scholarly journals EvoProDom: Evolutionary model of protein families by means of translocations of protein domains

2020 ◽  
Author(s):  
Gon Carmi ◽  
Alessandro Gorohovski ◽  
Milana Frenkel-Morgenstern
Keyword(s):  
Protein Design ◽  
Protein Domains ◽  
Evolutionary Model ◽  
Protein Domain ◽  
Protein Families ◽  
Orthologous Protein ◽  
Search Tool ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Evolution Of Proteins

AbstractHere, we developed a novel evolution of protein domains (EvoProDom) model for evolution of proteins, which was based on mix and merge of protein domains. We collected and integrated genomic and proteome data for 109 organisms. These data include protein domain content and orthologous protein families. In EvoProDom, we defined evolutionary events, such as translocations, as reciprocal exchanges of protein domains between orthologous proteins of different organisms. We found that protein domains, which frequently appear in translocation events, were enriched in trans-splicing events, i.e., producing novel transcripts fused from two distinct genes. We presented in EvoProDom, a general method to obtain protein domain content and orthologous protein annotation, by predicting these data from protein sequences using the Pfam search tool and KoFamKOALA, respectively. This method can be implemented in other research such as proteomics, protein design and host-virus interactions.

scholarly journals Integrative In Silico Investigation Reveals the Host-Virus Interactions in Repurposed Drugs Against SARS-CoV-2

2022 ◽  
Vol 1 ◽  
Author(s):  
Wenhui Yu ◽  
Yuxin Bai ◽  
Arjun Raha ◽  
Zhi Su ◽  
Fei Geng
Keyword(s):  
Molecular Docking ◽  
Drug Targets ◽  
Interaction Network ◽  
Dynamics Simulation ◽  
Search Tool ◽  
Direct Binding ◽  
Repurposed Drugs ◽  
Interaction Map ◽  
Host Virus Interactions ◽  
Virus Interactions

The ongoing COVID-19 outbreak have posed a significant threat to public health worldwide. Recently Toll-like receptor (TLR) has been proposed to be the drug target of SARS-CoV-2 treatment, the specificity and efficacy of such treatments remain unknown. In the present study we performed the investigation of repurposed drugs via a framework comprising of Search Tool for Interacting Chemicals (STITCH), Kyoto Encyclopedia of Genes and Genomes (KEGG), molecular docking, and virus-host-drug interactome mapping. Chloroquine (CQ) and hydroxychloroquine (HCQ) were utilized as probes to explore the interaction network that is linked to SARS-CoV-2. 47 drug targets were shown to be overlapped with SARS-CoV-2 network and were enriched in TLR signaling pathway. Molecular docking analysis and molecular dynamics simulation determined the direct binding affinity of TLR9 to CQ and HCQ. Furthermore, we established SARS-CoV-2-human-drug protein interaction map and identified the axis of TLR9-ERC1-Nsp13 and TLR9-RIPK1-Nsp12. Therefore, the elucidation of the interactions of SARS-CoV-2 with TLR9 axis will not only provide pivotal insights into SARS-CoV-2 infection and pathogenesis but also improve the treatment against COVID-19.

scholarly journals The molecular footprints of COVID-19

2020 ◽  
Vol 45 (3) ◽  
pp. 241-248
Author(s):  
Engin Yilmaz ◽  
Yakut Akyön ◽  
Muhittin Serdar
Keyword(s):  
Reaction Time ◽  
Changing Environment ◽  
The Third ◽  
The Past ◽  
The People ◽  
The World ◽  
The Future ◽  
Host Virus Interactions ◽  
Virus Interactions

AbstractCOVID-19 is the third spread of animal coronavirus over the past two decades, resulting in a major epidemic in humans after SARS and MERS. COVID-19 is responsible of the biggest biological earthquake in the world. In the global fight against COVID-19 some serious mistakes have been done like, the countries’ misguided attempts to protect their economies, lack of international co-operation. These mistakes that the people had done in previous deadly outbreaks. The result has been a greater economic devastation and the collapse of national and international trust for all. In this constantly changing environment, if we have a better understanding of the host-virus interactions than we can be more prepared to the future deadly outbreaks. When encountered with a disease which the causative is unknown, the reaction time and the precautions that should be taken matters a great deal. In this review we aimed to reveal the molecular footprints of COVID-19 scientifically and to get an understanding of the pandemia. This review might be a highlight to the possible outbreaks.

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.

Host-virus interactions: from the perspectives of epigenetics

2014 ◽  
Vol 24 (4) ◽  
pp. 223-241 ◽  
Author(s):  
Shanshan Li ◽  
Lingbao Kong ◽  
Xilan Yu ◽  
Yi Zheng
Keyword(s):  
Host Virus Interactions ◽  
Virus Interactions

Host–Virus Interactions from Potyvirus Replication to Translation

Plant Viruses ◽  
2018 ◽  
pp. 195-204
Author(s):  
Swarnalok De ◽  
Andres Lõhmus ◽  
Maija Pollari ◽  
Shreya Saha ◽  
Kristiina Mäkinen
Keyword(s):  
Host Virus Interactions ◽  
Virus Interactions

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.

scholarly journals Insights into the dynamics between viruses and their hosts in a hot spring microbial mat

2020 ◽  
Vol 14 (10) ◽  
pp. 2527-2541 ◽  
Author(s):  
Jessica K. Jarett ◽  
Mária Džunková ◽  
Frederik Schulz ◽  
Simon Roux ◽  
David Paez-Espino ◽  
...  
Keyword(s):  
Single Cell ◽  
Hot Spring ◽  
Current Knowledge ◽  
Single Cells ◽  
Metagenomic Data ◽  
Viral Genomes ◽  
Active Viral Replication ◽  
High Layer ◽  
Host Virus Interactions ◽  
Virus Interactions

Abstract Our current knowledge of host–virus interactions in biofilms is limited to computational predictions based on laboratory experiments with a small number of cultured bacteria. However, natural biofilms are diverse and chiefly composed of uncultured bacteria and archaea with no viral infection patterns and lifestyle predictions described to date. Herein, we predict the first DNA sequence-based host–virus interactions in a natural biofilm. Using single-cell genomics and metagenomics applied to a hot spring mat of the Cone Pool in Mono County, California, we provide insights into virus–host range, lifestyle and distribution across different mat layers. Thirty-four out of 130 single cells contained at least one viral contig (26%), which, together with the metagenome-assembled genomes, resulted in detection of 59 viruses linked to 34 host species. Analysis of single-cell amplification kinetics revealed a lack of active viral replication on the single-cell level. These findings were further supported by mapping metagenomic reads from different mat layers to the obtained host–virus pairs, which indicated a low copy number of viral genomes compared to their hosts. Lastly, the metagenomic data revealed high layer specificity of viruses, suggesting limited diffusion to other mat layers. Taken together, these observations indicate that in low mobility environments with high microbial abundance, lysogeny is the predominant viral lifestyle, in line with the previously proposed “Piggyback-the-Winner” theory.

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