scholarly journals Glucose-6-Phosphate Dehydrogenase Deficiency Enhances Human Coronavirus 229E Infection

2008 ◽  
Vol 197 (6) ◽  
pp. 812-816 ◽  
Author(s):  
Yi-Hsuan Wu ◽  
Ching-Ping Tseng ◽  
Mei-Ling Cheng ◽  
Hung-Yao Ho ◽  
Shin-Ru Shih ◽  
...  
Keyword(s):  
Particle Production ◽  
Ectopic Expression ◽  
Viral Gene Expression ◽  
Host Cells ◽  
Viral Gene ◽  
Human Coronavirus ◽  
Cellular Environment ◽  
Viral Particle Production ◽  
Oxidant Production ◽  
Glucose 6 Phosphate Dehydrogenase

Abstract The host cellular environment is a key determinant of pathogen infectivity. Viral gene expression and viral particle production of glucose-6-phosphate dehydrogenase (G6PD)–deficient and G6PD-knockdown cells were much higher than their counterparts when human coronavirus (HCoV) 229E was applied at 0.1 multiplicity of infection. These phenomena were correlated with increased oxidant production. Accordingly, ectopic expression of G6PD in G6PD-deficient cells or addition of antioxidant (such as α-lipoic acid) to G6PD-knockdown cells attenuated the increased susceptibility to HCoV 229E infection. All experimental data indicated that oxidative stress in host cells is an important factor in HCoV 229E infectivity

scholarly journals Herpesviral Latency—Common Themes

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 125 ◽  
Author(s):  
Magdalena Weidner-Glunde ◽  
Ewa Kruminis-Kaszkiel ◽  
Mamata Savanagouder
Keyword(s):  
Cell Biology ◽  
Particle Production ◽  
Viral Gene Expression ◽  
Lytic Cycle ◽  
Latent Reservoir ◽  
Viral Gene ◽  
Target Cells ◽  
Viral Particle Production ◽  
The Family ◽  
The Common

Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency.

scholarly journals Bacteriophage self-counting in the presence of viral replication

2021 ◽  
Vol 118 (51) ◽  
pp. e2104163118
Author(s):  
Tianyou Yao ◽  
Seth Coleman ◽  
Thu Vu Phuc Nguyen ◽  
Ido Golding ◽  
Oleg A. Igoshin
Keyword(s):  
Gene Expression ◽  
Viral Replication ◽  
Viral Gene Expression ◽  
Host Cells ◽  
Optimal Decision ◽  
Viral Gene ◽  
Viral Genomes ◽  
Viral Copy Number ◽  
Viral Copy ◽  
Type Phage

When host cells are in low abundance, temperate bacteriophages opt for dormant (lysogenic) infection. Phage lambda implements this strategy by increasing the frequency of lysogeny at higher multiplicity of infection (MOI). However, it remains unclear how the phage reliably counts infecting viral genomes even as their intracellular number increases because of replication. By combining theoretical modeling with single-cell measurements of viral copy number and gene expression, we find that instead of hindering lambda’s decision, replication facilitates it. In a nonreplicating mutant, viral gene expression simply scales with MOI rather than diverging into lytic (virulent) and lysogenic trajectories. A similar pattern is followed during early infection by wild-type phage. However, later in the infection, the modulation of viral replication by the decision genes amplifies the initially modest gene expression differences into divergent trajectories. Replication thus ensures the optimal decision—lysis upon single-phage infection and lysogeny at higher MOI.

scholarly journals LY6E Restricts Entry of Human Coronaviruses, Including Currently Pandemic SARS-CoV-2

2020 ◽  
Vol 94 (18) ◽  
Author(s):  
Xuesen Zhao ◽  
Shuangli Zheng ◽  
Danying Chen ◽  
Mei Zheng ◽  
Xinglin Li ◽  
...  
Keyword(s):  
Influenza A ◽  
Yellow Fever Virus ◽  
Virus Entry ◽  
Ectopic Expression ◽  
A549 Cells ◽  
Cellular Protein ◽  
Host Cells ◽  
Cellular Proteins ◽  
Human Coronavirus ◽  
Human Coronaviruses

ABSTRACT C3A is a subclone of the human hepatoblastoma HepG2 cell line with strong contact inhibition of growth. We fortuitously found that C3A was more susceptible to human coronavirus HCoV-OC43 infection than HepG2, which was attributed to the increased efficiency of virus entry into C3A cells. In an effort to search for the host cellular protein(s) mediating the differential susceptibility of the two cell lines to HCoV-OC43 infection, we found that ArfGAP with dual pleckstrin homology (PH) domains 2 (ADAP2), gamma-interferon-inducible lysosome/endosome-localized thiolreductase (GILT), and lymphocyte antigen 6 family member E (LY6E), the three cellular proteins identified to function in interference with virus entry, were expressed at significantly higher levels in HepG2 cells. Functional analyses revealed that ectopic expression of LY6E, but not GILT or ADAP2, in HEK 293 cells inhibited the entry of HCoV-O43. While overexpression of LY6E in C3A and A549 cells efficiently inhibited the infection of HCoV-OC43, knockdown of LY6E expression in HepG2 significantly increased its susceptibility to HCoV-OC43 infection. Moreover, we found that LY6E also efficiently restricted the entry mediated by the envelope spike proteins of other human coronaviruses, including the currently pandemic SARS-CoV-2. Interestingly, overexpression of serine protease TMPRSS2 or amphotericin treatment significantly neutralized the IFN-inducible transmembrane 3 (IFITM3) restriction of human coronavirus (CoV) entry, but did not compromise the effect of LY6E on the entry of human coronaviruses. The work reported herein thus demonstrates that LY6E is a critical antiviral immune effector that controls CoV infection and pathogenesis via a mechanism distinct from other factors that modulate CoV entry. IMPORTANCE Virus entry into host cells is one of the key determinants of host range and cell tropism and is subjected to the control of host innate and adaptive immune responses. In the last decade, several interferon-inducible cellular proteins, including IFITMs, GILT, ADAP2, 25CH, and LY6E, had been identified to modulate the infectious entry of a variety of viruses. Particularly, LY6E was recently identified as a host factor that facilitates the entry of several human-pathogenic viruses, including human immunodeficiency virus, influenza A virus, and yellow fever virus. Identification of LY6E as a potent restriction factor of coronaviruses expands the biological function of LY6E and sheds new light on the immunopathogenesis of human coronavirus infection.

scholarly journals Chromosomal resolution reveals symbiotic virus colonization of parasitic wasp genomes

2020 ◽  
Author(s):  
Jérémy Gauthier ◽  
Hélène Boulain ◽  
Joke J.F.A. van Vugt ◽  
Lyam Baudry ◽  
Emma Persyn ◽  
...  
Keyword(s):  
Particle Production ◽  
Parasitic Wasp ◽  
Viral Gene Expression ◽  
Parasitoid Wasp ◽  
Viral Gene ◽  
Parasitoid Wasps ◽  
Genomic Comparison ◽  
Immune Genes ◽  
Endogenous Viruses ◽  
First Time

AbstractMost endogenous viruses, an important proportion of eukaryote genomes, are doomed to slowly decay. Little is known, however, on how they evolve when they confer a benefit to their host. Bracoviruses are essential for the parasitism success of parasitoid wasps, whose genomes they integrated ~103 million years ago. Here we show, from the assembly of a parasitoid wasp genome, for the first time at a chromosomal scale, that symbiotic bracovirus genes spread to and colonized all the chromosomes. Moreover, large viral clusters are stably maintained suggesting strong evolutionary constraints. Genomic comparison with another wasps revealed that this organization was already established ~53 mya. Transcriptomic analyses highlight temporal synchronization of viral gene expression, leading to particle production. Immune genes are not induced, however, indicating the virus is not perceived as foreign by the wasp. This recognition suggests that no conflicts remain between symbiotic partners when benefits to them converge.

scholarly journals Antagonism to human BST-2/tetherin by Sendai virus glycoproteins

2013 ◽  
Vol 94 (6) ◽  
pp. 1211-1219 ◽  
Author(s):  
Carole Bampi ◽  
Lara Rasga ◽  
Laurent Roux
Keyword(s):  
Particle Production ◽  
Sendai Virus ◽  
Ectopic Expression ◽  
Mrna Levels ◽  
Madin Darby Canine Kidney ◽  
Virus Envelope ◽  
Viral Particle Production ◽  
Viral Glycoproteins ◽  
Matrix Fusion ◽  
Darby Canine Kidney

Tetherin is an interferon-inducible factor that restricts viral particle production. We show here that Sendai virus (SeV) induces a drastic decrease in tetherin levels in infected HeLa cells. Using ectopic expression of tetherin in Madin–Darby canine kidney cells, we find that infectious SeV production is sensitive to restriction by tetherin, suggesting that SeV downregulates tetherin to counter this form of cellular restriction. By using radioactive tetherin in pulse–chase experiments, applying conditions that limit protein degradation, and by estimating tetherin mRNA levels, we find that tetherin degradation is the mechanism of downregulation. Suppression of the virus envelope proteins matrix, fusion (F) or haemagglutinin-neuraminidase protein (HN) during the course of infection demonstrates that F and HN, in concert, are responsible for tetherin degradation. The mechanism(s) by which these two viral glycoproteins participate in degrading tetherin remains to be determined.

scholarly journals Bacteriophage self-counting in the presence of viral replication

2021 ◽  
Author(s):  
Seth Coleman ◽  
Tianyou Yao ◽  
Thu Vu Phuc Nguyen ◽  
Ido Golding ◽  
Oleg Igoshin
Keyword(s):  
Gene Expression ◽  
Viral Replication ◽  
Copy Number ◽  
Viral Gene Expression ◽  
Host Cells ◽  
Optimal Decision ◽  
Viral Gene ◽  
Viral Genomes ◽  
Viral Copy Number ◽  
Viral Copy

SUMMARYWhen host cells are in low abundance, temperate bacteriophages opt for dormant (lysogenic) infection. Phage lambda implements this strategy by increasing the frequency of lysogeny at higher multiplicity of infection (MOI). However, it remains unclear how the phage reliably counts infecting viral genomes even as their intracellular number increases due to replication. By combining theoretical modeling with single-cell measurements of viral copy number and gene expression, we find that, instead of hindering lambda’s decision, replication facilitates it. In a nonreplicating mutant, viral gene expression simply scales with MOI rather than diverging into lytic (virulent) and lysogenic trajectories. A similar pattern is followed during early infection by wildtype phage. However, later in the infection, the modulation of viral replication by the decision genes amplifies the initially modest gene expression differences into divergent trajectories. Replication thus ensures the optimal decision—lysis upon single-phage infection, lysogeny at higher MOI.

scholarly journals The Signal Peptide of a Simple Retrovirus Envelope Functions as a Posttranscriptional Regulator of Viral Gene Expression

2009 ◽  
Vol 83 (9) ◽  
pp. 4591-4604 ◽  
Author(s):  
Marco Caporale ◽  
Frederick Arnaud ◽  
Manuela Mura ◽  
Matthew Golder ◽  
Claudio Murgia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signal Peptide ◽  
Nuclear Export ◽  
Viral Particle ◽  
Particle Production ◽  
Rna Binding ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Binding Motif ◽  
Peptide Cleavage

ABSTRACT Retroviruses use different strategies to regulate transcription and translation and exploit the cellular machinery involved in these processes. This study shows that the signal peptide of the envelope glycoprotein (Env) of Jaagsiekte sheep retrovirus (JSRV) plays a major role in posttranscriptional viral gene expression. Expression of the JSRV Env in trans increases viral particle production by mechanisms dependent on (i) its leader sequence, (ii) an intact signal peptide cleavage site, (iii) a cis-acting RNA-responsive element located in the viral genome, (iv) Crm1, and (v) B23. The signal peptide of the JSRV Env (JSE-SP) is 80 amino acid residues in length and contains putative nuclear localization and export signals, in addition to an arginine-rich RNA binding motif. JSE-SP localizes both in the endoplasmic reticulum and in the nucleus, where it colocalizes with nucleolar markers. JSE-SP is a multifunctional protein, as it moderately enhances nuclear export of unspliced viral mRNA and considerably increases viral particle release by favoring a posttranslational step of the replication cycle.

scholarly journals Chromosomal scale assembly of parasitic wasp genome reveals symbiotic virus colonization

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Jérémy Gauthier ◽  
Hélène Boulain ◽  
Joke J. F. A. van Vugt ◽  
Lyam Baudry ◽  
Emma Persyn ◽  
...  
Keyword(s):  
Particle Production ◽  
Parasitic Wasp ◽  
Viral Gene Expression ◽  
Parasitoid Wasp ◽  
Viral Gene ◽  
Immune Gene ◽  
Genomic Comparison ◽  
Dna Viruses ◽  
Endogenous Viruses ◽  
A Genome

AbstractEndogenous viruses form an important proportion of eukaryote genomes and a source of novel functions. How large DNA viruses integrated into a genome evolve when they confer a benefit to their host, however, remains unknown. Bracoviruses are essential for the parasitism success of parasitoid wasps, into whose genomes they integrated ~103 million years ago. Here we show, from the assembly of a parasitoid wasp genome at a chromosomal scale, that bracovirus genes colonized all ten chromosomes of Cotesia congregata. Most form clusters of genes involved in particle production or parasitism success. Genomic comparison with another wasp, Microplitis demolitor, revealed that these clusters were already established ~53 mya and thus belong to remarkably stable genomic structures, the architectures of which are evolutionary constrained. Transcriptomic analyses highlight temporal synchronization of viral gene expression without resulting in immune gene induction, suggesting that no conflicts remain between ancient symbiotic partners when benefits to them converge.

scholarly journals Histone demethylase LSD1 promotes RIG-I poly-ubiquitination and anti-viral gene expression

2021 ◽  
Vol 17 (9) ◽  
pp. e1009918
Author(s):  
Qi-Xin Hu ◽  
Hui-Yi Wang ◽  
Lu Jiang ◽  
Chen-Yu Wang ◽  
Lin-Gao Ju ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathway ◽  
Rna Virus ◽  
Viral Gene Expression ◽  
Host Cells ◽  
Viral Gene ◽  
Type I ◽  
E3 Ligases ◽  
Positive Regulator

Under RNA virus infection, retinoic acid-inducible gene I (RIG-I) in host cells recognizes viral RNA and activates the expression of type I IFN. To investigate the roles of protein methyltransferases and demethylases in RIG-I antiviral signaling pathway, we screened all the known related enzymes with a siRNA library and identified LSD1 as a positive regulator for RIG-I signaling. Exogenous expression of LSD1 enhances RIG-I signaling activated by virus stimulation, whereas its deficiency restricts it. LSD1 interacts with RIG-I, promotes its K63-linked polyubiquitination and interaction with VISA/MAVS. Interestingly, LSD1 exerts its function in antiviral response not dependent on its demethylase activity but through enhancing the interaction between RIG-I with E3 ligases, especially TRIM25. Furthermore, we provide in vivo evidence that LSD1 increases antiviral gene expression and inhibits viral replication. Taken together, our findings demonstrate that LSD1 is a positive regulator of signaling pathway triggered by RNA-virus through mediating RIG-I polyubiquitination.

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