Author(s):  
Philip I. Marcus ◽  
John M. Ngunjiri ◽  
Margaret J. Sekellick
Keyword(s):  
Influenza Virus ◽  
Mdck Cells ◽  
Cell Killing ◽  
Biologically Active ◽  
High Multiplicity ◽  
Defective Interfering Particles ◽  
New Class ◽  
Active Particles ◽  
Large Numbers

ABSTRACT The dynamic changes in the temporal appearance and quantity of a new class of influenza virus, noninfectious cell-killing particles (niCKP), were compared to defective interfering particles (DIP). After a single high-multiplicity passage in MDCK cells of an egg-derived stock that lacked detectable niCKP or DIP, both classes of particles appeared in large numbers (>5 × 108/ml), and the plaque-forming particle (PFP) titer dropped ∼60-fold. After two additional serial high-multiplicity passages the DIP remained relatively constant, the DIP/niCKP ratio reached 10:1, and the PFP had declined by about 10,000-fold. Together, the niCKP and DIP subpopulations constituted ca. 20% of the total hemagglutinating particle population in which these noninfectious biologically active particles (niBAP) were subsumed. DIP neither killed cells nor interfered with the cell-killing (apoptosis-inducing) activity of niCKP or PFP (infectious CKP), even though they blocked the replication of PFP. Relative to the UV-target of ∼13,600 nucleotides (nt) for inactivation of PFP, the UV target for niCKP was ∼2,400 nt, consistent with one of the polymerase subunit genes, and that for DIP was ∼350 nt, consistent with the small DI-RNA responsible for DIP-mediated interference. Thus, niCKP and DIP are viewed as distinct particles with a propensity to form during infection at high multiplicities. These conditions are postulated to cause aberrations in the temporally regulated replication of virus and its packaging, leading to the production of niBAP. DIP have been implicated in the virulence of influenza virus, but the role of niCKP is yet unknown.

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