Relevant bibliographies by topics / Defective interference particle

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Academic literature on the topic 'Defective interference particle'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Defective interference particle"

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Bhat, Tara, Amy Cao, and John Yin. "Virus-like Particles: Measures and Biological Functions." Viruses 14, no. 2 (February 14, 2022): 383. http://dx.doi.org/10.3390/v14020383.

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Virus-like particles resemble infectious virus particles in size, shape, and molecular composition; however, they fail to productively infect host cells. Historically, the presence of virus-like particles has been inferred from total particle counts by microscopy, and infectious particle counts or plaque-forming-units (PFUs) by plaque assay; the resulting ratio of particles-to-PFUs is often greater than one, easily 10 or 100, indicating that most particles are non-infectious. Despite their inability to hijack cells for their reproduction, virus-like particles and the defective genomes they carry can exhibit a broad range of behaviors: interference with normal virus growth during co-infections, cell killing, and activation or inhibition of innate immune signaling. In addition, some virus-like particles become productive as their multiplicities of infection increase, a sign of cooperation between particles. Here, we review established and emerging methods to count virus-like particles and characterize their biological functions. We take a critical look at evidence for defective interfering virus genomes in natural and clinical isolates, and we review their potential as antiviral therapeutics. In short, we highlight an urgent need to better understand how virus-like genomes and particles interact with intact functional viruses during co-infection of their hosts, and their impacts on the transmission, severity, and persistence of virus-associated diseases.
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Marcus, Philip I., John M. Ngunjiri, and Margaret J. Sekellick. "Dynamics of Biologically Active Subpopulations of Influenza Virus: Plaque-Forming, Noninfectious Cell-Killing, and Defective Interfering Particles." Journal of Virology 83, no. 16 (June 3, 2009): 8122–30. http://dx.doi.org/10.1128/jvi.02680-08.

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ABSTRACT The dynamic changes in the temporal appearance and quantity of a new class of influenza virus, noninfectious cell-killing particles (niCKP), were compared to defective interfering particles (DIP). After a single high-multiplicity passage in MDCK cells of an egg-derived stock that lacked detectable niCKP or DIP, both classes of particles appeared in large numbers (>5 × 108/ml), and the plaque-forming particle (PFP) titer dropped ∼60-fold. After two additional serial high-multiplicity passages the DIP remained relatively constant, the DIP/niCKP ratio reached 10:1, and the PFP had declined by about 10,000-fold. Together, the niCKP and DIP subpopulations constituted ca. 20% of the total hemagglutinating particle population in which these noninfectious biologically active particles (niBAP) were subsumed. DIP neither killed cells nor interfered with the cell-killing (apoptosis-inducing) activity of niCKP or PFP (infectious CKP), even though they blocked the replication of PFP. Relative to the UV-target of ∼13,600 nucleotides (nt) for inactivation of PFP, the UV target for niCKP was ∼2,400 nt, consistent with one of the polymerase subunit genes, and that for DIP was ∼350 nt, consistent with the small DI-RNA responsible for DIP-mediated interference. Thus, niCKP and DIP are viewed as distinct particles with a propensity to form during infection at high multiplicities. These conditions are postulated to cause aberrations in the temporally regulated replication of virus and its packaging, leading to the production of niBAP. DIP have been implicated in the virulence of influenza virus, but the role of niCKP is yet unknown.
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Kim, Gyoung Nyoun, and C. Yong Kang. "Utilization of Homotypic and Heterotypic Proteins of Vesicular Stomatitis Virus by Defective Interfering Particle Genomes for RNA Replication and Virion Assembly: Implications for the Mechanism of Homologous Viral Interference." Journal of Virology 79, no. 15 (August 1, 2005): 9588–96. http://dx.doi.org/10.1128/jvi.79.15.9588-9596.2005.

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ABSTRACT Defective interfering (DI) particles of Indiana serotype of vesicular stomatitis virus (VSVInd) are capable of interfering with the replication of both homotypic VSVInd and heterotypic New Jersey serotype (VSVNJ) standard virus. In contrast, DI particles from VSVNJ do not interfere with the replication of VSVInd standard virus but do interfere with VSVNJ replication. The differences in the interfering activities of VSVInd DI particles and VSVNJ DI particles against heterotypic standard virus were investigated. We examined the utilization of homotypic and heterotypic VSV proteins by DI particle genomic RNAs for replication and maturation into infectious DI particles. Here we show that the RNA-nucleocapsid protein (N) complex of one serotype does not utilize the polymerase complex (P and L) of the other serotype for RNA synthesis, while DI particle genomic RNAs of both serotypes can utilize the N, P, and L proteins of either serotype without serotypic restriction but with differing efficiencies as long as all three proteins are derived from the same serotype. The genomic RNAs of VSVInd DI particles assembled and matured into DI particles by using either homotypic or heterotypic viral proteins. In contrast, VSVNJ DI particles could assemble only with homotypic VSVNJ viral proteins, although the genomic RNAs of VSVNJ DI particles could be replicated by using heterotypic VSVInd N, P, and L proteins. Thus, we concluded that both efficient RNA replication and assembly of DI particles are required for the heterotypic interference by VSV DI particles.
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Hein, Marc D., Heike Kollmus, Pavel Marichal-Gallardo, Sebastian Püttker, Dirk Benndorf, Yvonne Genzel, Klaus Schughart, Sascha Y. Kupke, and Udo Reichl. "OP7, a novel influenza A virus defective interfering particle: production, purification, and animal experiments demonstrating antiviral potential." Applied Microbiology and Biotechnology 105, no. 1 (December 4, 2020): 129–46. http://dx.doi.org/10.1007/s00253-020-11029-5.

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Abstract The novel influenza A virus (IAV) defective interfering particle “OP7” inhibits IAV replication in a co-infection and was previously suggested as a promising antiviral agent. Here, we report a batch-mode cell culture-based production process for OP7. In the present study, a seed virus containing standard virus (STV) and OP7 was used. The yield of OP7 strongly depended on the production multiplicity of infection. To inactivate infectious STV in the OP7 material, which may cause harm in a potential application, UV irradiation was used. The efficacy of OP7 in this material was preserved, as shown by an in vitro interference assay. Next, steric exclusion chromatography was used to purify and to concentrate (~ 13-fold) the UV-treated material. Finally, administration of produced OP7 material in mice did not show any toxic effects. Furthermore, all mice infected with a lethal dose of IAV survived the infection upon OP7 co-treatment. Thus, the feasibility of a production workflow for OP7 and its potential for antiviral treatment was demonstrated. Key points • OP7 efficacy strongly depended on the multiplicity of infection used for production • Purification by steric exclusion chromatography increased OP7 efficacy • OP7-treated mice were protected against a lethal infection with IAV
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Giachetti, C., and J. J. Holland. "Altered replicase specificity is responsible for resistance to defective interfering particle interference of an Sdi- mutant of vesicular stomatitis virus." Journal of Virology 62, no. 10 (1988): 3614–21. http://dx.doi.org/10.1128/jvi.62.10.3614-3621.1988.

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Poirier, Enzo Z., Bryan C. Mounce, Kathryn Rozen-Gagnon, Peter Jan Hooikaas, Kenneth A. Stapleford, Gonzalo Moratorio, and Marco Vignuzzi. "Low-Fidelity Polymerases of Alphaviruses Recombine at Higher Rates To Overproduce Defective Interfering Particles." Journal of Virology 90, no. 5 (December 16, 2015): 2446–54. http://dx.doi.org/10.1128/jvi.02921-15.

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ABSTRACTLow-fidelity RNA-dependent RNA polymerases for many RNA virus mutators have been shown to confer attenuated phenotypes, presumably due to increased mutation rates. Additionally, for many RNA viruses, replication to high titers results in the production of defective interfering particles (DIs) that also attenuate infection. We hypothesized that fidelity, recombination, and DI production are tightly linked. We show that a Sindbis virus mutator replicating at a high multiplicity of infection manifests an earlier and greater accumulation of DIs than its wild-type counterpart. The isolated DIs interfere with the replication of full-length virus in a dose-dependent manner. Importantly, the ability of the mutator virus to overproduce DIs could be linked to an increased recombination frequency. These data confirm that RNA-dependent RNA polymerase fidelity and recombination are inversely correlated for this mutator. Our findings suggest that defective interference resulting from higher recombination rates may be more detrimental to RNA virus mutators than the increase in mutational burden.IMPORTANCEReplication, adaptation, and evolution of RNA viruses rely in large part on their low-fidelity RNA-dependent RNA polymerase. Viruses artificially modified in their polymerases to decrease fidelity (mutator viruses) are attenuatedin vivo, demonstrating the important role of fidelity in viral fitness. However, attenuation was attributed solely to the modification of the viral mutation rate and the accumulation of detrimental point mutations. In this work, we described an additional phenotype of mutator viruses: an increased recombination rate leading to defective interfering particle (DI) overproduction. Because DIs are known for their inhibitory effect on viral replication, our work suggests that fidelity variants may be attenuatedin vivovia several mechanisms. This has important implications in the development of fidelity variants as live attenuated vaccine strains.
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Mao, Yuntao S., Masaki Yamaga, Xiaohui Zhu, Yongjie Wei, Hui-Qiao Sun, Jing Wang, Mia Yun, et al. "Essential and unique roles of PIP5K-γ and -α in Fcγ receptor-mediated phagocytosis." Journal of Cell Biology 184, no. 2 (January 19, 2009): 281–96. http://dx.doi.org/10.1083/jcb.200806121.

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The actin cytoskeleton is dynamically remodeled during Fcγ receptor (FcγR)-mediated phagocytosis in a phosphatidylinositol (4,5)-bisphosphate (PIP2)-dependent manner. We investigated the role of type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) γ and α isoforms, which synthesize PIP2, during phagocytosis. PIP5K-γ−/− bone marrow–derived macrophages (BMM) have a highly polymerized actin cytoskeleton and are defective in attachment to IgG-opsonized particles and FcγR clustering. Delivery of exogenous PIP2 rescued these defects. PIP5K-γ knockout BMM also have more RhoA and less Rac1 activation, and pharmacological manipulations establish that they contribute to the abnormal phenotype. Likewise, depletion of PIP5K-γ by RNA interference inhibits particle attachment. In contrast, PIP5K-α knockout or silencing has no effect on attachment but inhibits ingestion by decreasing Wiskott-Aldrich syndrome protein activation, and hence actin polymerization, in the nascent phagocytic cup. In addition, PIP5K-γ but not PIP5K-α is transiently activated by spleen tyrosine kinase–mediated phosphorylation. We propose that PIP5K-γ acts upstream of Rac/Rho and that the differential regulation of PIP5K-γ and -α allows them to work in tandem to modulate the actin cytoskeleton during the attachment and ingestion phases of phagocytosis.
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Ou, Yangli, Shuilong He, Chaofan Hu, Jiading Bao, and Wenjie Li. "Research on Rolling Bearing Fault Diagnosis Using Improved Majorization-Minimization-Based Total Variation and Empirical Wavelet Transform." Shock and Vibration 2020 (May 15, 2020): 1–11. http://dx.doi.org/10.1155/2020/3218564.

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Bearings are among the most widely used core components in mechanical equipment. Their failure creates the potential for serious accidents and economic losses. Vibration signature analyses are the most common approach to assess the viability of bearings due to its ease of measurement and high correlation with structural dynamics. However, the collected vibration signals of rolling bearings are usually nonstationary and are inevitably accompanied by noise interference. This makes it difficult to extract the feature frequency for the failed bearing and affects the diagnosis accuracy. The majorization-minimization-based total variation (TV-MM) denoising algorithm effectively removes the noise interference from the signal and highlights the related feature information. The value of its main parameter λ determines the quality of the denoising effect. However, manually selecting parameters requires professional experience in a process that it is time-consuming and laborious, while the use of genetic algorithms is cumbersome. Therefore, an improved particle swarm algorithm (IPSO) is used to find the optimal solution of λ. The IPSO utilises the mutation concept in genetic algorithms to reinitialise the particles with a certain probability after each update. In addition, the empirical wavelet transform (EWT) is an adaptive signal processing method suitable for processing nonlinear and nonstationary signals. Therefore, this paper presents an ensemble analysis method that combines the IPSO, TV-MM, and EWT. First, IPSO is used to optimise the denoising parameter λ. The TV-MM under this parameter effectively removes the background noise interference and improves the accuracy of the subsequent modal decomposition. Then, the EWT is used for the adaptive division to produce a set of sequences. Finally, Hilbert envelope demodulation is performed on each component to realise fault diagnosis. The results from simulations and signals received from defective bearings with outer race fault, inner race fault, and rolling element fault demonstrate the effectiveness of the proposed method for fault diagnosis of rolling bearings.
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Rossi, Marika, Marta Vallino, Simona Abbà, Marina Ciuffo, Raffaella Balestrini, Andrea Genre, and Massimo Turina. "The Importance of the KR-Rich Region of the Coat Protein of Ourmia melon virus for Host Specificity, Tissue Tropism, and Interference With Antiviral Defense." Molecular Plant-Microbe Interactions® 28, no. 1 (January 2015): 30–41. http://dx.doi.org/10.1094/mpmi-07-14-0197-r.

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The N-terminal region of the Ourmia melon virus (OuMV) coat protein (CP) contains a short lysine/arginine-rich (KR) region. By alanine scanning mutagenesis, we showed that the KR region influences pathogenicity and virulence of OuMV without altering viral particle assembly. A mutant, called OuMV6710, with three basic residue substitutions in the KR region, was impaired in the ability to maintain the initial systemic infection in Nicotiana benthamiana and to infect both cucumber and melon plants systemically. The integrity of this protein region was also crucial for encapsidation of viral genomic RNA; in fact, certain mutations within the KR region partially compromised the RNA encapsidation efficiency of the CP. In Arabidopsis thaliana Col-0, OuMV6710 was impaired in particle accumulation; however, this phenotype was abolished in dcl2/dcl4 and dcl2/dcl3/dcl4 Arabidopsis mutants defective for antiviral silencing. Moreover, in contrast to CPwt, in situ immunolocalization experiments indicated that CP6710 accumulates efficiently in the spongy mesophyll tissue of infected N. benthamiana and A. thaliana leaves but only occasionally infects palisade tissues. These results provided strong evidence of a crucial role for OuMV CP during viral infection and highlighted the relevance of the KR region in determining tissue tropism, host range, pathogenicity, and RNA affinity, which may be all correlated with a possible CP silencing-suppression activity.
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Bauerová, Petra, Adriana Šindelářová, Štěpán Rychlík, Zbyněk Novák, and Josef Keder. "Low-Cost Air Quality Sensors: One-Year Field Comparative Measurement of Different Gas Sensors and Particle Counters with Reference Monitors at Tušimice Observatory." Atmosphere 11, no. 5 (May 11, 2020): 492. http://dx.doi.org/10.3390/atmos11050492.

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With attention increasing regarding the level of air pollution in different metropolitan and industrial areas worldwide, interest in expanding the monitoring networks by low-cost air quality sensors is also increasing. Although the role of these small and affordable sensors is rather supplementary, determination of the measurement uncertainty is one of the main questions of their applicability because there is no certificate for quality assurance of these non-reference technologies. This paper presents the results of almost one-year field testing measurements, when the data from different low-cost sensors (for SO2, NO2, O3, and CO: Cairclip, Envea, FR; for PM1, PM2.5, and PM10: PMS7003, Plantower, CHN, and OPC-N2, Alphasense, UK) were compared with co-located reference monitors used within the Czech national ambient air quality monitoring network. The results showed that in addition to the given reduced measurement accuracy of the sensors, the data quality depends on the early detection of defective units and changes caused by the effect of meteorological conditions (effect of air temperature and humidity on gas sensors and effect of air humidity with condensation conditions on particle counters), or by the interference of different pollutants (especially in gas sensors). Comparative measurement is necessary prior to each sensor’s field applications.
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Dissertations / Theses on the topic "Defective interference particle"

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Rud, Erling William. "Defective interfering particles and viral interference: A model for the mechanism of heterotypic interference." Thesis, University of Ottawa (Canada), 1989. http://hdl.handle.net/10393/5869.

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BIANCO, ANNALISA. "Virus-host interactions in hepatitis C virus infection: implications for pathogenesis and therapy." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29914.

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Virus-host interactions are crucial for the pathogenesis of Hepatitis C. Disease progression and response to therapy depends from viral and host factors and from their mutual interactions. The study of host and viral factors is also of primary importance for the development of new antiviral therapies. The goal of this work was to investigate some of the most relevant viral and host factors in order to improve their knowledge and the possibility to translate this knowledge to a useful clinical application. CHAPTER 2: Metabolism of Phosphatidylinositol 4-Kinase IIIα-Dependent PI4P is Subverted by HCV and Is Targeted by a 4-Amino Quinazoline with Antiviral Activity The enzymatic activity of PI4KIIIα is required for efficient HCV RNA Replication and the direct activation of this lipid kinase by HCV is critical for the integrity of the viral replication complex. Since we demonstrated that the anti-HCV compound AL-9 is an inhibitor of PI4KIIIα, this kinase is a suitable antiviral target for the treatment of HCV. CHAPTERS 3-4: Unraveling host responses to the emergence of hepatitis C virus particles with defective RNA genomes HCV particles with defective RNA genomes have been recently identified in the serum of some patients with chronic HCV infection and represent a significant proportion of viral load. In order to investigate whether HCV defective genomes could play a role in any of the hepatic disease manifestations associated with chronic HCV infection, or affect response to antiviral therapy, we adopted a two-fold ex vivo/in vitro approach. On one hand, we performed a retrospective screening campaign aiming at assessing the presence of defective genomes in the serum of HCV-infected individuals stratified according to disease severity as well as response to PEG-IFNα/RBV combination therapy (CHAPTER 3). On another hand, we studied the direct role of defective HCV genomes in hepatocyte injury using an infectivity model system in vitro (CHAPTER 4).
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Tuffereau, Marie-Christine. "Infections persistantes in vitro par le virus sendai : etablissement de l'infection par un melange de particules standart et defectives interferentes sur cellules bhk21." Paris 7, 1987. http://www.theses.fr/1987PA077245.

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Pál, Karina Alexandra. "Intracellular Stochastic Modelling of Influenza A Virus and DIP Replication." Master's thesis, 2018. http://hdl.handle.net/10362/65246.

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Defective interfering particles (DIPs) are mutated versions of viruses that are characterized by carrying internal deletions in their genome. These deletions are introduced randomly during virus replication and the truncated genomes interfere with the propagation of their standard virus (STV) leading to reduced infectious virus titers. Therefore, DIPs were recently proposed to be used for antiviral therapy which increased the demand for a reliable production process and a better understanding of the interference mechanism. The infection dynamics were analysed by a deterministic modelling approach, however, the impact of stochastic effects introduced by cell-to-cell variability, different coinfection scenarios and an independent genome segment replication remain largely elusive. Hence, we developed a stochastic model of influenza A virus and DIP replication which considers the influence of these random effects on STV and DIP release. We found that the viral nucleoprotein (NP), which is essential for encapsidation of the naked viral RNA (vRNA), is strongly affected by fluctuations and three distinct sub-populations emerged in our model. Furthermore, simulations performed with one DIP and one STV infecting the cell resulted in mostly non-productive simulations, mainly caused by failures during the endocytosis of particles and by the random degradation of vRNAs. Moreover, the optimal DIP production was achieved when STV enters nucleus first and the DIP entry is delayed between 1.5 and 3 hours. Lastly, we demonstrate that the implementation of a two-step packaging process, which separates the formation of genome complexes and the assembly of all required proteins for release, is crucial to achieve a substantial DIP advantage over STV production. Overall, our simulations suggest that a combination of various random effects influences the replication of STVs and DIPs inducing a broad distribution of progeny particle release. The stochastic model developed in this thesis provides an ideal basis for the analysis of these effects and their impact on DIP interference and production.
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LIN, MAO-XIANG, and 林茂香. "Viral interference and defective interfering particles of infections pancreatic necrosis virus HB-1 isolate from clam meretrix iusoria." Thesis, 1987. http://ndltd.ncl.edu.tw/handle/13692382735402652981.

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碩士
輔仁大學
生物學研究所
75
IPN 病毒類，HB-1文蛤病毒分離株在高濃度下經4 個月繼代培養，發現病毒效價有波 動情形，其波動度高於以低濃度感染之病毒，因其教價會降低，且皆低於以低濃度接 種之繼代病毒，顯示有病毒干擾現象。取經40代高濃度繼代之高毒與正常低濃度感染 之病毒，於同時間內分別純化，取得多DI病毒及多正常病毒之收集管。將兩者之收隻 管加以分析，多DI管感染效價最高在第7 收集管，干擾效價最高在第9 收集管，正常 病毒之感染效價最高在第7 收集管，且其所有收集管均測不到干擾現象，觀測其蛋白 質電泳分析圖譜，發現兩者之α、β蛋白質群有差異，γ蛋白質群則其相同分子量之 蛋白質，多成熟DI管之α蛋白質分子量分別為94Kd ，105Kd，成熟正常病毒為94Kd， 多成熟DI管之β蛋白質分子量分別為50Kd ，51Kd，成熟正常病毒為52.3Kd ，推測分 子量50Kd及105Kd 者為成熟DI特有之蛋白質，應和干擾現象有關。至於以10％聚烯醯 胺分析基因組核酸，發現多正常病毒僅有兩條核酸片段，而多DI病毒核酸則有三條， 若多正常病毒與多DI病毒核酸混合後，亦只有三條核酸片段。根據結果分析該異常RN A 分子應為DI粒子RNA 的大片段。所以IPN 病毒HB-1分離株之DI粒子為核酸缺失性突 變種（deletion mutant ）。
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Arora, Prerna. "Novel production system for influenza A virus-derived defective interfering particles and analysis of antiviral activity." Doctoral thesis, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-148F-4.

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Book chapters on the topic "Defective interference particle"

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Kang, A. Yong. "Interference Induced by Defective Interfering Particles." In Rhabdoviruses, 201–19. CRC Press, 2018. http://dx.doi.org/10.1201/9781351076395-12.

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Faulkner, G. P., and Robert A. Lazzarini. "Homologous Interference by Defective Virus Particles." In Rhabdoviruses, 163–76. CRC Press, 2018. http://dx.doi.org/10.1201/9781351076395-9.

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