A viral protein orchestrates rice ethylene signaling to coordinate viral infection and insect vector-mediated transmission

ABSTRACTInterferons (IFNs) restrict various kinds of viral infection via induction of hundreds of IFN-stimulated genes (ISGs), while the functions of the majority of ISGs are broadly unclear. Here, we show that a high-IFN-inducible gene, ISG12a (also known as IFI27), exhibits a nonapoptotic antiviral effect on hepatitis C virus (HCV) infection. Viral NS5A protein is targeted specifically by ISG12a, which mediates NS5A degradation via a ubiquitination-dependent proteasomal pathway. K374R mutation in NS5A domain III abrogates ISG12a-induced ubiquitination and degradation of NS5A. S-phase kinase-associated protein 2 (SKP2) is identified as an ubiquitin E3 ligase for NS5A. ISG12a functions as a crucial adaptor that promotes SKP2 to interact with and degrade viral protein. Moreover, the antiviral effect of ISG12a is dependent on the E3 ligase activity of SKP2. These findings uncover an intriguing mechanism by which ISG12a restricts viral infection and provide clues for understanding the actions of innate immunity.IMPORTANCEUpon virus invasion, IFNs induce numerous ISGs to control viral spread, while the functions of the majority of ISGs are broadly unclear. The present study shows a novel antiviral mechanism of ISGs and elucidated that ISG12a recruits an E3 ligase, SKP2, for ubiquitination and degradation of viral protein and restricts viral infection. These findings provide important insights into exploring the working principles of innate immunity.

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The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells

Journal of General Virology ◽

10.1099/vir.0.80813-0 ◽

2005 ◽

Vol 86 (7) ◽

pp. 1921-1930 ◽

Cited By ~ 77

Author(s):

Patrick T. W. Law ◽

Chi-Hang Wong ◽

Thomas C. C. Au ◽

Chi-Pang Chuck ◽

Siu-Kai Kong ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Severe Acute Respiratory Syndrome ◽

Viral Infection ◽

Viral Protein ◽

Host Response ◽

Transmembrane Protein ◽

Chromatin Condensation ◽

Aetiological Agent ◽

First Case

An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid-November 2002. The aetiological agent of this disease was found to be a previously unknown coronavirus, SARS-associated coronavirus (SARS-CoV). The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein, which is predicted to be a transmembrane protein. In this study, it was shown that the 3a protein was expressed in the lungs and intestinal tissues of SARS patients and that the protein localized to the endoplasmic reticulum in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggested that the 3a protein may trigger apoptosis. These data showed that overexpression of a single SARS-CoV protein can induce apoptosis in vitro.

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An insect cell line derived from the small brown planthopper supports replication of rice stripe virus, a tenuivirus

Journal of General Virology ◽

10.1099/vir.0.050104-0 ◽

2013 ◽

Vol 94 (6) ◽

pp. 1421-1425 ◽

Cited By ~ 17

Author(s):

Yuanyuan Ma ◽

Wei Wu ◽

Hongyan Chen ◽

Qifei Liu ◽

Dongsheng Jia ◽

...

Keyword(s):

Viral Infection ◽

Cell Line ◽

Persistent Infection ◽

Brown Planthopper ◽

Insect Cell Line ◽

Rice Stripe Virus ◽

Insect Vector ◽

Structural Protein ◽

Small Brown Planthopper ◽

A Cell

A cell line from the small brown planthopper (SBPH; Laodelphax striatellus) was established to study replication of rice stripe virus (RSV), a tenuivirus. The SBPH cell line, which had been subcultured through 30 passages, formed monolayers of epithelial-like cells. Inoculation of cultured vector cells with RSV resulted in a persistent infection. During viral infection in the SBPH cell line, the viral non-structural protein NS3 co-localized with the filamentous ribonucleoprotein particles of RSV, as revealed by electron and confocal microscopy. The knockdown of NS3 expression due to RNA interference induced by synthesized double-stranded RNAs from the NS3 gene significantly inhibited viral infection in the SBPH cell line. These results demonstrated that NS3 of RSV might be involved in viral replication or assembly. The persistent infection of the SBPH cell line by RSV will enable a better understanding of the complex relationship between RSV and its insect vector.

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C19ORF66 broadly escapes viral-induced endonuclease cleavage and restricts Kaposi’s Sarcoma Associated Herpesvirus (KSHV)

10.1101/506410 ◽

2018 ◽

Cited By ~ 1

Author(s):

William Rodriguez ◽

Aman Srivastav ◽

Mandy Muller

Keyword(s):

Viral Infection ◽

Viral Protein ◽

Host Response ◽

Rna Decay ◽

Comparative Approach ◽

Restriction Factor ◽

Rna Seq ◽

Gain Access ◽

In Cells ◽

Hsv 1

AbstractOne striking characteristic of certain herpesviruses is their ability to induce rapid and widespread RNA decay in order to gain access to host resources. This phenotype is induced by viral endoribonucleases, including SOX in KSHV, muSOX in MHV68, BGLF5 in EBV and vhs in HSV-1. Here, we performed comparative RNA-seq upon expression of these herpesviral endonucleases in order to characterize their effect on the host transcriptome. Consistent with previous reports, we found that approximately two thirds of transcripts are downregulated in cells expressing any of these viral endonucleases. Among transcripts spared from degradation, we uncovered a cluster of transcripts that systematically escape degradation from all tested endonucleases. Among these escapees, we identified C19ORF66 and reveal that like the previously identified escapees, this transcript is protected from degradation by its 3’UTR. We then show that C19ORF66, a known anti-viral protein, is a potent KSHV restriction factor, suggesting that its ability to escape viral cleavage may be an important component of the host response to viral infection. Collectively, our comparative approach is a powerful tool to pinpoint key regulators of the viral-host interplay and led us to uncover a novel KSHV regulator.

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Pressure-driven release of viral genome into a host nucleus is a mechanism leading to herpes infection

eLife ◽

10.7554/elife.47212 ◽

2019 ◽

Vol 8 ◽

Cited By ~ 5

Author(s):

Alberto Brandariz-Nuñez ◽

Ting Liu ◽

Te Du ◽

Alex Evilevitch

Keyword(s):

Nucleic Acids ◽

Viral Infection ◽

Host Cell ◽

Cell Nucleus ◽

Viral Protein ◽

Viral Genome ◽

Eukaryotic Cells ◽

Host Nucleus ◽

Protein Shell ◽

Dependent Mechanism

Many viruses previously have been shown to have pressurized genomes inside their viral protein shell, termed the capsid. This pressure results from the tight confinement of negatively charged viral nucleic acids inside the capsid. However, the relevance of capsid pressure to viral infection has not been demonstrated. In this work, we show that the internal DNA pressure of tens of atmospheres inside a herpesvirus capsid powers ejection of the viral genome into a host cell nucleus. To our knowledge, this provides the first demonstration of a pressure-dependent mechanism of viral genome penetration into a host nucleus, leading to infection of eukaryotic cells.

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Why do we die? Uncovering the genetic connections causing COVID-19 disease severity

10.21203/rs.3.rs-33174/v1 ◽

2020 ◽

Author(s):

Keyana Cordoza ◽

Magen Hoch ◽

Frederic B. Montz ◽

Bridgette F. Froeschke ◽

Kimberly P. Dobrinski

Keyword(s):

Single Nucleotide Polymorphisms ◽

Protein Expression ◽

Viral Infection ◽

X Chromosome ◽

Viral Protein ◽

Cell Receptor ◽

Nucleotide Polymorphisms ◽

Single Nucleotide ◽

Viral Binding ◽

Host Cell Receptor

Abstract SARS-CoV-2 attacks randomly causing deaths among certain populations. Additionally, this disease seems to kill males preferentially. This study investigates why by examining single nucleotide polymorphisms (SNPs) correlated with increased protein expression associated with viral infection of cells leading to disease proliferation. ACE2, the assumed host cell receptor for the virus is believed to be assisted by co-receptors ENPEP and ANPEP. TMPRSS2 cleaves the S viral protein into two sub-units allowing viral binding to the ACE2 receptor. ACE2 found on the X-chromosome has SNPs increasing ACE2 expression found at frequencies greater than 50% in all male populations analyzed which could account for the increase in male deaths. Females would undergo X-inactivation for the SNPs and have protection from the increased ACE2 expression in all their cells. ACE2, ENPEP, and TMPRSS2 were also found to have population specific SNP patterns which could account for the increased prevalence of disease among certain populations.

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Nonstructural protein Pns4 of rice dwarf virus is essential for viral infection in its insect vector

Virology Journal ◽

10.1186/s12985-015-0438-6 ◽

2015 ◽

Vol 12 (1) ◽

Cited By ~ 5

Author(s):

Qian Chen ◽

Linghua Zhang ◽

Hongyan Chen ◽

Lianhui Xie ◽

Taiyun Wei

Keyword(s):

Viral Infection ◽

Nonstructural Protein ◽

Dwarf Virus ◽

Insect Vector ◽

Rice Dwarf Virus

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The Spread of Rice Dwarf Virus among Cells of Its Insect Vector Exploits Virus-Induced Tubular Structures

Journal of Virology ◽

10.1128/jvi.00537-06 ◽

2006 ◽

Vol 80 (17) ◽

pp. 8593-8602 ◽

Cited By ~ 71

Author(s):

Taiyun Wei ◽

Akira Kikuchi ◽

Yusuke Moriyasu ◽

Nobuhiro Suzuki ◽

Takumi Shimizu ◽

...

Keyword(s):

Viral Protein ◽

Neutralizing Antibodies ◽

Specific Binding ◽

Host Cells ◽

Dwarf Virus ◽

Insect Vector ◽

Rice Dwarf Virus ◽

Tubular Structures ◽

Intercellular Spread

ABSTRACT Various cytopathological structures, known as inclusion bodies, are formed upon infection of cultured leafhopper cells by Rice dwarf virus, a member of the family Reoviridae. These structures include tubules of approximately 85 nm in diameter which are composed of the nonstructural viral protein Pns10 and contain viral particles. Such tubular structures were produced in heterologous non-host insect cells that expressed Pns10 of the virus. These tubules, when associated with actin-based filopodia, were able to protrude from the surface of cells and to penetrate neighboring cells. A binding assay in vitro revealed the specific binding of Pns10 to actin. Infection of clusters of cells was readily apparent 5 days after inoculation at a low multiplicity of infection with the virus, even in the presence of neutralizing antibodies. However, treatment of host cells with drugs that inhibited the elongation of actin filaments abolished the extension of Pns10 tubules from the surface of cells, with a significant simultaneous decrease in the extent of infection of neighboring cells. These results together revealed a previously undescribed aspect of the intercellular spread of Rice dwarf virus, wherein the virus exploits tubules composed of a nonstructural viral protein and actin-based filopodia to move into neighboring cells.

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A viral protein utilizes the NDP52/CALCOCO2 selective autophagy receptor to disassemble processing bodies

10.1101/2021.02.07.430164 ◽

2021 ◽

Author(s):

Carolyn-Ann Robinson ◽

Gillian K. Singh ◽

Elizabeth L. Castle ◽

Bre Q. Boudreau ◽

Jennifer A. Corcoran

Keyword(s):

Virus Infection ◽

Viral Infection ◽

Inflammatory Mediators ◽

Viral Protein ◽

Inflammatory Mediator ◽

Fine Tuning ◽

Messenger Rnas ◽

Processing Bodies ◽

Selective Autophagy ◽

Inflammatory Processes

AbstractSelective autophagy receptors contribute to host defence by targeting intracellular microbes for degradation and fine-tuning inflammatory processes by directing the degradation of macromolecular immune signaling platforms. Processing bodies (PBs) are cytoplasmic ribonucleoprotein granules that control inflammation by silencing and/or degrading labile messenger RNAs (mRNAs) that encode inflammatory mediator proteins. PBs often disassemble in response to virus infection, which correlates with increased synthesis of inflammatory mediator proteins; however, PB disassembly mechanisms remain largely obscure. Here, we demonstrate that the Kaposi’s sarcoma-associated herpesvirus (KSHV) KapB protein increases the synthesis of inflammatory mediators by driving autophagy and triggering PB disassembly. This could be prevented by silencing of Atg5 or the selective autophagy receptor NDP52/CALCOCO2, whereas silencing other selective autophagy receptors p62 and OPTN had no effect on PB turnover or inflammatory mediator synthesis. These studies reveal a new role for NDP52 in regulating PB turnover in response to viral infection.

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A scanning electron microscopic study of the eggs of Culicoides variipennis (Diptera: Ceratopogonidae)

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100128705 ◽

1987 ◽

Vol 45 ◽

pp. 884-885 ◽

Cited By ~ 1

Author(s):

R. A. Nunamaker ◽

C. E. Nunamaker ◽

B. C. Wick

Keyword(s):

Distinct Species ◽

Hemorrhagic Disease ◽

Insect Vector ◽

Electron Microscopic ◽

Important Species ◽

Scanning Electron Microscopic Study ◽

Laboratory Colony ◽

Culicoides Variipennis ◽

Morphological Differences ◽

Scanning Electron

Culicoides variipennis (Coquillett) is probably the most economically important species of biting midge in the U.S. due to its involvement in the transmission of bluetongue (BT) disease of sheep, cattle and ruminant wildlife, and epizootic hemorrhagic disease (EHD) of deer. Proposals have been made to recognize the eastern and western populations of this insect vector as distinct species. Others recommend use of the term “variipennis complex” until such time that the necessary biosystematic studies have been made to determine the genetic nature and/or minute morphological differences within the population structure over the entire geographic range of the species. Increasingly, students of ootaxonomy are relying on scanning electron microscopy (SEM) to assess chorionic features. This study was undertaken to provide comparative chorionic data for the C. variipennis complex.Culicoides variipennis eggs were collected from a laboratory colony maintained in Laramie, Wyoming.

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