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Relevant bibliographies by topics / Flock house virus

Academic literature on the topic 'Flock house virus'

Author: Grafiati

Published: 6 September 2023

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Dissertations / Theses
Book chapters
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Journal articles on the topic "Flock house virus"

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Fisher, A. J., B. R. McKinney, J. P. Wery, and J. E. Johnson. "Crystallization and preliminary data analysis of flock house virus." Acta Crystallographica Section B Structural Science 48, no. 4 (August 1, 1992): 515–20. http://dx.doi.org/10.1107/s0108768192000053.

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A. McCormick, Alison, Payal D. Maharaj, Jyothi K. Mallajosyula, Philip Thi, Gloria Lee, Yiyang Zhou, and Christopher Kearney. "Trans-Encapsidation of Flock House virus with Tobacco Mosaic virus Structural Proteins." Journal of Advanced Biotechnology and Bioengineering 2, no. 2 (November 2014): 49–59. http://dx.doi.org/10.12970/2311-1755.2014.02.02.2.

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Johnson, Kyle L., and L. Andrew Ball. "Induction and Maintenance of Autonomous Flock House Virus RNA1 Replication." Journal of Virology 73, no. 10 (1999): 7933–42. http://dx.doi.org/10.1128/jvi.73.10.7933-7942.1999.

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The nodavirus flock house virus (FHV) has a bipartite, positive-sense, RNA genome that encodes the catalytic subunit of the RNA replicase and the viral capsid protein precursor on separate genomic segments (RNA1 and RNA2, respectively). RNA1 can replicate autonomously when transfected into permissive cells, allowing study of the kinetics of RNA1 replication in the absence of either RNA2 or capsid proteins. However, RNA1 replication ceases ca. 3 days after transfection despite the presence of replication-competent RNA. We examined this inhibition by inducing the expression of RNA1 in cells from a cDNA copy that was under the control of a hormone-regulated RNA polymerase II promoter. This system reproduced the shutoff of RNA replication when DNA-templated primary transcription was turned off. Continued primary transcription partially alleviated the shutoff and maintained the rate of RNA replication for several days at a steady-state level approximately one-third that of the peak rate. After shutoff, RNA replication could be restored by transferring the resulting intracellular RNA to fresh cells or by reinducing primary transcription, indicating that cessation of replication occurred despite the competence of both the viral RNA and the cytoplasmic environment. These data suggest that there is a mechanism by which replication is shut off at late times after transfection, which may reflect the natural endpoint of the replicative cycle.

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Short, James R., Jeffrey A. Speir, Radhika Gopal, Logan M. Pankratz, Jason Lanman, and Anette Schneemann. "Role of Mitochondrial Membrane Spherules in Flock House Virus Replication." Journal of Virology 90, no. 7 (January 20, 2016): 3676–83. http://dx.doi.org/10.1128/jvi.03080-15.

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ABSTRACTViruses that generate double-stranded RNA (dsRNA) during replication must overcome host defense systems designed to detect this infection intermediate. All positive-sense RNA viruses studied to date modify host membranes to help facilitate the sequestration of dsRNA from host defenses and concentrate replication factors to enhance RNA production. Flock House virus (FHV) is an attractive model for the study of these processes since it is well characterized and infectsDrosophilacells, which are known to have a highly effective RNA silencing system. During infection, FHV modifies the outer membrane of host mitochondria to form numerous membrane invaginations, called spherules, that are ∼50 nm in diameter and known to be the site of viral RNA replication. While previous studies have outlined basic structural features of these invaginations, very little is known about the mechanism underlying their formation. Here we describe the optimization of an experimental system for the analysis of FHV host membrane modifications using crude mitochondrial preparations from infectedDrosophilacells. These preparations can be programmed to synthesize both single- and double-stranded FHV RNA. The system was used to demonstrate that dsRNA is protected from nuclease digestion by virus-induced membrane invaginations and that spherules play an important role in stimulating RNA replication. Finally, we show that spherules generated during FHV infection appear to be dynamic as evidenced by their ability to form or disperse based on the presence or absence of RNA synthesis.IMPORTANCEIt is well established that positive-sense RNA viruses induce significant membrane rearrangements in infected cells. However, the molecular mechanisms underlying these rearrangements, particularly membrane invagination and spherule formation, remain essentially unknown. How the formation of spherules enhances viral RNA synthesis is also not understood, although it is assumed to be partly a result of evading host defense pathways. To help interrogate some of these issues, we optimized a cell-free replication system consisting of mitochondria isolated from Flock House virus-infectedDrosophilacells for use in biochemical and structural studies. Our data suggest that spherules generated during Flock House virus replication are dynamic, protect double-stranded RNA, and enhance RNA replication in general. Cryo-electron microscopy suggests that the samples are amenable to detailed structural analyses of spherules engaged in RNA synthesis. This system thus provides a foundation for understanding the molecular mechanisms underlying spherule formation, maintenance, and function during positive-sense viral RNA replication.

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Thomson, Travis C., and Joshua Johnson. "Infection with Flock House Virus Induces Oocyte Destruction in Drosophila." Biology of Reproduction 83, Suppl_1 (November 1, 2010): 662. http://dx.doi.org/10.1093/biolreprod/83.s1.662.

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Bong, Dennis T., Andreas Janshoff, Claudia Steinem, and M. Reza Ghadiri. "Membrane Partitioning of the Cleavage Peptide in Flock House Virus." Biophysical Journal 78, no. 2 (February 2000): 839–45. http://dx.doi.org/10.1016/s0006-3495(00)76641-0.

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Hiscox, J. A., and L. A. Ball. "Cotranslational disassembly of flock house virus in a cell-free system." Journal of virology 71, no. 10 (1997): 7974–77. http://dx.doi.org/10.1128/jvi.71.10.7974-7977.1997.

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Jovel, Juan, and Anette Schneemann. "Molecular characterization of Drosophila cells persistently infected with Flock House virus." Virology 419, no. 1 (October 2011): 43–53. http://dx.doi.org/10.1016/j.virol.2011.08.002.

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Dasgupta, Ranjit, Li-Lin Cheng, Lyric C. Bartholomay, and Bruce M. Christensen. "Flock house virus replicates and expresses green fluorescent protein in mosquitoes." Journal of General Virology 84, no. 7 (July 1, 2003): 1789–97. http://dx.doi.org/10.1099/vir.0.18938-0.

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McMenamin, Alexander J., Fenali Parekh, Verena Lawrence, and Michelle L. Flenniken. "Investigating Virus–Host Interactions in Cultured Primary Honey Bee Cells." Insects 12, no. 7 (July 17, 2021): 653. http://dx.doi.org/10.3390/insects12070653.

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Honey bee (Apis mellifera) health is impacted by viral infections at the colony, individual bee, and cellular levels. To investigate honey bee antiviral defense mechanisms at the cellular level we further developed the use of cultured primary cells, derived from either larvae or pupae, and demonstrated that these cells could be infected with a panel of viruses, including common honey bee infecting viruses (i.e., sacbrood virus (SBV) and deformed wing virus (DWV)) and an insect model virus, Flock House virus (FHV). Virus abundances were quantified over the course of infection. The production of infectious virions in cultured honey bee pupal cells was demonstrated by determining that naïve cells became infected after the transfer of deformed wing virus or Flock House virus from infected cell cultures. Initial characterization of the honey bee antiviral immune responses at the cellular level indicated that there were virus-specific responses, which included increased expression of bee antiviral protein-1 (GenBank: MF116383) in SBV-infected pupal cells and increased expression of argonaute-2 and dicer-like in FHV-infected hemocytes and pupal cells. Additional studies are required to further elucidate virus-specific honey bee antiviral defense mechanisms. The continued use of cultured primary honey bee cells for studies that involve multiple viruses will address this knowledge gap.

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Dissertations / Theses on the topic "Flock house virus"

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Bajaj, Saumya. "Studies on membrane penetration and heterologous packaging ability of a non-enveloped insect virus, flock house virus." Thesis, IIT Delhi, 2017. http://localhost:8080/xmlui/handle/12345678/7238.

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Walukiewicz, Hanna Ewa. "Structural and functional studies of the Flock House virus cell entry mechanism /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3177888.

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Zhong, Weidong. "Flock house virus, a small insect ribovirus replication and encapsidation of RNA2 /." 1993. http://catalog.hathitrust.org/api/volumes/oclc/31251192.html.

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Kopek, Benjamin G. "Structure, organization, and formation of the flock house virus RNA replication complex." 2008. http://www.library.wisc.edu/databases/connect/dissertations.html.

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Schneemann, Anette. "Studies on assembly and maturation of Flock House virus, a small insect ribovirus." 1992. http://catalog.hathitrust.org/api/volumes/oclc/28757797.html.

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Thesis (Ph. D.)--University of Wisconsin--Madison, 1992.
Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 160-164).

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Settles, Erik W. "Flock house virus induces replication-dependent apoptosis by depleting the Drosophila inhibitor-of-apoptosis protein, DIAP1 /." 2008. http://www.library.wisc.edu/databases/connect/dissertations.html.

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Book chapters on the topic "Flock house virus"

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Odegard, Amy, Manidipa Banerjee, and John E. Johnson. "Flock House Virus: A Model System for Understanding Non-Enveloped Virus Entry and Membrane Penetration." In Current Topics in Microbiology and Immunology, 1–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_35.

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Dasgupta, R., B. Selling, and R. Rueckert. "Flock house virus: a simple model for studying persistent infection in cultured Drosophila cells." In Positive-Strand RNA Viruses, 121–32. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9326-6_13.

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Reports on the topic "Flock house virus"

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Malkinson, Mertyn, Irit Davidson, Moshe Kotler, and Richard L. Witter. Epidemiology of Avian Leukosis Virus-subtype J Infection in Broiler Breeder Flocks of Poultry and its Eradication from Pedigree Breeding Stock. United States Department of Agriculture, March 2003. http://dx.doi.org/10.32747/2003.7586459.bard.

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Objectives 1. Establish diagnostic procedures to identify tolerant carrier birds based on a) Isolation of ALV-J from blood, b) Detection of group-specific antigen in cloacal swabs and egg albumen. Application of these procedures to broiler breeder flocks with the purpose of removing virus positive birds from the breeding program. 2. Survey the AL V-J infection status of foundation lines to estimate the feasibility of the eradication program 3. Investigate virus transmission through the embryonated egg (vertical) and between chicks in the early post-hatch period (horizontal). Establish a model for limiting horizontal spread by analyzing parameters operative in the hatchery and brooder house. 4. Compare the pathogenicity of AL V-J isolates for broiler chickens. 5. Determine whether AL V-J poses a human health hazard by examining its replication in mammalian and human cells. Revisions. The: eradication objective had to be terminated in the second year following the closing down of the Poultry Breeders Union (PBU) in Israel. This meant that their foundation flocks ceased to be available for selection. Instead, the following topics were investigated: a) Comparison of commercial breeding flocks with and without myeloid leukosis (matched controls) for viremia and serum antibody levels. b) Pathogenicity of Israeli isolates for turkey poults. c) Improvement of a diagnostic ELISA kit for measuring ALV-J antibodies Background. ALV-J, a novel subgroup of the avian leukosis virus family, was first isolated in 1988 from broiler breeders presenting myeloid leukosis (ML). The extent of its spread among commercial breeding flocks was not appreciated until the disease appeared in the USA in 1994 when it affected several major breeding companies almost simultaneously. In Israel, ML was diagnosed in 1996 and was traced to grandparent flocks imported in 1994-5, and by 1997-8, ML was present in one third of the commercial breeding flocks It was then realized that ALV-J transmission was following a similar pattern to that of other exogenous ALVs but because of its unusual genetic composition, the virus was able to establish an extended tolerant state in infected birds. Although losses from ML in affected flocks were somewhat higher than normal, both immunosuppression and depressed growth rates were encountered in affected broiler flocks and affected their profitability. Conclusions. As a result of the contraction in the number of international primary broiler breeders and exchange of male and female lines among them, ALV-J contamination of broiler breeder flocks affected the broiler industry worldwide within a short time span. The Israeli national breeding company (PBU) played out this scenario and presented us with an opportunity to apply existing information to contain the virus. This BARD project, based on the Israeli experience and with the aid of the ADOL collaborative effort, has managed to offer solutions for identifying and eliminating infected birds based on exhaustive virological and serological tests. The analysis of factors that determine the efficiency of horizontal transmission of virus in the hatchery resulted in the workable solution of raising young chicks in small groups through the brooder period. These results were made available to primary breeders as a strategy for reducing viral transmission. Based on phylogenetic analysis of selected Israeli ALV-J isolates, these could be divided into two groups that reflected the countries of origin of the grandparent stock. Implications. The availability of a simple and reliable means of screening day old chicks for vertical transmission is highly desirable in countries that rely on imported breeding stock for their broiler industry. The possibility that AL V-J may be transmitted to human consumers of broiler meat was discounted experimentally.

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