The Experts below are selected from a list of 19050 Experts worldwide ranked by ideXlab platform
Thomas Hohn - One of the best experts on this subject based on the ideXlab platform.
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interaction between cauliflower mosaic Virus Inclusion body protein and capsid protein implications for viral assembly
1996Co-Authors: Axel Himmelbach, Yvan Chapdelaine, Thomas HohnAbstract:Abstract The cauliflower mosaic Virus (CaMV) Inclusion body protein (pVI) is able to specifically interact with the viral capsid precursor protein (pIV). By using the yeast two-hybrid system and a blot assay, the pIV region required for the recognition of pVI was mapped to the lysine-rich domain. This region of only 48 amino acids when fused to dihydrofolate reductase (DHFR) mediated pVI and DNA binding in vitro. Competition experiments confirmed that pVI and DNA bind to the same region of pIV. Since pVI is absent from the mature Virus, models are discussed in which pVI plays an accessory role in CaMV assembly, in addition to its function in transactivating translation.
Richard E. Randall - One of the best experts on this subject based on the ideXlab platform.
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interferon induced inhibition of parainfluenza Virus type 5 the roles of mxa pkr and oligo a synthetase rnase l
2007Co-Authors: T. S. Carlos, D. F. Young, Silke Stertz, Georg Kochs, Richard E. RandallAbstract:Abstract We have previously reported that the addition of interferon (IFN) to the culture medium of Vero cells (which cannot produce IFN) that were infected with the CPI− strain of parainfluenza Virus 5 (PIV5, formally known as SV5), that fails to block IFN signaling, rapidly induces alterations in the relative levels of Virus mRNA and protein synthesis. In addition, IFN treatment also caused a rapid redistribution of Virus proteins and enhanced the formation of cytoplasmic viral Inclusion bodies. The most studied IFN-induced genes with known anti-viral activity are MxA, PKR and the Oligo A synthetase/RNase L system. We therefore examined the effects of these proteins on the replication cycle of PIV5. These studies revealed that while these proteins had some anti-viral activity against PIV5 they were not primarily responsible for the very rapid alteration in Virus protein synthesis observed following IFN treatment, nor for the IFN-induced formation of Virus Inclusion bodies, in CPI− infected cells.
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Interferon-Induced Alterations in the Pattern of Parainfluenza Virus 5 Transcription and Protein Synthesis and the Induction of Virus Inclusion Bodies
2005Co-Authors: T. S. Carlos, Rachel Fearns, Richard E. RandallAbstract:Although parainfluenza Virus 5 (simian Virus 5 [SV5]) circumvents the interferon (IFN) response by blocking IFN signaling and by reducing the amount of IFN released by infected cells, its ability to circumvent the IFN response is not absolute. The effects of IFN on SV5 infection were examined in Vero cells, which do not produce but can respond to IFN, using a strain of SV5 (CPI−) which does not block IFN signaling. Thus, by infecting Vero cells with CPI− and subsequently treating the cells with exogenous IFN, it was possible to observe the effects that IFN had on SV5 infection in the absence of Virus countermeasures. IFN rapidly (within 6 h) induced alterations in the relative levels of Virus mRNA and protein synthesis and caused a redistribution of Virus proteins within infected cells that led to the enhanced formation of Virus cytoplasmic Inclusion bodies. IFN induced a steeper gradient of mRNA transcription from the 3′ to the 5′ end of the genome and the production of Virus mRNAs with longer poly(A) tails, suggesting that the processivity of the Virus polymerase was altered in cells in an IFN-induced antiviral state. Additional evidence is presented which suggests that these findings also apply to the replication of strains of SV5, parainfluenza Virus type 2, and mumps Virus that block IFN signaling when they infect cells that are already in an IFN-induced antiviral state.
Pierre-edouard Fournier - One of the best experts on this subject based on the ideXlab platform.
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genomic diversity and evolution of coronaVirus sars cov 2 in france from 309 covid 19 infected patients
2020Co-Authors: Anthony Levasseur, Aurelia Caputo, Ludivine Brechard, Jeremy Delerce, Jean Christophe Lagier, Philippe Colson, Pierre-edouard FournierAbstract:The novel coronaVirus (SARS-CoV-2) causes pandemic of viral pneumonia. The evolution and mutational events of the SARS-CoV-2 genomes are critical for controlling virulence, transmissibility, infectivity, severity of symptoms and mortality associated to this infectious disease. We collected and investigated 309 SARS-CoV-2 genomes from patients infected in France. Detailed genome cartography of all mutational events (SNPs, indels) was reported and correlated to clinical features of patients. A comparative analysis between our 309 SARS-CoV-2 genomes from French patients and the reference Wuhan coronaVirus genome revealed 315 substitution mutations and six deletion events: ten were in 5/3 UTR, 178 were nonsynonymous, 126 were synonymous and one generated a stop codon. Six different deleted areas were also identified in nine viral variants. In particular, 30 substitution mutations (18 nonsynonymous) and one deletion ({Delta}21765-21770) concerned the spike S glycoprotein. An average of 7.8 mutational events (+/- 1.7 SD) and a median of 8 (range, 7-9) were reported per viral isolate. Comparative analyses and clustering of specific mutational signatures in 309 genomes disclose several divisions in groups and subgroups combining their geographical and phylogenetic origin. Clinical outcomes of the 309 COVID-19-infected patients were investigated according to the mutational signatures of viral variants. These findings highlight the genome dynamics of the coronaVirus 2019-20 and shed light on the mutational landscape and evolution of this Virus. Inclusion of the French cohort enabled us to identify 161 novel mutations never reported in SARS-CoV-2 genomes collected worldwide. These results support a global and continuing surveillance of the emerging variants of the coronaVirus SARS-CoV-2.
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genomic diversity and evolution of coronaVirus sars cov 2 in france from 309 covid 19 infected patients
2020Co-Authors: Aurelia Caputo, Ludivine Brechard, Jeremy Delerce, Anthony Levasseur, Jean Christophe Lagier, Philippe Colson, Pierre-edouard FournierAbstract:ABSTRACT The novel coronaVirus (SARS-CoV-2) causes pandemic of viral pneumonia. The evolution and mutational events of the SARS-CoV-2 genomes are critical for controlling virulence, transmissibility, infectivity, severity of symptoms and mortality associated to this infectious disease. We collected and investigated 309 SARS-CoV-2 genomes from patients infected in France. Detailed genome cartography of all mutational events (SNPs, indels) was reported and correlated to clinical features of patients. A comparative analysis between our 309 SARS-CoV-2 genomes from French patients and the reference Wuhan coronaVirus genome revealed 315 substitution mutations and six deletion events: ten were in 5’/3’ UTR, 178 were nonsynonymous, 126 were synonymous and one generated a stop codon. Six different deleted areas were also identified in nine viral variants. In particular, 30 substitution mutations (18 nonsynonymous) and one deletion (Δ21765-21770) concerned the spike S glycoprotein. An average of 7.8 mutational events (+/- 1.7 SD) and a median of 8 (range, 7-9) were reported per viral isolate. Comparative analyses and clustering of specific mutational signatures in 309 genomes disclose several divisions in groups and subgroups combining their geographical and phylogenetic origin. Clinical outcomes of the 309 COVID-19-infected patients were investigated according to the mutational signatures of viral variants. These findings highlight the genome dynamics of the coronaVirus 2019-20 and shed light on the mutational landscape and evolution of this Virus. Inclusion of the French cohort enabled us to identify 161 novel mutations never reported in SARS-CoV-2 genomes collected worldwide. These results support a global and continuing surveillance of the emerging variants of the coronaVirus SARS-CoV-2.
Anthony Levasseur - One of the best experts on this subject based on the ideXlab platform.
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genomic diversity and evolution of coronaVirus sars cov 2 in france from 309 covid 19 infected patients
2020Co-Authors: Anthony Levasseur, Aurelia Caputo, Ludivine Brechard, Jeremy Delerce, Jean Christophe Lagier, Philippe Colson, Pierre-edouard FournierAbstract:The novel coronaVirus (SARS-CoV-2) causes pandemic of viral pneumonia. The evolution and mutational events of the SARS-CoV-2 genomes are critical for controlling virulence, transmissibility, infectivity, severity of symptoms and mortality associated to this infectious disease. We collected and investigated 309 SARS-CoV-2 genomes from patients infected in France. Detailed genome cartography of all mutational events (SNPs, indels) was reported and correlated to clinical features of patients. A comparative analysis between our 309 SARS-CoV-2 genomes from French patients and the reference Wuhan coronaVirus genome revealed 315 substitution mutations and six deletion events: ten were in 5/3 UTR, 178 were nonsynonymous, 126 were synonymous and one generated a stop codon. Six different deleted areas were also identified in nine viral variants. In particular, 30 substitution mutations (18 nonsynonymous) and one deletion ({Delta}21765-21770) concerned the spike S glycoprotein. An average of 7.8 mutational events (+/- 1.7 SD) and a median of 8 (range, 7-9) were reported per viral isolate. Comparative analyses and clustering of specific mutational signatures in 309 genomes disclose several divisions in groups and subgroups combining their geographical and phylogenetic origin. Clinical outcomes of the 309 COVID-19-infected patients were investigated according to the mutational signatures of viral variants. These findings highlight the genome dynamics of the coronaVirus 2019-20 and shed light on the mutational landscape and evolution of this Virus. Inclusion of the French cohort enabled us to identify 161 novel mutations never reported in SARS-CoV-2 genomes collected worldwide. These results support a global and continuing surveillance of the emerging variants of the coronaVirus SARS-CoV-2.
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genomic diversity and evolution of coronaVirus sars cov 2 in france from 309 covid 19 infected patients
2020Co-Authors: Aurelia Caputo, Ludivine Brechard, Jeremy Delerce, Anthony Levasseur, Jean Christophe Lagier, Philippe Colson, Pierre-edouard FournierAbstract:ABSTRACT The novel coronaVirus (SARS-CoV-2) causes pandemic of viral pneumonia. The evolution and mutational events of the SARS-CoV-2 genomes are critical for controlling virulence, transmissibility, infectivity, severity of symptoms and mortality associated to this infectious disease. We collected and investigated 309 SARS-CoV-2 genomes from patients infected in France. Detailed genome cartography of all mutational events (SNPs, indels) was reported and correlated to clinical features of patients. A comparative analysis between our 309 SARS-CoV-2 genomes from French patients and the reference Wuhan coronaVirus genome revealed 315 substitution mutations and six deletion events: ten were in 5’/3’ UTR, 178 were nonsynonymous, 126 were synonymous and one generated a stop codon. Six different deleted areas were also identified in nine viral variants. In particular, 30 substitution mutations (18 nonsynonymous) and one deletion (Δ21765-21770) concerned the spike S glycoprotein. An average of 7.8 mutational events (+/- 1.7 SD) and a median of 8 (range, 7-9) were reported per viral isolate. Comparative analyses and clustering of specific mutational signatures in 309 genomes disclose several divisions in groups and subgroups combining their geographical and phylogenetic origin. Clinical outcomes of the 309 COVID-19-infected patients were investigated according to the mutational signatures of viral variants. These findings highlight the genome dynamics of the coronaVirus 2019-20 and shed light on the mutational landscape and evolution of this Virus. Inclusion of the French cohort enabled us to identify 161 novel mutations never reported in SARS-CoV-2 genomes collected worldwide. These results support a global and continuing surveillance of the emerging variants of the coronaVirus SARS-CoV-2.
Axel Himmelbach - One of the best experts on this subject based on the ideXlab platform.
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interaction between cauliflower mosaic Virus Inclusion body protein and capsid protein implications for viral assembly
1996Co-Authors: Axel Himmelbach, Yvan Chapdelaine, Thomas HohnAbstract:Abstract The cauliflower mosaic Virus (CaMV) Inclusion body protein (pVI) is able to specifically interact with the viral capsid precursor protein (pIV). By using the yeast two-hybrid system and a blot assay, the pIV region required for the recognition of pVI was mapped to the lysine-rich domain. This region of only 48 amino acids when fused to dihydrofolate reductase (DHFR) mediated pVI and DNA binding in vitro. Competition experiments confirmed that pVI and DNA bind to the same region of pIV. Since pVI is absent from the mature Virus, models are discussed in which pVI plays an accessory role in CaMV assembly, in addition to its function in transactivating translation.
