vhfRNAi: a web-platform for analysis of host genes involved in viral infections discovered by genome wide RNAi screens

2017 ◽  
Vol 13 (7) ◽  
pp. 1377-1387 ◽  
Author(s):  
Anamika Thakur ◽  
Abid Qureshi ◽  
Manoj Kumar
Keyword(s):  
Rna Interference ◽  
High Throughput ◽  
Viral Infections ◽  
Host Factors ◽  
Genome Wide ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Web Platform ◽  
Host Genes

Knockdown of host genes using high-throughput genome-wide RNA interference screens has identified numerous host factors that affect viral infections, which would be helpful in understanding host–virus interactions.

Exploring the associations of host genes for viral infection revealed by genome-wide RNAi and virus–host protein interactions

2015 ◽  
Vol 11 (9) ◽  
pp. 2511-2519 ◽  
Author(s):  
Dafei Xie ◽  
Lu Han ◽  
Yifu Luo ◽  
Yang Liu ◽  
Song He ◽  
...  
Keyword(s):  
Rna Interference ◽  
Viral Infection ◽  
Cell Viability ◽  
Virus Replication ◽  
Protein Interactions ◽  
Viral Infections ◽  
Host Factors ◽  
Host Protein ◽  
Genome Wide ◽  
Host Genes

Genome-wide RNA interference screens have greatly facilitated the identification of essential host factors (EHFs) for viral infections, whose knockdown effects significantly influence virus replication but not host cell viability.

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 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 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 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 Nudivirus Remnants in the Genomes of Arthropods

2020 ◽  
Vol 12 (5) ◽  
pp. 578-588 ◽  
Author(s):  
Ruo-Lin Cheng ◽  
Xiao-Feng Li ◽  
Chuan-Xi Zhang
Keyword(s):  
Viral Infections ◽  
Phylogenetic Analyses ◽  
Open Reading Frames ◽  
Endogenous Viral Elements ◽  
Host Virus Interactions ◽  
Fossil Records ◽  
Virus Interactions ◽  
Flanking Regions ◽  
Eukaryotic Genomes ◽  
Reading Frames

Abstract Endogenous viral elements (EVEs), derived from all major types of viruses, have been discovered in many eukaryotic genomes, representing “fossil records” of past viral infections. The endogenization of nudiviruses has been reported in several insects, leading to the question of whether genomic integration is a common phenomenon for these viruses. In this study, genomic assemblies of insects and other arthropods were analyzed to identify endogenous sequences related to Nudiviridae. A total of 359 nudivirus-like genes were identified in 43 species belonging to different groups; however, none of these genes were detected in the known hosts of nudiviruses. A large proportion of the putative EVEs identified in this study encode intact open reading frames or are transcribed as mRNAs, suggesting that they result from recent endogenization of nudiviruses. Phylogenetic analyses of the identified EVEs and inspections of their flanking regions indicated that integration of nudiviruses has occurred recurrently during the evolution of arthropods. This is the first report of a comprehensive screening for nudivirus-derived EVEs in arthropod genomes. The results of this study demonstrated that a large variety of arthropods, especially hemipteran and hymenopteran insects, have previously been or are still infected by nudiviruses. These findings have greatly extended the host range of Nudiviridae and provide new insights into viral diversity, evolution, and host–virus interactions.

scholarly journals To TRIM or not to TRIM: the balance of host–virus interactions mediated by the ubiquitin system

2019 ◽  
Vol 100 (12) ◽  
pp. 1641-1662 ◽  
Author(s):  
Adam Hage ◽  
Ricardo Rajsbaum
Keyword(s):  
Innate Immunity ◽  
Viral Replication ◽  
Viral Infections ◽  
Ubiquitin Ligases ◽  
Innate Immune ◽  
Future Research ◽  
Post Translational Modifications ◽  
Ubiquitin System ◽  
Host Virus Interactions ◽  
Virus Interactions

The innate immune system responds rapidly to protect against viral infections, but an overactive response can cause harmful damage. To avoid this, the response is tightly regulated by post-translational modifications (PTMs). The ubiquitin system represents a powerful PTM machinery that allows for the reversible linkage of ubiquitin to activate and deactivate a target’s function. A precise enzymatic cascade of ubiquitin-activating, conjugating and ligating enzymes facilitates ubiquitination. Viruses have evolved to take advantage of the ubiquitin pathway either by targeting factors to dampen the antiviral response or by hijacking the system to enhance their replication. The tripartite motif (TRIM) family of E3 ubiquitin ligases has garnered attention as a major contributor to innate immunity. Many TRIM family members limit viruses either indirectly as components in innate immune signalling, or directly by targeting viral proteins for degradation. In spite of this, TRIMs and other ubiquitin ligases can be appropriated by viruses and repurposed as valuable tools in viral replication. This duality of function suggests a new frontier of research for TRIMs and raises new challenges for discerning the subtleties of these pro-viral mechanisms. Here, we review current findings regarding the involvement of TRIMs in host–virus interactions. We examine ongoing developments in the field, including novel roles for unanchored ubiquitin in innate immunity, the direct involvement of ubiquitin ligases in promoting viral replication, recent controversies on the role of ubiquitin and TRIM25 in activation of the pattern recognition receptor RIG-I, and we discuss the implications these studies have on future research directions.

Innate and adaptive immunity toward influenza B viruses

2020 ◽  
Vol 15 (11) ◽  
pp. 1045-1058
Author(s):  
Luca Hensen ◽  
Katherine Kedzierska ◽  
Marios Koutsakos
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Host Factors ◽  
Influenza B ◽  
Innate And Adaptive Immunity ◽  
Vaccination Strategies ◽  
Immunological Mechanisms ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Significant Disease

Despite annual vaccination, influenza B viruses (IBV) cause significant disease with substantial health and socio-economic impacts. Novel vaccination strategies inducing broadly protective and long-lasting immunity across IBV lineages are needed. However, as immune responses toward IBV are largely understudied, host–virus interactions and protective immune mechanisms need to be defined to rationally design such vaccines. Here, we summarize recent advances in our understanding of immunological mechanisms underpinning protection from IBV. We discuss how innate antiviral host factors inhibit IBV replication and the ways by which IBV escapes such restriction. We review the specificity of broadly cross-reactive antibodies and universal T cells, and the mechanisms by which they mediate protection. We highlight important knowledge gaps needing to be addressed to design improved IBV vaccines.

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