The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Takaji Wakita - One of the best experts on this subject based on the ideXlab platform.
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hepatitis c Viral life cycle
Advanced Drug Delivery Reviews, 2007Co-Authors: Tetsuro Suzuki, Koji Ishii, Hideki Aizaki, Takaji WakitaAbstract:Hepatitis C virus (HCV) has been recognized as a major cause of chronic liver diseases worldwide. Molecular studies of the virus became possible with the successful cloning of its genome in 1989. Although much work remains to be done regarding early and late stages of the HCV life cycle, significant progress has been made with respect to the molecular biology of HCV, especially the Viral Protein processing and the genome replication. This review summarizes our current understanding of genomic organization of HCV, features of the Viral Protein characteristics, and the Viral life cycle.
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Hepatitis C Viral life cycle
Advanced Drug Delivery Reviews, 2007Co-Authors: Tetsuro Suzuki, Koji Ishii, Hideki Aizaki, Takaji WakitaAbstract:Hepatitis C virus (HCV) has been recognized as a major cause of chronic liver diseases worldwide. Molecular studies of the virus became possible with the successful cloning of its genome in 1989. Although much work remains to be done regarding early and late stages of the HCV life cycle, significant progress has been made with respect to the molecular biology of HCV, especially the Viral Protein processing and the genome replication. This review summarizes our current understanding of genomic organization of HCV, features of the Viral Protein characteristics, and the Viral life cycle. © 2007 Elsevier B.V. All rights reserved.
Emily D Ledgerwood - One of the best experts on this subject based on the ideXlab platform.
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mammalian orthoreovirus infection is enhanced in cells pre treated with sodium arsenite
Viruses, 2019Co-Authors: Michael M Lutz, Megan P Worth, Meleana M Hinchman, John S L Parker, Emily D LedgerwoodAbstract:Following reovirus infection, cells activate stress responses that repress canonical translation as a mechanism to limit progeny virion production. Work by others suggests that these stress responses, which are part of the integrated stress response (ISR), may benefit rather than repress reovirus replication. Here, we report that compared to untreated cells, treating cells with sodium arsenite (SA) to activate the ISR prior to infection enhanced Viral Protein expression, percent infectivity, and Viral titer. SA-mediated enhancement was not strain-specific, but was cell-type specific. While SA pre-treatment of cells offered the greatest enhancement, treatment within the first 4 h of infection increased the percent of cells infected. SA activates the heme-regulated eIF2α (HRI) kinase, which phosphorylates eukaryotic translation initiation factor 2 alpha (eIF2α) to induce stress granule (SG) formation. Heat shock (HS), another activator of HRI, also induced eIF2α phosphorylation and SGs in cells. However, HS had no effect on percent infectivity or Viral yield but did enhance Viral Protein expression. These data suggest that SA pre-treatment perturbs the cell in a way that is beneficial for reovirus and that this enhancement is independent of SG induction. Understanding how to manipulate the cellular stress responses during infection to enhance replication could help to maximize the oncolytic potential of reovirus.
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mammalian orthoreovirus infection is enhanced in cells pre treated with sodium arsenite
bioRxiv, 2019Co-Authors: Michael M Lutz, Megan P Worth, Meleana M Hinchman, John S L Parker, Emily D LedgerwoodAbstract:Following reovirus infection, cells activate stress responses that repress canonical cellular translation as a mechanism to limit production of progeny virions. This includes the formation of stress granules (SG) that sequester translationally-stalled cellular transcripts, translation initiation factors, ribosomal Proteins, and RNA binding Proteins until conditions improve and translation can resume. Work by others suggests that these cellular stress responses, which are part of the integrated stress response, may benefit rather than repress reovirus replication. In agreement with this, we report that stressing cells prior to infection with sodium arsenite (SA), a robust inducer of SG and activator of eIF2α kinases, enhanced Viral Protein expression, percent infectivity and Viral titer in SA-treated cells compared to untreated cells. SA-mediated enhancement of reovirus replication was not strain-specific, but was cell-type specific. While pre-treatment of cells with SA offered the greatest enhancement, treatment of infected cultures as late as 4 h post infection resulted in an increase in the percent of cells infected. SA activates the HRI kinase, which phosphorylates eIF2α and subsequently induces SG formation. Other stresses, such as heat shock (HS) and osmotic shock also activate HRI. Heat shock of cells prior to reovirus infection readily induced SG in greater than 85% of cells. Although HS pre-treatment had no effect on the percentage of infected cells or Viral yield, it did enhance Viral Protein expression. These data suggest that SA pre-treatment perturbs the cell in a way that is beneficial for reovirus and that neither HRI activation nor SG induction is sufficient for reovirus infection enhancement.
Yoshihiro Kawaoka - One of the best experts on this subject based on the ideXlab platform.
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Host Protein mimics Viral Protein to hinder infection by Ebola virus
Nature, 2019Co-Authors: Seiya Yamayoshi, Yoshihiro KawaokaAbstract:Infection by Ebola virus can be fatal. The discovery of a human Protein that mimics one type of Ebola Protein and binds to another to suppress Viral RNA production might aid the development of clinical treatments for the disease. The production of RNA by Ebola virus is suppressed by a human Protein.
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Identification of a Novel Viral Protein Expressed from the PB2 Segment of Influenza A Virus
Journal of Virology, 2015Co-Authors: Seiya Yamayoshi, Mariko Watanabe, Hideo Goto, Yoshihiro KawaokaAbstract:ABSTRACT Over the past 2 decades, several novel influenza virus Proteins have been identified that modulate Viral infections in vitro and/or in vivo . The PB2 segment, which is one of the longest influenza A virus segments, is known to encode only one Viral Protein, PB2. In the present study, we used reverse transcription-PCR (RT-PCR) targeting Viral mRNAs transcribed from the PB2 segment to look for novel Viral Proteins encoded by spliced mRNAs. We identified a new Viral Protein, PB2-S1, encoded by a novel spliced mRNA in which the region corresponding to nucleotides 1513 to 1894 of the PB2 mRNA is deleted. PB2-S1 was detected in virus-infected cells and in cells transfected with a Protein expression plasmid encoding PB2. PB2-S1 localized to mitochondria, inhibited the RIG-I-dependent interferon signaling pathway, and interfered with Viral polymerase activity (dependent on its PB1-binding capability). The nucleotide sequences around the splicing donor and acceptor sites for PB2-S1 were highly conserved among pre-2009 human H1N1 viruses but not among human H1N1pdm and H3N2 viruses. PB2-S1-deficient viruses, however, showed growth kinetics in MDCK cells and virulence in mice similar to those of wild-type virus. The biological significance of PB2-S1 to the replication and pathogenicity of seasonal H1N1 influenza A viruses warrants further investigation. IMPORTANCE Transcriptome analysis of cells infected with influenza A virus has improved our understanding of the host response to Viral infection, because such analysis yields considerable information about both in vitro and in vivo Viral infections. However, little attention has been paid to transcriptomes derived from the Viral genome. Here we focused on the splicing of mRNA expressed from the PB2 segment and identified a spliced Viral mRNA encoding a novel Viral Protein. This result suggests that other, as yet unidentified Viral Proteins encoded by spliced mRNAs could be expressed in virus-infected cells. A Viral transcriptome including the Viral spliceosome should be evaluated to gain new insights into influenza virus infection.
Michael Bukrinsky - One of the best experts on this subject based on the ideXlab platform.
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vpr host interactions during hiv 1 Viral life cycle
Journal of Neuroimmune Pharmacology, 2011Co-Authors: Richard Y. Zhao, Ge Li, Michael BukrinskyAbstract:Human immunodeficiency virus type 1 (HIV-1) Viral Protein R (Vpr) is a multifunctional Viral Protein that plays important role at multiple stages of the HIV-1 Viral life cycle. Although the molecular mechanisms underlying these activities are subject of ongoing investigations, overall, these activities have been linked to promotion of Viral replication and impairment of anti-HIV immunity. Importantly, functional defects of Vpr have been correlated with slow disease progression of HIV-infected patients. Vpr is required for efficient Viral replication in non-dividing cells such as macrophages, and it promotes, to some extent, Viral replication in proliferating CD4+ T cells. The specific activities of Vpr include modulation of fidelity of Viral reverse transcription, nuclear import of the HIV-1 pre-integration complex, transactivation of the HIV-1 LTR promoter, induction of cell cycle G2 arrest and cell death via apoptosis. In this review, we focus on description of the cellular Proteins that specifically interact with Vpr and discuss their significance with regard to the known Vpr activities at each step of the Viral life cycle in proliferating and non-proliferating cells.
Tetsuro Suzuki - One of the best experts on this subject based on the ideXlab platform.
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hepatitis c Viral life cycle
Advanced Drug Delivery Reviews, 2007Co-Authors: Tetsuro Suzuki, Koji Ishii, Hideki Aizaki, Takaji WakitaAbstract:Hepatitis C virus (HCV) has been recognized as a major cause of chronic liver diseases worldwide. Molecular studies of the virus became possible with the successful cloning of its genome in 1989. Although much work remains to be done regarding early and late stages of the HCV life cycle, significant progress has been made with respect to the molecular biology of HCV, especially the Viral Protein processing and the genome replication. This review summarizes our current understanding of genomic organization of HCV, features of the Viral Protein characteristics, and the Viral life cycle.
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Hepatitis C Viral life cycle
Advanced Drug Delivery Reviews, 2007Co-Authors: Tetsuro Suzuki, Koji Ishii, Hideki Aizaki, Takaji WakitaAbstract:Hepatitis C virus (HCV) has been recognized as a major cause of chronic liver diseases worldwide. Molecular studies of the virus became possible with the successful cloning of its genome in 1989. Although much work remains to be done regarding early and late stages of the HCV life cycle, significant progress has been made with respect to the molecular biology of HCV, especially the Viral Protein processing and the genome replication. This review summarizes our current understanding of genomic organization of HCV, features of the Viral Protein characteristics, and the Viral life cycle. © 2007 Elsevier B.V. All rights reserved.
