scholarly journals The Multifarious Role of 14-3-3 Family of Proteins in Viral Replication

Viruses ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 436 ◽  
Author(s):  
Kavitha Ganesan Nathan ◽  
Sunil K. Lal
Keyword(s):  
Protein Interactions ◽  
Viral Infections ◽  
Pharmaceutical Research ◽  
Host Protein ◽  
Dna Viruses ◽  
Wide Range ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Rna And Dna

The 14-3-3 proteins are a family of ubiquitous and exclusively eukaryotic proteins with an astoundingly significant number of binding partners. Their binding alters the activity, stability, localization, and phosphorylation state of a target protein. The association of 14-3-3 proteins with the regulation of a wide range of general and specific signaling pathways suggests their crucial role in health and disease. Recent studies have linked 14-3-3 to several RNA and DNA viruses that may contribute to the pathogenesis and progression of infections. Therefore, comprehensive knowledge of host–virus interactions is vital for understanding the viral life cycle and developing effective therapeutic strategies. Moreover, pharmaceutical research is already moving towards targeting host proteins in the control of virus pathogenesis. As such, targeting the right host protein to interrupt host–virus interactions could be an effective therapeutic strategy. In this review, we generated a 14-3-3 protein interactions roadmap in viruses, using the freely available Virusmentha network, an online virus–virus or virus–host interaction tool. Furthermore, we summarize the role of the 14-3-3 family in RNA and DNA viruses. The participation of 14-3-3 in viral infections underlines its significance as a key regulator for the expression of host and viral proteins.

scholarly journals Role of Mitochondria in Viral Infections

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 232
Author(s):  
Srikanth Elesela ◽  
Nicholas W. Lukacs
Keyword(s):  
Viral Infections ◽  
Mitochondrial Dynamics ◽  
The Body ◽  
Viral Diseases ◽  
Multiple Organs ◽  
Innate Immune Signaling ◽  
Mitochondrial Functions ◽  
Host Virus Interactions ◽  
Virus Interactions

Viral diseases account for an increasing proportion of deaths worldwide. Viruses maneuver host cell machinery in an attempt to subvert the intracellular environment favorable for their replication. The mitochondrial network is highly susceptible to physiological and environmental insults, including viral infections. Viruses affect mitochondrial functions and impact mitochondrial metabolism, and innate immune signaling. Resurgence of host-virus interactions in recent literature emphasizes the key role of mitochondria and host metabolism on viral life processes. Mitochondrial dysfunction leads to damage of mitochondria that generate toxic compounds, importantly mitochondrial DNA, inducing systemic toxicity, leading to damage of multiple organs in the body. Mitochondrial dynamics and mitophagy are essential for the maintenance of mitochondrial quality control and homeostasis. Therefore, metabolic antagonists may be essential to gain a better understanding of viral diseases and develop effective antiviral therapeutics. This review briefly discusses how viruses exploit mitochondrial dynamics for virus proliferation and induce associated diseases.

scholarly journals Exploring the Human-Nipah Virus Protein-Protein Interactome

2017 ◽  
Vol 91 (23) ◽  
Author(s):  
Luis Martinez-Gil ◽  
Natalia M. Vera-Velasco ◽  
Ismael Mingarro
Keyword(s):  
Protein Interactions ◽  
Affinity Purification ◽  
Nipah Virus ◽  
Productive Infection ◽  
Virus Protein ◽  
Protein Protein Interactions ◽  
Data Set ◽  
Wide Range ◽  
Host Virus Interactions ◽  
Virus Interactions

ABSTRACT Nipah virus is an emerging, highly pathogenic, zoonotic virus of the Paramyxoviridae family. Human transmission occurs by close contact with infected animals, the consumption of contaminated food, or, occasionally, via other infected individuals. Currently, we lack therapeutic or prophylactic treatments for Nipah virus. To develop these agents we must now improve our understanding of the host-virus interactions that underpin a productive infection. This aim led us to perform the present work, in which we identified 101 human-Nipah virus protein-protein interactions (PPIs), most of which (88) are novel. This data set provides a comprehensive view of the host complexes that are manipulated by viral proteins. Host targets include the PRP19 complex and the microRNA (miRNA) processing machinery. Furthermore, we explored the biologic consequences of the interaction with the PRP19 complex and found that the Nipah virus W protein is capable of altering p53 control and gene expression. We anticipate that these data will help in guiding the development of novel interventional strategies to counter this emerging viral threat. IMPORTANCE Nipah virus is a recently discovered virus that infects a wide range of mammals, including humans. Since its discovery there have been yearly outbreaks, and in some of them the mortality rate has reached 100% of the confirmed cases. However, the study of Nipah virus has been largely neglected, and currently we lack treatments for this infection. To develop these agents we must now improve our understanding of the host-virus interactions that underpin a productive infection. In the present work, we identified 101 human-Nipah virus protein-protein interactions using an affinity purification approach coupled with mass spectrometry. Additionally, we explored the cellular consequences of some of these interactions. Globally, this data set offers a comprehensive and detailed view of the host machinery's contribution to the Nipah virus's life cycle. Furthermore, our data present a large number of putative drug targets that could be exploited for the treatment of this infection.

Poly(A)-binding protein (PABP): a common viral target

2010 ◽  
Vol 426 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Richard W. P. Smith ◽  
Nicola K. Gray
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Intracellular Localization ◽  
Mrna Translation ◽  
Dna Viruses ◽  
Multifunctional Protein ◽  
Wide Range ◽  
Viral Target ◽  
Rna And Dna

Cytoplasmic PABP [poly(A)-binding protein] is a multifunctional protein with well-studied roles in mRNA translation and stability. In the present review, we examine recent evidence that the activity of PABP is altered during infection with a wide range of viruses, bringing about changes in its stability, complex formation and intracellular localization. Targeting of PABP by both RNA and DNA viruses highlights the role of PABP as a central regulator of gene expression.

scholarly journals Poxviral Strategies to Overcome Host Cell Apoptosis

Pathogens ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 6
Author(s):  
Chathura D. Suraweera ◽  
Mark G. Hinds ◽  
Marc Kvansakul
Keyword(s):  
Viral Infections ◽  
B Cell Lymphoma ◽  
Intrinsic Apoptosis ◽  
Host Cell Apoptosis ◽  
Successful Infection ◽  
Infected Cells ◽  
Host Virus Interactions ◽  
Almost All ◽  
Virus Interactions ◽  
Multicellular Organisms

Apoptosis is a form of cellular suicide initiated either via extracellular (extrinsic apoptosis) or intracellular (intrinsic apoptosis) cues. This form of programmed cell death plays a crucial role in development and tissue homeostasis in multicellular organisms and its dysregulation is an underlying cause for many diseases. Intrinsic apoptosis is regulated by members of the evolutionarily conserved B-cell lymphoma-2 (Bcl-2) family, a family that consists of pro- and anti-apoptotic members. Bcl-2 genes have also been assimilated by numerous viruses including pox viruses, in particular the sub-family of chordopoxviridae, a group of viruses known to infect almost all vertebrates. The viral Bcl-2 proteins are virulence factors and aid the evasion of host immune defenses by mimicking the activity of their cellular counterparts. Viral Bcl-2 genes have proved essential for the survival of virus infected cells and structural studies have shown that though they often share very little sequence identity with their cellular counterparts, they have near-identical 3D structures. However, their mechanisms of action are varied. In this review, we examine the structural biology, molecular interactions, and detailed mechanism of action of poxvirus encoded apoptosis inhibitors and how they impact on host–virus interactions to ultimately enable successful infection and propagation of viral infections.

scholarly journals A functional spleen contributes to afucosylated IgG in humans

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Iwona Wojcik ◽  
David E. Schmidt ◽  
Lisa A. de Neef ◽  
Minke A. E. Rab ◽  
Bob Meek ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Immune Cell ◽  
Lymphoid Organ ◽  
Immune Effector ◽  
Adaptive Immune ◽  
Wide Range ◽  
Humoral Responses ◽  
First Time

AbstractAs a lymphoid organ, the spleen hosts a wide range of immune cell populations, which not only remove blood-borne antigens, but also generate and regulate antigen-specific immune responses. In particular, the splenic microenvironment has been demonstrated to play a prominent role in adaptive immune responses to enveloped viral infections and alloantigens. During both types of immunizations, antigen-specific immunoglobulins G (IgGs) have been characterized by the reduced amount of fucose present on N-linked glycans of the fragment crystallizable (Fc) region. These glycans are essential for mediating the induction of immune effector functions. Therefore, we hypothesized that a spleen may modulate humoral responses and serve as a preferential site for afucosylated IgG responses, which potentially play a role in immune thrombocytopenia (ITP) pathogenesis. To determine the role of the spleen in IgG-Fc glycosylation, we performed IgG subclass-specific liquid chromatography–mass spectrometry (LC–MS) analysis of Fc glycosylation in a large cohort of individuals splenectomized due to trauma, due to ITP, or spherocytosis. IgG-Fc fucosylation was consistently increased after splenectomy, while no effects for IgG-Fc galactosylation and sialylation were observed. An increase in IgG1- and IgG2/3-Fc fucosylation level upon splenectomy has been reported here for the first time, suggesting that immune responses occurring in the spleen may be particularly prone to generate afucosylated IgG responses. Surprisingly, the level of total IgG-Fc fucosylation was decreased in ITP patients compared to healthy controls. Overall, our results suggest a yet unrecognized role of the spleen in either the induction or maintenance of afucosylated IgG responses by B cells.

Novel syntaxin gene sequences from Giardia, Trypanosoma and algae: implications for the ancient evolution of the eukaryotic endomembrane system

2002 ◽  
Vol 115 (8) ◽  
pp. 1635-1642 ◽  
Author(s):  
Joel B. Dacks ◽  
W. Ford Doolittle
Keyword(s):  
Protein Interactions ◽  
Calcium Binding ◽  
Parallel Evolution ◽  
Membrane System ◽  
Compartment System ◽  
Eukaryotic Diversity ◽  
Wide Range ◽  
Membrane Compartment ◽  
Isoleucine Residue

SNAP receptors or SNARES are crucial components of the intracellular membrane system of eukaryotes. The syntaxin family of SNAREs have been shown to have roles in neurotransmission, vesicular transport, membrane fusion and even internal membrane compartment reconstruction. While syntaxins and SNAREs in general have been well characterized in mammalian and yeast models, little is known about their overall distribution across eukaryotic diversity or about the evolution of the syntaxin gene family. By combining bioinformatic,molecular biological and phylogenetic approaches, we demonstrate that various syntaxin homologs are not only present in `eukaryotic crown taxa' but across a wide range of eukaryotic lineages. The alignment of evolutionarily diverse syntaxin paralogs shows that an isoleucine residue critical to nSec1—syntaxin complex formation and the characteristic syntaxin glutamine residue are nearly universally conserved, implying a general functional importance for these residues. Other identified functional residues involved in botulism toxicity and calcium-binding-protein interactions are also compared. The presence of Golgi-related syntaxins in the intestinal parasite Giardia intestinalis provides further evidence for a cryptic Golgi in this `adictyosomal' taxon, and another likely case of secondary reduction in this parasite. The phylogeny of syntaxins shows a number of nested duplications, including a case of parallel evolution in the plasma membrane-associated syntaxins, and ancestral duplications in the other syntaxin paralogs. These speak to ancient events in the evolution of the syntaxin system and emphasize the universal role of the syntaxins in the eukaryotic intracellular compartment system.

scholarly journals Alternative Experimental Models for Studying Influenza Proteins, Host–Virus Interactions and Anti-Influenza Drugs

2019 ◽  
Vol 12 (4) ◽  
pp. 147 ◽  
Author(s):  
Sonja C. J. H. Chua ◽  
Hui Qing Tan ◽  
David Engelberg ◽  
Lina H. K. Lim
Keyword(s):  
Protein Function ◽  
Viral Infections ◽  
Experimental Models ◽  
Host Proteins ◽  
Physiological Basis ◽  
Host Interactions ◽  
Experimental Systems ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Unique Potential

Ninety years after the discovery of the virus causing the influenza disease, this malady remains one of the biggest public health threats to mankind. Currently available drugs and vaccines only partially reduce deaths and hospitalizations. Some of the reasons for this disturbing situation stem from the sophistication of the viral machinery, but another reason is the lack of a complete understanding of the molecular and physiological basis of viral infections and host–pathogen interactions. Even the functions of the influenza proteins, their mechanisms of action and interaction with host proteins have not been fully revealed. These questions have traditionally been studied in mammalian animal models, mainly ferrets and mice (as well as pigs and non-human primates) and in cell lines. Although obviously relevant as models to humans, these experimental systems are very complex and are not conveniently accessible to various genetic, molecular and biochemical approaches. The fact that influenza remains an unsolved problem, in combination with the limitations of the conventional experimental models, motivated increasing attempts to use the power of other models, such as low eukaryotes, including invertebrate, and primary cell cultures. In this review, we summarized the efforts to study influenza in yeast, Drosophila, zebrafish and primary human tissue cultures and the major contributions these studies have made toward a better understanding of the disease. We feel that these models are still under-utilized and we highlight the unique potential each model has for better comprehending virus–host interactions and viral protein function.

scholarly journals IgG2a restriction of murine antibodies elicited by viral infections.

1987 ◽  
Vol 165 (1) ◽  
pp. 64-69 ◽  
Author(s):  
J P Coutelier ◽  
J T van der Logt ◽  
F W Heessen ◽  
G Warnier ◽  
J Van Snick
Keyword(s):  
Viral Infections ◽  
Antiviral Response ◽  
Igg Antibodies ◽  
Dna Viruses ◽  
Rna And Dna

The isotypic distribution of IgG antibodies was determined in the serum of mice after infection with a panel of RNA and DNA viruses representative of 11 different genera. The antiviral response induced by all these viruses showed a striking preponderance of the IgG2a subclass whatever the strain of mice tested or the time elapsed after infection. Together with the predominance of IgG1 in antiprotein and of IgG3 in anticarbohydrate response, this IgG2a restriction of antiviral antibodies strongly suggests the existence of highly specific mechanisms for the regulation of individual subclasses in the mouse.

scholarly journals Recent Updates on Research Models and Tools to Study Virus–Host Interactions at the Placenta

Viruses ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 5 ◽  
Author(s):  
Jae Kyung Lee ◽  
Soo-Jin Oh ◽  
Hosun Park ◽  
Ok Sarah Shin
Keyword(s):  
Viral Infections ◽  
Protective Role ◽  
Biological Mechanisms ◽  
Cellular Targets ◽  
Host Interactions ◽  
Wide Range ◽  
Hofbauer Cells ◽  
Maternal Fetal Transmission ◽  
Immunological Barrier

The placenta is a unique mixed organ, composed of both maternal and fetal tissues, that is formed only during pregnancy and serves as the key physiological and immunological barrier preventing maternal–fetal transmission of pathogens. Several viruses can circumvent this physical barrier and enter the fetal compartment, resulting in miscarriage, preterm birth, and birth defects, including microcephaly. The mechanisms underlying viral strategies to evade the protective role of placenta are poorly understood. Here, we reviewed the role of trophoblasts and Hofbauer cells in the placenta and have highlighted characteristics of vertical and perinatal infections caused by a wide range of viruses. Moreover, we explored current progress and future opportunities in cellular targets, pathogenesis, and underlying biological mechanisms of congenital viral infections, as well as novel research models and tools to study the placenta.

scholarly journals RdDM pathway is required for Tobamovirus-induced symptomatology production

2020 ◽  
Author(s):  
Melisa Leone ◽  
Diego Zavallo ◽  
Andrea Venturuzzi ◽  
Sebastián Asurmendi
Keyword(s):  
Dna Methylation ◽  
Viral Infection ◽  
Viral Infections ◽  
Expression Patterns ◽  
Initial Step ◽  
List Type ◽  
Direct Role ◽  
Transcriptional Changes ◽  
Virus Interactions

SummarySmall RNAs (sRNA) are important molecules for gene regulation in plants and play an essential role in plant-pathogen interactions. Researchers have evaluated the relationship between viral infections as well as the endogenous accumulation of sRNAs and the transcriptional changes associated with the production of symptoms, little is known about a possible direct role of epigenetics, mediated by 24-nt sRNAs, in the induction of these symptoms.With the use of different RNA directed DNA methylation pathway mutants and triple demethylase mutants, here we demonstrate that the disruption of RdDM pathway during viral infection produced alterations in the plant transcriptomic changes (because of the infection) and in symptomatology.This study represents the initial step in exposing that DNA methylation directed by endogenous sRNAs has an important role, uncoupled to defense, in the production of symptoms associated with plant-virus interactions.Significance statementThe crop yield losses induced by phytoviruses are mainly associated with the symptoms of the disease. DNA modifications as methylation, can modulate the information coded by the sequence, process named epigenetics. Viral infection can change the expression patterns of different genes linked to defenses and symptoms. This work represents the initial step to expose the role of epigenetic process, in the production of symptoms associated with plants-virus interactions.

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