The Experts below are selected from a list of 267 Experts worldwide ranked by ideXlab platform
Miguel A. Aranda - One of the best experts on this subject based on the ideXlab platform.
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A comparison between Virus Replication and abiotic stress (heat) as modifiers of host gene expression in pea
Molecular plant pathology, 2000Co-Authors: Margarita Escaler, Miguel A. Aranda, I. M. Roberts, Carole L. Thomas, Andrew J. MauleAbstract:Abstract Pea embryonic tissues respond to active Replication of pea seed-borne mosaic potyVirus (PSbMV) by the down-regulation of a range of genes and the induction of others. Both of these responses can be seen when tissues are subjected to abiotic stress, particularly heat. We have compared the effects of the two inducers to assess whether the host alterations following Virus Replication represent generic responses to stress, or more specific effects. Five classes of response were identified: (i) genes induced by both stresses (e.g. heat shock protein 70, hsp70); (ii) genes induced by Virus Replication but unaffected by heat (e.g. glutathione reductase 2, gor2); (iii) genes induced by heat but unaffected by Virus Replication (e.g. heat shock factor, hsf); (iv) genes down-regulated by Virus Replication and unaffected by heat (e.g. vicilin, vic); and (v) genes unaffected by both inducers (e.g. actin, act and beta-tubulin, tub). A change in the appearance and organization of the endoplasmic reticulum (ER) was also seen in cells actively replicating PSbMV RNA. Heat treatment of pea embryonic tissues also produced altered ER, although the changes were different from those seen following Virus infection. Collectively, these data show that, while there are some common features of the responses to Virus infection and heat, there are also substantial differences. Hence, it appears that the host response to Virus Replication is not a general stress response.
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Programmed responses to Virus Replication in plants.
Molecular plant pathology, 2000Co-Authors: Andrew J. Maule, Margarita Escaler, Miguel A. ArandaAbstract:Abstract Despite their economic importance, we understand very little about the mechanism leading to symptom formation in compatible Virus infections. By applying a spatial analysis to advancing infection fronts, we have been able to relate molecular events in small groups of cells to a sequence of Virus-induced changes. This sequence starts ahead of the main front of Virus Replication and Virus protein accumulation and lasts beyond the time at which Virus Replication has ceased. The host changes include alterations in gene expression, physiology and cellular ultrastructure. The relationship between these effects has been analysed in comparative studies between different Virus infections in different hosts and abiotic stress. The research points to there being common features for different Viruses leading to common effects. Also, although many of the consequences of Virus infection are similar to the effects of heat shock, there are sufficient differences to suggest that the two inducers use distinct control pathways. The immediate challenge for the future is to establish synchronous infections of tissues so that the complex relationship between the Virus and the host can be investigated using temporal rather than spatial analyses.
L Gras - One of the best experts on this subject based on the ideXlab platform.
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Ectromelia Virus Replication in major target organs of innately resistant and susceptible mice after intravenous infection.
Archives of virology, 1993Co-Authors: D G Brownstein, P N Bhatt, L GrasAbstract:The kinetics of ectromelia Virus Replication in the spleen and liver and of alpha/beta interferon production in the spleen were determined during the first 3 days after intravenous infection with the virulent Moscow strain in resistant C57 BL/6 and susceptible DBA/2 mice. Virus Replication in the spleen as measured by assays for Virus DNA and infectious centers was suppressed in C57BL/6 mice relative to DBA/2 mice within the first 1 or 2 days of infection. Infectious centers increased in DBA/2 mice but not in C57 BL/6 mice. Differences in Virus Replication between strains were less discrete when spleens were assayed for infectious Virus than when they were assayed for infectious centers because infectious centers of most C57 BL/6 mice had more infectious Virus than infectious centers of DBA/2 mice. Virus Replication in the liver, the major target organ, as measured by Virus DNA and infectious Virus assays, was suppressed in C57 BL/6 mice relative to DBA/2 mice 3 days after infection but not before that interval. The results indicate that genetic control of ectromelia Virus Replication begins within the first 1 or 2 days of infection in the spleen but is delayed in the liver and that genetic control is directed at the prevention of Virus spread more than at Virus Replication.
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ectromelia Virus Replication in major target organs of innately resistant and susceptible mice after intravenous infection
Archives of Virology, 1993Co-Authors: D G Brownstein, P N Bhatt, L GrasAbstract:The kinetics of ectromelia Virus Replication in the spleen and liver and of α/β interferon production in the spleen were determined during the first 3 days after intravenous infection with the virulent Moscow strain in resistant C57 BL/6 and susceptible DBA/2 mice. Virus Replication in the spleen as measured by assays for Virus DNA and infectious centers was suppressed in C57 BL/6 mice relative to DBA/2 mice within the first 1 or 2 days of infection. Infectious centers increased in DBA/2 mice but not in C57 BL/6 mice. Differences in Virus Replication between strains were less discrete when spleens were assayed for infectious Virus than when they were assayed for infectious centers because infectious centers of most C57 BL/6 mice had more infectious Virus than infectious centers of DBA/2 mice. Virus Replication in the liver, the major target organ, as measured by Virus DNA and infectious Virus assays, was suppressed in C57 BL/6 mice relative to DBA/2 mice 3 days after infection but not before that interval. The results indicate that genetic control of ectromelia Virus Replication begins within the first 1 or 2 days of infection in the spleen but is delayed in the liver and that genetic control is directed at the prevention of Virus spread more than at Virus Replication.
Andrew J. Maule - One of the best experts on this subject based on the ideXlab platform.
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A comparison between Virus Replication and abiotic stress (heat) as modifiers of host gene expression in pea
Molecular plant pathology, 2000Co-Authors: Margarita Escaler, Miguel A. Aranda, I. M. Roberts, Carole L. Thomas, Andrew J. MauleAbstract:Abstract Pea embryonic tissues respond to active Replication of pea seed-borne mosaic potyVirus (PSbMV) by the down-regulation of a range of genes and the induction of others. Both of these responses can be seen when tissues are subjected to abiotic stress, particularly heat. We have compared the effects of the two inducers to assess whether the host alterations following Virus Replication represent generic responses to stress, or more specific effects. Five classes of response were identified: (i) genes induced by both stresses (e.g. heat shock protein 70, hsp70); (ii) genes induced by Virus Replication but unaffected by heat (e.g. glutathione reductase 2, gor2); (iii) genes induced by heat but unaffected by Virus Replication (e.g. heat shock factor, hsf); (iv) genes down-regulated by Virus Replication and unaffected by heat (e.g. vicilin, vic); and (v) genes unaffected by both inducers (e.g. actin, act and beta-tubulin, tub). A change in the appearance and organization of the endoplasmic reticulum (ER) was also seen in cells actively replicating PSbMV RNA. Heat treatment of pea embryonic tissues also produced altered ER, although the changes were different from those seen following Virus infection. Collectively, these data show that, while there are some common features of the responses to Virus infection and heat, there are also substantial differences. Hence, it appears that the host response to Virus Replication is not a general stress response.
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Programmed responses to Virus Replication in plants.
Molecular plant pathology, 2000Co-Authors: Andrew J. Maule, Margarita Escaler, Miguel A. ArandaAbstract:Abstract Despite their economic importance, we understand very little about the mechanism leading to symptom formation in compatible Virus infections. By applying a spatial analysis to advancing infection fronts, we have been able to relate molecular events in small groups of cells to a sequence of Virus-induced changes. This sequence starts ahead of the main front of Virus Replication and Virus protein accumulation and lasts beyond the time at which Virus Replication has ceased. The host changes include alterations in gene expression, physiology and cellular ultrastructure. The relationship between these effects has been analysed in comparative studies between different Virus infections in different hosts and abiotic stress. The research points to there being common features for different Viruses leading to common effects. Also, although many of the consequences of Virus infection are similar to the effects of heat shock, there are sufficient differences to suggest that the two inducers use distinct control pathways. The immediate challenge for the future is to establish synchronous infections of tissues so that the complex relationship between the Virus and the host can be investigated using temporal rather than spatial analyses.
John D. Morrey - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of synthetic oligonucleotides as inhibitors of West Nile Virus Replication
Antiviral Research, 2006Co-Authors: Paul F. Torrence, Nidhi Gupta, Carol Whitney, John D. MorreyAbstract:A series of synthetic oligonucleotide phosphorothioate 15-mers were generated against specific sequences in the West Nile Virus RNA genome. These antisense oligonucleotides targeted (1) conserved features of the West Nile Virus RNA genome that may be expected to lead to inhibition of Virus Replication since such features play essential roles in the Virus lifecycle; (2) G-quartet oligonucleotides with potential facilitated uptake properties and that also targeted conserved sequences among a range of West Nile Virus strains. Several formulations with significant in vitro antiviral activity were found. Among the active oligonucleotides were examples that targeted both C-rich RNA sequences of the West Nile RNA genome as well as recognized conserved sequences key to West Nile Virus Replication. Since the antiviral activity of the latter oligonucleotides diminished upon 2'-O-methyl substitution, it is likely that their activity involves RNase H-catalyzed RNA degradation. One G-rich oligonucleotide that did not target a West Nile Virus RNA sequence also was found. These results suggest the potential of antisense strategies for the control of West Nile Virus Replication if the attendant problem of oligonucleotide delivery can be adequately addressed.
Margarita Escaler - One of the best experts on this subject based on the ideXlab platform.
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A comparison between Virus Replication and abiotic stress (heat) as modifiers of host gene expression in pea
Molecular plant pathology, 2000Co-Authors: Margarita Escaler, Miguel A. Aranda, I. M. Roberts, Carole L. Thomas, Andrew J. MauleAbstract:Abstract Pea embryonic tissues respond to active Replication of pea seed-borne mosaic potyVirus (PSbMV) by the down-regulation of a range of genes and the induction of others. Both of these responses can be seen when tissues are subjected to abiotic stress, particularly heat. We have compared the effects of the two inducers to assess whether the host alterations following Virus Replication represent generic responses to stress, or more specific effects. Five classes of response were identified: (i) genes induced by both stresses (e.g. heat shock protein 70, hsp70); (ii) genes induced by Virus Replication but unaffected by heat (e.g. glutathione reductase 2, gor2); (iii) genes induced by heat but unaffected by Virus Replication (e.g. heat shock factor, hsf); (iv) genes down-regulated by Virus Replication and unaffected by heat (e.g. vicilin, vic); and (v) genes unaffected by both inducers (e.g. actin, act and beta-tubulin, tub). A change in the appearance and organization of the endoplasmic reticulum (ER) was also seen in cells actively replicating PSbMV RNA. Heat treatment of pea embryonic tissues also produced altered ER, although the changes were different from those seen following Virus infection. Collectively, these data show that, while there are some common features of the responses to Virus infection and heat, there are also substantial differences. Hence, it appears that the host response to Virus Replication is not a general stress response.
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Programmed responses to Virus Replication in plants.
Molecular plant pathology, 2000Co-Authors: Andrew J. Maule, Margarita Escaler, Miguel A. ArandaAbstract:Abstract Despite their economic importance, we understand very little about the mechanism leading to symptom formation in compatible Virus infections. By applying a spatial analysis to advancing infection fronts, we have been able to relate molecular events in small groups of cells to a sequence of Virus-induced changes. This sequence starts ahead of the main front of Virus Replication and Virus protein accumulation and lasts beyond the time at which Virus Replication has ceased. The host changes include alterations in gene expression, physiology and cellular ultrastructure. The relationship between these effects has been analysed in comparative studies between different Virus infections in different hosts and abiotic stress. The research points to there being common features for different Viruses leading to common effects. Also, although many of the consequences of Virus infection are similar to the effects of heat shock, there are sufficient differences to suggest that the two inducers use distinct control pathways. The immediate challenge for the future is to establish synchronous infections of tissues so that the complex relationship between the Virus and the host can be investigated using temporal rather than spatial analyses.
