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1

Stone, Jeffrey K., Rene Rijnbrand, David A. Stein, et al. "A Morpholino Oligomer Targeting Highly Conserved Internal Ribosome Entry Site Sequence Is Able To Inhibit Multiple Species of Picornavirus." Antimicrobial Agents and Chemotherapy 52, no. 6 (2008): 1970–81. http://dx.doi.org/10.1128/aac.00011-08.

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ABSTRACT Members of the genera Enterovirus and Rhinovirus (family Picornaviridae) cause a wide range of human diseases. An established vaccine is available only for poliovirus, and no effective therapy is available for the treatment of infections caused by any pathogenic picornavirus. Peptide-conjugated phosphorodiamidate morpholino oligomers (PPMO) are single-stranded DNA-like antisense agents that readily enter cells. A panel of PPMO was tested for their antiviral activities against various picornaviruses. PPMO targeting conserved internal ribosome entry site (IRES) sequence were highly acti
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2

Li, Qisheng, Catherine Sodroski, Brianna Lowey, et al. "Hepatitis C virus depends on E-cadherin as an entry factor and regulates its expression in epithelial-to-mesenchymal transition." Proceedings of the National Academy of Sciences 113, no. 27 (2016): 7620–25. http://dx.doi.org/10.1073/pnas.1602701113.

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Hepatitis C virus (HCV) enters the host cell through interactions with a cascade of cellular factors. Although significant progress has been made in understanding HCV entry, the precise mechanisms by which HCV exploits the receptor complex and host machinery to enter the cell remain unclear. This intricate process of viral entry likely depends on additional yet-to-be-defined cellular molecules. Recently, by applying integrative functional genomics approaches, we identified and interrogated distinct sets of host dependencies in the complete HCV life cycle. Viral entry assays using HCV pseudopar
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3

Muralinath, E., G. Srinivas, D.V. Ramanjaneyulu, et al. "An Important Parameters of Entero Virus Include Etiologhy, Epidemiology, Patho Physiology, Diagnosis, Differential Diagnosis, Treatment, Prognosis and Complications." Journal of Cardiovascular, Cardiopulmonary Rehabilitation Nursing 3, no. 2 (2025): 11–21. https://doi.org/10.5281/zenodo.15532695.

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<em>Enteroviruses are a class of viruses comprising approximately 300 serotypes. These common viruses have a broad range of illnesses, diverse presentations, widespread morbidity, and an economic burden. The pathologic basis of these diseases is explained in this exercise, which also goes over the interprofessional team's involvement in diagnosing and treating patients with enteroviral infections.</em>
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4

Licursi, Maria, Yumiko Komatsu, Theerawat Pongnopparat, and Kensuke Hirasawa. "Promotion of viral internal ribosomal entry site-mediated translation under amino acid starvation." Journal of General Virology 93, no. 5 (2012): 951–62. http://dx.doi.org/10.1099/vir.0.040386-0.

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Cap-dependent and internal ribosomal entry site (IRES)-mediated translation are regulated differently within cells. Viral IRES-mediated translation often remains active when cellular cap-dependent translation is severely impaired under cellular stresses induced by virus infection. To investigate how cellular stresses influence the efficiency of viral IRES-mediated translation, we used a bicistronic luciferase reporter construct harbouring IRES elements from the following viruses: encephalomyocarditis virus (EMCV), foot-and-mouth disease virus (FMDV), hepatitis C virus (HCV) or human rhinovirus
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5

Tripathi, Sachin Kumar, Ashish Aneja, Teji Borgaonkar, and Saumitra Das. "PSPC1 Binds to HCV IRES and Prevents Ribosomal Protein S5 Binding, Inhibiting Viral RNA Translation." Viruses 16, no. 5 (2024): 738. http://dx.doi.org/10.3390/v16050738.

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Hepatitis C virus (HCV) infects the human liver, and its chronic infection is one of the major causes of Hepatocellular carcinoma. Translation of HCV RNA is mediated by an Internal Ribosome Entry Site (IRES) element located in the 5’UTR of viral RNA. Several RNA Binding proteins of the host interact with the HCV IRES and modulate its function. Here, we demonstrate that PSPC1 (Paraspeckle Component 1), an essential paraspeckle component, upon HCV infection is relocalized and interacts with HCV IRES to prevent viral RNA translation. Competition UV-crosslinking experiments showed that PSPC1 inter
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6

Gallego, J., and G. Varani. "The hepatitis C virus internal ribosome-entry site: a new target for antiviral research." Biochemical Society Transactions 30, no. 2 (2002): 140–45. http://dx.doi.org/10.1042/bst0300140.

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The hepatitis C virus (HCV) is the main causative agent of non-A, non-B hepatitis in humans and a major cause of mortality and morbidity in the world. Currently there is no effective treatment available for the infection caused by this virus, whose replication depends on an unusual translation-initiation mechanism. The viral RNA contains an internal ribosome-entry site (IRES) that is recognized specifically by the small ribosomal subunit and by eukaryotic initiation factor 3, and these interactions allow cap (7-methylguanine nucleotide)-independent initiation of viral protein synthesis. In thi
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7

Chen, L. L., Y. A. Kung, K. F. Weng, J. Y. Lin, J. T. Horng, and S. R. Shih. "Enterovirus 71 Infection Cleaves a Negative Regulator for Viral Internal Ribosomal Entry Site-Driven Translation." Journal of Virology 87, no. 7 (2013): 3828–38. http://dx.doi.org/10.1128/jvi.02278-12.

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8

Svitkin, Yuri V., Barbara Herdy, Mauro Costa-Mattioli, Anne-Claude Gingras, Brian Raught, and Nahum Sonenberg. "Eukaryotic Translation Initiation Factor 4EAvailability Controls the Switch between Cap-Dependent andInternal Ribosomal Entry Site-MediatedTranslation." Molecular and Cellular Biology 25, no. 23 (2005): 10556–65. http://dx.doi.org/10.1128/mcb.25.23.10556-10565.2005.

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ABSTRACT Translation of m7G-capped cellular mRNAs is initiated by recruitment of ribosomes to the 5′ end of mRNAs via eukaryotic translation initiation factor 4F (eIF4F), a heterotrimeric complex comprised of a cap-binding subunit (eIF4E) and an RNA helicase (eIF4A) bridged by a scaffolding molecule (eIF4G). Internal translation initiation bypasses the requirement for the cap and eIF4E and occurs on viral and cellular mRNAs containing internal ribosomal entry sites (IRESs). Here we demonstrate that eIF4E availability plays a critical role in the switch from cap-dependent to IRES-mediated trans
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9

Fernández-Miragall, Olga, and Encarnación Martínez-Salas. "In vivo footprint of a picornavirus internal ribosome entry site reveals differences in accessibility to specific RNA structural elements." Journal of General Virology 88, no. 11 (2007): 3053–62. http://dx.doi.org/10.1099/vir.0.83218-0.

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Internal ribosome entry site (IRES) elements were described in picornaviruses as an essential region of the viral RNA. Understanding of IRES function requires a detailed knowledge of each step involved in the internal initiation process, from RNA folding and IRES–protein interaction to ribosome recruitment. Thus, deciphering IRES accessibility to external agents due to RNA structural features, as well as RNA–protein protection within living cells, is of primary importance. In this study, two chemical reagents, dimethylsulfate (DMS) and aminomethylpsoralen, have been used to footprint the entir
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10

Cheng, Yuan-Lung, Keng-Hsueh Lan, Wei-Ping Lee, et al. "Amiodarone inhibits the entry and assembly steps of hepatitis C virus life cycle." Clinical Science 125, no. 9 (2013): 439–48. http://dx.doi.org/10.1042/cs20120594.

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HCV (hepatitis C virus) infection affects an estimated 180 million people in the world's population. Adverse effects occur frequently with current standard treatment of interferon and ribavirin, while resistance of new direct anti-viral agents, NS3 protease inhibitors, is a major concern because of their single anti-HCV mechanism against the viral factor. New anti-viral agents are needed to resolve the problems. Amiodarone, an anti-arrhythmic drug, has recently been shown to inhibit HCV infection in vitro. The detailed mechanism has yet to be clarified. The aim of the present study was to eluc
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11

Yuan, Ji, David A. Stein, Travis Lim, et al. "Inhibition of Coxsackievirus B3 in Cell Cultures and in Mice by Peptide-Conjugated Morpholino Oligomers Targeting the Internal Ribosome Entry Site." Journal of Virology 80, no. 23 (2006): 11510–19. http://dx.doi.org/10.1128/jvi.00900-06.

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ABSTRACT Coxsackievirus B3 (CVB3) is a primary cause of viral myocarditis, yet no effective therapeutic against CVB3 is available. Nucleic acid-based interventional strategies against various viruses, including CVB3, have shown promise experimentally, but limited stability and inefficient delivery in vivo remain as obstacles to their potential as therapeutics. We employed phosphorodiamidate morpholino oligomers (PMO) conjugated to a cell-penetrating arginine-rich peptide, P007 (to form PPMO), to address these issues. Eight CVB3-specific PPMO were evaluated with HeLa cells and HL-1 cardiomyocyt
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12

Gutiérrez-Escolano, Ana Lorena, Zamirath Uribe Brito, Rosa M. del Angel, and Xi Jiang. "Interaction of Cellular Proteins with the 5′ End of Norwalk Virus Genomic RNA." Journal of Virology 74, no. 18 (2000): 8558–62. http://dx.doi.org/10.1128/jvi.74.18.8558-8562.2000.

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ABSTRACT The lack of a susceptible cell line and an animal model for Norwalk virus (NV) infection has prompted the development of alternative strategies to generate in vitro RNAs that approximate the authentic viral genome. This approach has allowed the study of viral RNA replication and gene expression. In this study, using mobility shift and cross-linking assays, we detected several cellular proteins from HeLa and CaCo-2 cell extracts that bind to, and form stable complexes with, the first 110 nucleotides of the 5′ end of NV genomic RNA, a region previously predicted to form a double stem-lo
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13

Hirasawa, Kensuke, Angus Kim, Hye-Seung Han, Jaeseok Han, Hee-Sook Jun, and Ji-Won Yoon. "Effect of p38 Mitogen-Activated Protein Kinase on the Replication of Encephalomyocarditis Virus." Journal of Virology 77, no. 10 (2003): 5649–56. http://dx.doi.org/10.1128/jvi.77.10.5649-5656.2003.

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ABSTRACT Cellular phosphorylation events during viral infection are necessary for effective viral replication. Encephalomyocarditis (EMC) virus has been used for studies on the molecular mechanisms of viral replication, but little is known about the cellular signaling pathways involved. This investigation was initiated to determine whether mitogen-activated protein kinases (MAPKs), which are central components of signal transduction pathways in the regulation of cell proliferation, play a role in the replication of EMC virus. We examined the phosphorylation of MAPKs, including extracellular si
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14

Abdullah, Sahibzada Waheed, Shichong Han, Jin’en Wu, et al. "The DDX23 Negatively Regulates Translation and Replication of Foot-and-Mouth Disease Virus and Is Degraded by 3C Proteinase." Viruses 12, no. 12 (2020): 1348. http://dx.doi.org/10.3390/v12121348.

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DEAD-box helicase 23 (DDX23) is a host nuclear helicase, which is a part of the spliceosomal complex and involved in pre-mRNA splicing. To investigate whether DDX23, an internal ribosomal entry sites transacting factor (ITAF) affects foot-and-mouth disease virus (FMDV) replication and translation through internal ribosome entry site (IRES)-dependent manner. For this, we utilized a pull-down assay, Western blotting, quantitative real-time PCR, confocal microscopy, overexpression and small interfering RNA knockdown, as well as the median tissue culture infective dose. Our findings showed that FM
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15

Rheault, Marylin, Sophie E. Cousineau, Danielle R. Fox, Quinn H. Abram, and Selena M. Sagan. "Elucidating the distinct contributions of miR-122 in the HCV life cycle reveals insights into virion assembly." Nucleic Acids Research 51, no. 5 (2023): 2447–63. http://dx.doi.org/10.1093/nar/gkad094.

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Abstract Efficient hepatitis C virus (HCV) RNA accumulation is dependent upon interactions with the human liver-specific microRNA, miR-122. MiR-122 has at least three roles in the HCV life cycle: it acts as an RNA chaperone, or ‘riboswitch’, allowing formation of the viral internal ribosomal entry site; it provides genome stability; and promotes viral translation. However, the relative contribution of each role in HCV RNA accumulation remains unclear. Herein, we used point mutations, mutant miRNAs, and HCV luciferase reporter RNAs to isolate each of the roles and evaluate their contribution to
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16

Arita, Minetaro, Hiroyuki Shimizu, and Tatsuo Miyamura. "Characterization of in vitro and in vivo phenotypes of poliovirus type 1 mutants with reduced viral protein synthesis activity." Journal of General Virology 85, no. 7 (2004): 1933–44. http://dx.doi.org/10.1099/vir.0.19768-0.

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Sabin vaccine strains of poliovirus (PV) contain major attenuation determinants in the internal ribosomal entry site (IRES), an area that directs viral protein synthesis. To examine the effect of reduced viral protein synthesis on PV neurovirulence, spacer sequences, consisting of short open reading frames of different lengths, were introduced between the IRES and the initiation codon of viral polyprotein, resulting in PV mutants with reduced viral protein synthesis. These PV mutants had a viral protein synthesis activity 8·8–55 % of that of the parental Mahoney strain as measured in HeLa S3 c
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17

Forton, Daniel M., Peter Karayiannis, Nadiya Mahmud, Simon D. Taylor-Robinson, and Howard C. Thomas. "Identification of Unique Hepatitis C Virus Quasispecies in the Central Nervous System and Comparative Analysis of Internal Translational Efficiency of Brain, Liver, and Serum Variants." Journal of Virology 78, no. 10 (2004): 5170–83. http://dx.doi.org/10.1128/jvi.78.10.5170-5183.2004.

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ABSTRACT Reports of cerebral dysfunction in chronic hepatitis C virus (HCV) infection have led to the suggestion that HCV may infect the central nervous system (CNS). We used reverse transcription-PCR, cloning, and sequencing to define quasispecies for the HCV internal ribosomal entry site (IRES) and hypervariable region 1 (HVR1) in autopsy-derived brain, liver, lymph node, and serum samples. There was evidence of tissue compartmentalization of sequences in the brain in two patients, with between 24 and 55% of brain-derived IRES sequences absent from the serum, and significant phylogenetic and
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18

Toyoda, Hidemi, David Franco, Kentaro Fujita, Aniko V. Paul, and Eckard Wimmer. "Replication of Poliovirus Requires Binding of the Poly(rC) Binding Protein to the Cloverleaf as Well as to the Adjacent C-Rich Spacer Sequence between the Cloverleaf and the Internal Ribosomal Entry Site." Journal of Virology 81, no. 18 (2007): 10017–28. http://dx.doi.org/10.1128/jvi.00516-07.

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ABSTRACT The 5′ nontranslated region of poliovirus RNA contains two highly structured regions, the cloverleaf (CL) and the internal ribosomal entry site (IRES). A cellular protein, the poly(rC) binding protein (PCBP), has been reported to interact with the CL either alone or in combination with viral protein 3CDpro. The formation of the ternary complex is essential for RNA replication and, hence, viral proliferation. PCBP also interacts with stem-loop IV of the IRES, an event critical for the initiation of cap-independent translation. Until recently, no special function was assigned to a space
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19

Rahmagiarti, Cintera, Silvia Tri Widyaningtyas, and Budiman Bela. "Konstruksi Plasmid Rekombinan untuk Inisiasi Translasi Enhance Green Fluorescent Protein oleh Internal Ribosomal Entry Site HIV-1." Media Penelitian dan Pengembangan Kesehatan 28, no. 2 (2018): 67–72. http://dx.doi.org/10.22435/mpk.v28i2.181.

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Human immunodeficiency virus (HIV) is a virus that causes acquired immunodeficiency virus syndrome (AIDS). The HIV genome has a cap structure at 5’ and polyadenylation at 3’ on mRNA resulting in a translation initiation through scanning at 5'untranslated region (UTR). The Vpr protein produced during viral replication causes the 5'cap scanning to be inhibited so HIV-1 can directly recruit the ribosome at the start codon via internal ribosomal entry site (IRES). IRES activity is high at G2/M phase and highest expression in monocyte cell line (THP-1) and lymphocyte (HPB-ALL). The role of HIV IRES
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20

Yamasaki, Kenji, Conrad C. Weihl, and Raymond P. Roos. "Alternative Translation Initiation of Theiler’s Murine Encephalomyelitis Virus." Journal of Virology 73, no. 10 (1999): 8519–26. http://dx.doi.org/10.1128/jvi.73.10.8519-8526.1999.

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ABSTRACT DA strain and other members of the TO subgroup of Theiler’s murine encephalomyelitis virus (TMEV) produce a chronic demyelinating disease in which the virus persists but has a restricted expression. We previously reported that TO subgroup strains, in addition to synthesizing the picornaviral polyprotein, use an alternative initiation codon just downstream from the polyprotein’s AUG to translate an 18-kDa protein called L* that is out of frame with the polyprotein (H. H. Chen et al., Nat. Med. 1:927–931, 1995; W. P. Kong and R. P. Roos, J. Virol. 65:3395–3399, 1991). L* is critically i
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21

Klemens, O., D. Dubrau, and N. Tautz. "Characterization of the Determinants of NS2-3-Independent Virion Morphogenesis of Pestiviruses." Journal of Virology 89, no. 22 (2015): 11668–80. http://dx.doi.org/10.1128/jvi.01646-15.

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ABSTRACTA peculiarity of theFlaviviridaeis the critical function of nonstructural (NS) proteins for virus particle formation. For pestiviruses, like bovine viral diarrhea virus (BVDV), uncleaved NS2-3 represents an essential factor for virion morphogenesis, while NS3 is an essential component of the viral replicase. Accordingly, in natural pestivirus isolates, processing at the NS2-3 cleavage site is not complete, to allow for virion morphogenesis. Virion morphogenesis of the related hepatitis C virus (HCV) shows a major deviation from that of pestiviruses: while RNA replication also requires
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22

Peoples, M., S. Sadeghieh, E. Hwang, et al. "5 INHIBITION OF FOOT AND MOUTH DISEASE VIRUS IN VITRO USING RNA INTERFERENCE." Reproduction, Fertility and Development 21, no. 1 (2009): 103. http://dx.doi.org/10.1071/rdv21n1ab5.

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The use of short-hairpin RNA (shRNA) targeting viral genomes has shown great promise in human medicine and in vitro research in animal agriculture. However, this research has not been extrapolated into livestock applications. Foot and mouth disease virus (FMDV) is a world-wide disease resulting in decreased production and export limitations in countries with endemic FMDV, as well as severe economical impacts if an outbreak occurs in an FMDV-free country. The long-term goal for this project is to produce transgenic cattle that express shRNA targeting the FMDV genome resulting in resistance to i
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23

Corman, Victor Max, Adam Grundhoff, Christine Baechlein, et al. "Highly Divergent Hepaciviruses from African Cattle." Journal of Virology 89, no. 11 (2015): 5876–82. http://dx.doi.org/10.1128/jvi.00393-15.

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ABSTRACTThe hepatitis C virus (HCV; genusHepacivirus) is a highly relevant human pathogen. Unique hepaciviruses (HV) were discovered recently in animal hosts. The direct ancestor of HCV has not been found, but the genetically most closely related animal HVs exist in horses. To investigate whether other peridomestic animals also carry HVs, we analyzed sera from Ghanaian cattle for HVs by reverse transcription-PCR (RT-PCR). Nine of 106 specimens from different sampling sites contained HV RNA (8.5%) at median viral loads of 1.6 × 105copies/ml. Infection seemed unrelated to cattle age and gender.
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Gruber, Charlotte, Rebekka Grundler, Georg Haecker, Falco Fend, Christian Peschel, and Justus Duyster. "NPM-ALK Induces Tumour Development in a Murine Model of Anaplastic Large Cell Lymphoma (ALCL) Independently of Bcl-3 Expression." Blood 110, no. 11 (2007): 460. http://dx.doi.org/10.1182/blood.v110.11.460.460.

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Abstract Anaplastic large cell lymphomas (ALCLs) define a subgroup of aggressive non-Hodgkin’s lymphomas. In 40–60% of systemic ALCLs, a t(2;5) (p23;q35) translocation is found, which generates a fusion gene between nucleophosmin (NPM) and the receptor tyrosine kinase gene ALK (anaplastic lymphoma kinase). The NPM-ALK chimeric gene encodes a constitutively activated tyrosine kinase and is believed to initiate the process of lymphomagenesis. Since NPM-ALK has been shown to activate PI3-kinase and STAT3, proteins that are involved in apoptosis regulation, altered apoptosis might contribute to AL
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Needham, J. M., T. M. Greco, I. M. Cristea, and S. R. Thompson. "Ribosomal protein S25 promotes cell cycle entry for a productive BK polyomavirus infection." Philosophical Transactions of the Royal Society B: Biological Sciences 380, no. 1921 (2025). https://doi.org/10.1098/rstb.2023.0390.

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Many viruses use alternate mechanisms to initiate protein translation owing to their limited coding capacity. The ribosomal protein S25 (RPS25/eS25) is required for efficient non-canonical mechanisms of translation initiation, such as internal ribosomal entry site (IRES) initiation or ribosomal shunting, but eS25 is not required for efficient cap-dependent initiation. Thus, eS25 knockdown can be used to evaluate whether a virus relies on alternative mechanisms of initiation. Since earlier studies suggest that simian virus 40 (SV40) uses an IRES to translate a minor capsid protein VP3, which is
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Kirby, Mathew P., Ciara Stevenson, Liam J. Worrall, et al. "The Hinge Region of the Israeli Acute Paralysis Virus Internal Ribosome Entry Site Directs Ribosomal Positioning, Translational Activity, and Virus Infection." Journal of Virology 96, no. 5 (2022). http://dx.doi.org/10.1128/jvi.01330-21.

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Viruses must use the host cell machinery to direct viral protein expression for productive infection. One such mechanism is an internal ribosome entry site that can directly recruit host cell machinery. In this study, we have identified a novel sequence in an IRES that provides insight into the mechanism of viral gene expression. Specifically, this novel sequence promotes viral IRES activity by directly guiding the host cell machinery to start gene expression at a specific site.
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Su, Yu-Siang, Lih-Hwa Hwang, and Chi-Ju Chen. "Heat Shock Protein A6, a Novel HSP70, Is Induced During Enterovirus A71 Infection to Facilitate Internal Ribosomal Entry Site-Mediated Translation." Frontiers in Microbiology 12 (May 7, 2021). http://dx.doi.org/10.3389/fmicb.2021.664955.

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Enterovirus A71 (EV-A71) is a human pathogen causing hand, foot, and mouth disease (HFMD) in children. Its infection can lead to severe neurological diseases or even death in some cases. While being produced in a large quantity during infection, viral proteins often require the assistance from cellular chaperones for proper folding. In this study, we found that heat shock protein A6 (HSPA6), whose function in viral life cycle is scarcely studied, was induced and functioned as a positive regulator for EV-A71 infection. Depletion of HSPA6 led to the reductions of EV-A71 viral proteins, viral RNA
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Liu, Wenming, Decheng Yang, Chao Sun, et al. "hnRNP K Is a Novel Internal Ribosomal Entry Site-Transacting Factor That Negatively Regulates Foot-and-Mouth Disease Virus Translation and Replication and Is Antagonized by Viral 3C Protease." Journal of Virology 94, no. 17 (2020). http://dx.doi.org/10.1128/jvi.00803-20.

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ABSTRACT Cap-independent translation initiation on picornavirus mRNAs is mediated by an internal ribosomal entry site (IRES) in the 5′ untranslated region. The regulation of internal initiation requires the interaction of IRES-transacting factors (ITAFs) with the IRES. In this study, we identified a novel ITAF, heterogeneous nuclear ribonucleoprotein K (hnRNP K), which negatively regulates foot-and-mouth disease virus (FMDV) translation and viral replication. Further investigation revealed that the KH2 and KH3 domains of hnRNP K directly bind to domains II, III, and IV of the FMDV IRES, result
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Lin, Jhao‐Yin, Jing‐Yi Lin, Rei‐Lin Kuo, and Hsing‐I Huang. "Heterogeneous nuclear ribonucleoprotein A3 binds to the internal ribosomal entry site of enterovirus A71 and affects virus replication in neural cells." Journal of Cellular Biochemistry, May 9, 2024. http://dx.doi.org/10.1002/jcb.30575.

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AbstractEnterovirus A71 (EV‐A71) belongs to the genus Enterovirus of the Picornaviridae family and often causes outbreaks in Asia. EV‐A71 infection usually causes hand, foot, and mouth disease and can even affect the central nervous system, causing neurological complications or death. The 5′‐untranslated region (5′‐UTR) of EV‐A71 contains an internal ribosome entry site (IRES) that is responsible for the translation of viral proteins. IRES‐transacting factors can interact with the EV‐A71 5′‐UTR to regulate IRES activity. Heterogeneous nuclear ribonucleoprotein (hnRNP) A3 is a member of the hnR
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30

Hao, Haojie, Weichi Liu, Yuanjiu Miao, et al. "N4-acetylcytidine regulates the replication and pathogenicity of enterovirus 71." Nucleic Acids Research, August 16, 2022. http://dx.doi.org/10.1093/nar/gkac675.

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Abstract Chemical modifications are important for RNA function and metabolism. N4-acetylcytidine (ac4C) is critical for the translation and stability of mRNA. Although ac4C is found in RNA viruses, the detailed mechanisms through which ac4C affects viral replication are unclear. Here, we reported that the 5′ untranslated region of the enterovirus 71 (EV71) genome was ac4C modified by the host acetyltransferase NAT10. Inhibition of NAT10 and mutation of the ac4C sites within the internal ribosomal entry site (IRES) suppressed EV71 replication. ac4C enhanced viral RNA translation via selective r
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31

Lai, Ming-Chih, Han-Hsiang Chen, Peng Xu, and Robert Y. L. Wang. "Translation control of Enterovirus A71 gene expression." Journal of Biomedical Science 27, no. 1 (2020). http://dx.doi.org/10.1186/s12929-019-0607-9.

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AbstractUpon EV-A71 infection of a host cell, EV-A71 RNA is translated into a viral polyprotein. Although EV-A71 can use the cellular translation machinery to produce viral proteins, unlike cellular translation, which is cap-dependent, the viral RNA genome of EV-A71 does not contain a 5′ cap and the translation of EV-A71 protein is cap-independent, which is mediated by the internal ribosomal entry site (IRES) located in the 5′ UTR of EV-A71 mRNA. Like many other eukaryotic viruses, EV-A71 manipulates the host cell translation devices, using an elegant RNA-centric strategy in infected cells. Du
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Han, Shichong, Shiqi Sun, Pinghua Li, et al. "Ribosomal Protein L13 Promotes IRES-Driven Translation of Foot-and-Mouth Disease Virus in a Helicase DDX3-Dependent Manner." Journal of Virology 94, no. 2 (2019). http://dx.doi.org/10.1128/jvi.01679-19.

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ABSTRACT Internal ribosome entry site (IRES)-driven translation is a common strategy among positive-sense, single-stranded RNA viruses for bypassing the host cell requirement of a 5′ cap structure. In the current study, we identified the ribosomal protein L13 (RPL13) as a critical regulator of IRES-driven translation of foot-and-mouth disease virus (FMDV) but found that it is not essential for cellular global translation. RPL13 is also a determinant for translation and infection of Seneca Valley virus (SVV) and classical swine fever virus (CSFV), and this suggests that its function may also be
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Walton, Ross W., Michael C. Brown, Matthew T. Sacco, and Matthias Gromeier. "Engineered Oncolytic Poliovirus PVSRIPO Subverts MDA5-Dependent Innate Immune Responses in Cancer Cells." Journal of Virology 92, no. 19 (2018). http://dx.doi.org/10.1128/jvi.00879-18.

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ABSTRACTWe are pursuing cancer immunotherapy with a neuro-attenuated recombinant poliovirus, PVSRIPO. PVSRIPO is the live attenuated type 1 (Sabin) poliovirus vaccine carrying a heterologous internal ribosomal entry site (IRES) of human rhinovirus type 2 (HRV2). Intratumoral infusion of PVSRIPO is showing promise in the therapy of recurrent WHO grade IV malignant glioma (glioblastoma), a notoriously treatment-refractory cancer with dismal prognosis. PVSRIPO exhibits profound cytotoxicity in infected neoplastic cells expressing the poliovirus receptor CD155. In addition, it elicits intriguing p
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