scholarly journals Cellular Gene Expression Survey of Vaccinia Virus Infection of Human HeLa Cells

2003 ◽  
Vol 77 (11) ◽  
pp. 6493-6506 ◽  
Author(s):  
Susana Guerra ◽  
Luis A. López-Fernández ◽  
Alberto Pascual-Montano ◽  
Manuel Muñoz ◽  
Keith Harshman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virus Infection ◽  
Vaccinia Virus ◽  
Family Member ◽  
Hela Cells ◽  
De Novo ◽  
Host Gene ◽  
Global Changes ◽  
Host Gene Expression ◽  
Regulatory Pathways

ABSTRACT Vaccinia virus (VV) is a cytocidal virus that causes major changes in host cell machinery shortly after infecting cells. To define the consequences of virus infection on host gene expression, we used microarrays of approximately 15,000 human cDNAs to examine expression levels of mRNAs isolated at 2, 6, and 16 h postinfection from cultures of infected HeLa cells. The majority of profiling changes during VV infection corresponded to downregulation of genes at 16 h postinfection. Differentially expressed genes were clustered into seven groups to identify common regulatory pathways, with most of them (90%) belonging to clusters 6 and 7, which represent genes whose expression was repressed after infection. Cluster 1, however, contained 37 transcripts (2.81%) showing a robust pattern of induction that was maintained during the course of infection. Genes in cluster 1 included those for Wiskott-Aldrich syndrome protein (WASP) family member WASF1, thymosine, adenosine A2a receptor, glutamate decarboxylase 2, CD-80 antigen, KIAA0888 protein, selenophosphate synthetase, pericentrin, and attractin as well as several expressed sequence tags. We analyzed in more detail the fate of WASP protein in VV-infected cells, because a related family member, N-WASP, is involved in viral motility. WASP protein accumulated in the course of infection; its increase required viral DNA replication and de novo protein synthesis, and it localized in cytoplasmic structures distinct from uninfected cells. This study is the first quantitative analysis of host gene expression following VV infection of cultured human cells, demonstrating global changes in the expression profile, and identifies upregulated genes with potential roles in the virus replication cycle.

Trends in symbiont-induced host cellular differentiation

2020 ◽  
Author(s):  
Shelbi Russell ◽  
Jennie Ruelas Castillo
Keyword(s):  
Gene Expression ◽  
Cellular Differentiation ◽  
Cost Benefit ◽  
Regulatory Elements ◽  
Host Gene ◽  
Bacterial Symbionts ◽  
Host Gene Expression ◽  
Associated Bacteria ◽  
Regulatory Pathways ◽  
Symbiotic Associations

Bacteria participate in a wide diversity of symbiotic associations with eukaryotic hosts that require precise interactions for bacterial recognition and persistence. Most commonly, host-associated bacteria interfere with host gene expression to modulate the immune response to the infection. However, many of these bacteria also interfere with host cellular differentiation pathways to create a hospitable niche, resulting in the formation of novel cell types, tissues, and organs. In both of these situations, bacterial symbionts must interact with eukaryotic regulatory pathways. Here, we detail what is known about how bacterial symbionts, from pathogens to mutualists, control host cellular differentiation across the central dogma, from epigenetic chromatin modifications, to transcription and mRNA processing, to translation and protein modifications. We identify four main trends from this survey. First, mechanisms for controlling host gene expression appear to evolve from symbionts co-opting cross-talk between host signalling pathways. Second, symbiont regulatory capacity is constrained by the processes that drive reductive genome evolution in host-associated bacteria. Third, the regulatory mechanisms symbionts exhibit correlate with the cost/benefit nature of the association. And, fourth symbiont mechanisms for interacting with host genetic regulatory elements are not bound by native bacterial capabilities. Using this knowledge, we explore how the ubiquitous intracellular Wolbachia symbiont of arthropods and nematodes may modulate host cellular differentiation to manipulate host reproduction. Our survey of the literature on how infection alters gene expression in Wolbachia and its hosts revealed that, despite their intermediate-sized genomes, different strains appear capable of a wide diversity of regulatory manipulations. Given this and Wolbachia’s diversity of phenotypes and eukaryotic-like proteins, we expect that many symbiont-induced host differentiation mechanisms will be discovered in this system.

scholarly journals Host Gene Expression Profiling of Dengue Virus Infection in Cell Lines and Patients

2007 ◽  
Vol 1 (2) ◽  
pp. e86 ◽  
Author(s):  
Joshua Fink ◽  
Feng Gu ◽  
Ling Ling ◽  
Thomas Tolfvenstam ◽  
Farzad Olfat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virus Infection ◽  
Dengue Virus ◽  
Gene Expression Profiling ◽  
Cell Lines ◽  
Expression Profiling ◽  
Host Gene ◽  
Host Gene Expression ◽  
Dengue Virus Infection

scholarly journals Erratum: Dynamic changes in host gene expression associated with H5N8 avian influenza virus infection in mice

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Su-Jin Park ◽  
Mukesh Kumar ◽  
Hyeok-il Kwon ◽  
Rak-Kyun Seong ◽  
Kyudong Han ◽  
...  
Keyword(s):  
Gene Expression ◽  
Influenza Virus ◽  
Virus Infection ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Influenza Virus Infection ◽  
Host Gene ◽  
Host Gene Expression ◽  
Dynamic Changes

scholarly journals Suppression of Proinflammatory Signal Transduction and Gene Expression by the DualNucleic Acid Binding Domains of the Vaccinia Virus E3L Proteins

2006 ◽  
Vol 80 (20) ◽  
pp. 10083-10095 ◽  
Author(s):  
Jeffrey O. Langland ◽  
John C. Kash ◽  
Victoria Carter ◽  
Matthew J. Thomas ◽  
Michael G. Katze ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Vaccinia Virus ◽  
Cellular Response ◽  
Viral Infections ◽  
Host Gene ◽  
Host Gene Expression ◽  
Danger Signals ◽  
Binding Domains ◽  
Z Dna

ABSTRACT Cells have evolved elaborate mechanisms to counteract the onslaught of viral infections. To activate these defenses, the viral threat must be recognized. Danger signals, or pathogen-associated molecular patterns, that are induced by pathogens include double-stranded RNA (dsRNA), viral single-stranded RNA, glycolipids, and CpG DNA. Understanding the signal transduction pathways activated and host gene expression induced by these danger signals is vital to understanding virus-host interactions. The vaccinia virus E3L protein is involved in blocking the host antiviral response and increasing pathogenesis, functions that map to separate C-terminal dsRNA- and N-terminal Z-DNA-binding domains. Viruses containing mutations in these domains allow modeling of the role of dsRNA and Z-form nucleic acid in the host response to virus infection. Deletions in the Z-DNA- or dsRNA-binding domains led to activation of signal transduction cascades and up-regulation of host gene expression, with many genes involved in the inflammatory response. These data suggest that poxviruses actively inhibit cellular recognition of viral danger signals and the subsequent cellular response to the viral threat.

scholarly journals Highly Selective Escape from KSHV-mediated Host mRNA Shutoff and Its Implications for Viral Pathogenesis

2004 ◽  
Vol 200 (3) ◽  
pp. 391-398 ◽  
Author(s):  
Britt Glaunsinger ◽  
Don Ganem
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
De Novo ◽  
Signaling Molecules ◽  
Lytic Cycle ◽  
Host Gene ◽  
Host Gene Expression ◽  
Disease States ◽  
Cellular Genes ◽  
Host Shutoff

During Kaposi's sarcoma (KS)–associated herpesvirus (KSHV) lytic infection, many virus-encoded signaling molecules (e.g., viral G protein–coupled receptor [vGPCR]) are produced that can induce host gene expression in transiently transfected cells, and roles for such induced host genes have been posited in KS pathogenesis. However, we have recently found that host gene expression is strongly inhibited by 10–12 h after lytic reactivation of KSHV, raising the question of whether and to what extent de novo host gene expression induced by viral signaling molecules can proceed during the lytic cycle. Here, we show by microarray analysis that expression of most vGPCR target genes is drastically curtailed by this host shutoff. However, rare cellular genes can escape the host shutoff and are potently up-regulated during lytic KSHV growth. Prominent among these is human interleukin-6, whose striking induction may contribute to the overexpression of this cytokine in several disease states linked to KSHV infection.

scholarly journals Trends in Symbiont-Induced Host Cellular Differentiation

2020 ◽  
Author(s):  
Shelbi Russell ◽  
Jennie Ruelas Castillo
Keyword(s):  
Gene Expression ◽  
Cellular Differentiation ◽  
Cost Benefit ◽  
Regulatory Elements ◽  
Host Gene ◽  
Bacterial Symbionts ◽  
Host Gene Expression ◽  
Associated Bacteria ◽  
Regulatory Pathways ◽  
Symbiotic Associations

Bacteria participate in a wide diversity of symbiotic associations with eukaryotic hosts that require precise interactions for bacterial recognition and persistence. Most commonly, host-associated bacteria interfere with host gene expression to modulate the immune response to the infection. However, many of these bacteria also interfere with host cellular differentiation pathways to create a hospitable niche, resulting in the formation of novel cell types, tissues, and organs. In both of these situations, bacterial symbionts must interact with eukaryotic regulatory pathways. Here, we detail what is known about how bacterial symbionts, from pathogens to mutualists, control host cellular differentiation across the central dogma, from epigenetic chromatin modifications, to transcription and mRNA processing, to translation and protein modifications. We identify four main trends from this survey. First, mechanisms for controlling host gene expression appear to evolve from symbionts co-opting cross-talk between host signalling pathways. Second, symbiont regulatory capacity is constrained by the processes that drive reductive genome evolution in host-associated bacteria. Third, the regulatory mechanisms symbionts exhibit correlate with the cost/benefit nature of the association. And, fourth symbiont mechanisms for interacting with host genetic regulatory elements are not bound by native bacterial capabilities. Using this knowledge, we explore how the ubiquitous intracellular Wolbachia symbiont of arthropods and nematodes may modulate host cellular differentiation to manipulate host reproduction. Our survey of the literature on how infection alters gene expression in Wolbachia and its hosts revealed that, despite their intermediate-sized genomes, different strains appear capable of a wide diversity of regulatory manipulations. Given this and Wolbachia’s diversity of phenotypes and eukaryotic-like proteins, we expect that many symbiont-induced host differentiation mechanisms will be discovered in this system.

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