Academic literature on the topic 'Antiviral immunity'

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Journal articles on the topic "Antiviral immunity"

1

Alderton, Gemma. "Antiviral immunity." Science 371, no. 6528 (2021): 477.10–479. http://dx.doi.org/10.1126/science.371.6528.477-j.

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Maria Navarro, Jose, and Mercedes Perez-Ruiz. "Antiviral Immunity." Current Immunology Reviews 7, no. 1 (2011): 19–24. http://dx.doi.org/10.2174/157339511794474244.

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Zinkernagel, Rolf, and Hans Hengartner. "Antiviral immunity." Immunology Today 18, no. 6 (1997): 258–60. http://dx.doi.org/10.1016/s0167-5699(97)80017-5.

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M, Yamashita, Millward CA, Inoshita H, et al. "Antiviral innate immunity disturbs podocyte cell function." Nihon Shoni Jinzobyo Gakkai Zasshi 28, no. 1 (2015): 81–82. http://dx.doi.org/10.3165/jjpn.28.81.

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Yan, Nan, and Zhijian J. Chen. "Intrinsic antiviral immunity." Nature Immunology 13, no. 3 (2012): 214–22. http://dx.doi.org/10.1038/ni.2229.

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Hope, Jennifer L., and Linda M. Bradley. "Lessons in antiviral immunity." Science 371, no. 6528 (2021): 464–65. http://dx.doi.org/10.1126/science.abf6446.

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Chen, Guangchun, and Jacques Robert. "Antiviral Immunity in Amphibians." Viruses 3, no. 11 (2011): 2065–86. http://dx.doi.org/10.3390/v3112065.

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De Clercq, Erik. "Antiviral agents and immunity." Clinical Immunology Newsletter 6, no. 7 (1985): 103–7. http://dx.doi.org/10.1016/s0197-1859(85)80043-1.

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Lee, Heung Kyu, and Akiko Iwasaki. "Autophagy and antiviral immunity." Current Opinion in Immunology 20, no. 1 (2008): 23–29. http://dx.doi.org/10.1016/j.coi.2008.01.001.

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Kemp, Cordula, and Jean-Luc Imler. "Antiviral immunity in drosophila." Current Opinion in Immunology 21, no. 1 (2009): 3–9. http://dx.doi.org/10.1016/j.coi.2009.01.007.

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Dissertations / Theses on the topic "Antiviral immunity"

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Arnaout, Ramy A. "Mathematical models of antiviral immunity." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325989.

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Palmer, William Hunt. "Evolution and genetics of antiviral immunity in Drosophila." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31557.

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Virus-host interactions determine virus transmissibility and virulence, and underlie coevolution that shapes interesting biological phenomena such as the genetic architecture of host resistance and host range. Characterization of the virus factors that exert selective pressure on the host, and the host genes which underlie resistance and adaptation against viruses will help to define the mechanistic pathways embroiled in host-virus coevolution. In this thesis, I describe the viral causes and host consequences of host-virus coevolution. These include genomic signatures consistent with antagonistic coevolution in antiviral RNA interference pathway genes such as high rates of positive selection and polymorphism, loci that underlie genetic variation in resistance to virus infection, and apparent conflict between NF-κB signalling and DNA virus infection. The RNA interference (RNAi) pathway is the most general innate immune pathway in insects, underlined by the observation that many viruses encode suppressors of RNAi (VSRs). The relationship between RNAi and VSRs has garnered attention as a plausible battleground for host-virus antagonistic coevolution, and genomic patterns in Drosophila support this hypothesis. However, genomic patterns in the N-terminal domain of the key RNAi effector gene, Argonaute-2, have not been described. In Chapter 2, I sequence the Argonaute-2 N-terminal domain using PacBio long-read sequencing technology to describe variation within and across Drosophila species, and test whether this variation is associated with resistance to Drosophila C Virus. The RNAi pathway evolves adaptively in Drosophila, but this has not been formally extended across invertebrate species. In Chapter 3, I quantify rates of adaptive protein evolution and describe evidence for selective sweeps in RNAi pathway genes using population genomic data from 8 insect and nematode species. These analyses indicate that RNAi genes involved in suppression of transposable elements and defence against viruses evolve rapidly across invertebrates, and I identify genes with signatures of elevated adaptation in multiple insect species. Host genes that underlie host-virus interactions have been described in RNA virus infection of Drosophila, however substantially less attention has focussed on the host response to DNA viruses, primarily because no DNA viruses have been isolated from Drosophila. In Chapter 4, I describe the isolation of Kallithea virus, a Drosophila dsDNA nudivirus, and characterise the host response to infection and genetic variation in resistance. I find that Kallithea virus infection causes early male-specific lethality, a cessation of oogenesis, and induction of undescribed virus-responsive genes. Further, I describe genetic variation in resistance and tolerance to Kallithea virus infection, and identify a potential causal variant for virus-induced mortality in Cip4. Insect viruses commonly encode viral suppressors of RNAi, however there are a multitude of antiviral immune mechanisms besides RNAi which may select for viral-encoded inhibitors. In Chapter 5, I describe the requirement for RNAi and NF-κB in immunity against Kallithea virus, and map gp83 as a virus-encoded inhibitor of NF-κB signalling. I find that gp83 inhibits Toll signalling at the level of, or downstream of NF-κB transcription factors, and that this immunosuppressive function is conserved in other nudiviruses.
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Carissimo, Guillaume. "Caractérisation et rôle de l'immunité antivirale des anophèles dans la compétence vectorielle pour les arbovirus et parasites." Electronic Thesis or Diss., Paris 6, 2014. http://www.theses.fr/2014PA066293.

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Dans une ère où les moustiques modifiés commencent à être utilisés ou envisagés pour contrôler les épidémies de Dengue ou malaria, le manque de connaissance sur l’immunité des insectes vecteurs envers certains pathogènes se fait cruellement ressentir. Pourtant la possibilité de changements de vecteurs, dû à un changement de leur immunité, provoquée par l’Homme est réelle. Pour déterminer la contribution de l’immunité dans différents compartiments du vecteur contre divers pathogènes avons étudié la réponse antivirale dans la première barrière de transmission chez le moustique vecteur de la malaria après une infection par un repas sanguin. Nous montrons que les réponses antivirales sont différentes entre compartiments, et proposons un modèle où des interactions tripartites entre le virus, l’immunité du moustique et la flore entérique interagissent pour contrôler l’infection précoce du moustique après le repas sanguin. De façon surprenante, nous avons également montré que la voie de l’ARN interférence n’a pas d’effet antiviral dans ce compartiment. Nous suggérons que cette voie est utilisée par le parasite Plasmodium pour détourner la réponse antiparasitaire médiée par Toll, grâce à un facteur de virulence de nature ARN double brin. Nous avons également montré que des biais expérimentaux lors de l’infection des insectes ont conduit à l’élaboration d’un dogme disant que la voie de l’ARN interférence est la voie antivirale principale des insectes, mais nos resultats suggèrent que malgré l’importance de cette voie pour controler l’intensité de la réplication virale lors de l’infection disséminée, cette voie n’a aucune fonction antivirale lors de l’infection initiale du tube digestif. Néanmoins, le séquençage des produits de cette voie permet d’assembler de-novo des génomes de virus commensaux. Les résultats de ces travaux montrent très clairement qu’il faut évaluer le rôle et l’impact de toute modification d’insectes vecteurs pour plusieurs classes de pathogènes. Cela ouvre également de nombreux nouveaux champs de recherches et pose de nombreuses nouvelles questions<br>In an era where modified mosquitoes are starting to be used in nature for controlling malaria and Dengue, lack of knowledge about immunity of mosquito vectors to some pathogen classes are becoming more evident. The risks for human-provoked vector shifts of pathogens transmission have not been examined. To fill these gaps, we assessed the antiviral immunity of the malaria vector, Anopheles gambiae, in the strongest mosquito bottleneck for pathogens, the midgut infection barrier after an infective bloodmeal. This work shows that the antiviral responses are different and highly compartmentalized between the midgut and systemic immunity. We propose a model where tripartite interactions between virus, mosquito immunity and enteric flora control early arboviral infection in the midgut. Surprisingly, we showed that while the siRNA pathway had no evident anti-arbovirus activity in the midgut, it was used by Plasmodium to evade mosquito immunity. A virus-like elicitor of double strand RNA nature is transferred from the parasite at the ookinete stage to the mosquito midgut cells, resulting in a shift of immune balance from anti-parasite response to an antiviral-like response. Importantly, our work shows that biases in experimental infection methods led to the misconstruction of a dogma stating that siRNA is the main antiviral pathways in insects, at least in the midgut compartment. And that the use of the pathway products can be successfully used to de-novo assemble previously unknown viruses from the virome. This work indicates that immune modifications in vectors need to be evaluated for changes of vectorial competence to different pathogens. It also opens numerous avenues of research and raises a lot of interesting questions that will need to be investigated in the future
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Carissimo, Guillaume. "Caractérisation et rôle de l'immunité antivirale des anophèles dans la compétence vectorielle pour les arbovirus et parasites." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066293.

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Dans une ère où les moustiques modifiés commencent à être utilisés ou envisagés pour contrôler les épidémies de Dengue ou malaria, le manque de connaissance sur l’immunité des insectes vecteurs envers certains pathogènes se fait cruellement ressentir. Pourtant la possibilité de changements de vecteurs, dû à un changement de leur immunité, provoquée par l’Homme est réelle. Pour déterminer la contribution de l’immunité dans différents compartiments du vecteur contre divers pathogènes avons étudié la réponse antivirale dans la première barrière de transmission chez le moustique vecteur de la malaria après une infection par un repas sanguin. Nous montrons que les réponses antivirales sont différentes entre compartiments, et proposons un modèle où des interactions tripartites entre le virus, l’immunité du moustique et la flore entérique interagissent pour contrôler l’infection précoce du moustique après le repas sanguin. De façon surprenante, nous avons également montré que la voie de l’ARN interférence n’a pas d’effet antiviral dans ce compartiment. Nous suggérons que cette voie est utilisée par le parasite Plasmodium pour détourner la réponse antiparasitaire médiée par Toll, grâce à un facteur de virulence de nature ARN double brin. Nous avons également montré que des biais expérimentaux lors de l’infection des insectes ont conduit à l’élaboration d’un dogme disant que la voie de l’ARN interférence est la voie antivirale principale des insectes, mais nos resultats suggèrent que malgré l’importance de cette voie pour controler l’intensité de la réplication virale lors de l’infection disséminée, cette voie n’a aucune fonction antivirale lors de l’infection initiale du tube digestif. Néanmoins, le séquençage des produits de cette voie permet d’assembler de-novo des génomes de virus commensaux. Les résultats de ces travaux montrent très clairement qu’il faut évaluer le rôle et l’impact de toute modification d’insectes vecteurs pour plusieurs classes de pathogènes. Cela ouvre également de nombreux nouveaux champs de recherches et pose de nombreuses nouvelles questions<br>In an era where modified mosquitoes are starting to be used in nature for controlling malaria and Dengue, lack of knowledge about immunity of mosquito vectors to some pathogen classes are becoming more evident. The risks for human-provoked vector shifts of pathogens transmission have not been examined. To fill these gaps, we assessed the antiviral immunity of the malaria vector, Anopheles gambiae, in the strongest mosquito bottleneck for pathogens, the midgut infection barrier after an infective bloodmeal. This work shows that the antiviral responses are different and highly compartmentalized between the midgut and systemic immunity. We propose a model where tripartite interactions between virus, mosquito immunity and enteric flora control early arboviral infection in the midgut. Surprisingly, we showed that while the siRNA pathway had no evident anti-arbovirus activity in the midgut, it was used by Plasmodium to evade mosquito immunity. A virus-like elicitor of double strand RNA nature is transferred from the parasite at the ookinete stage to the mosquito midgut cells, resulting in a shift of immune balance from anti-parasite response to an antiviral-like response. Importantly, our work shows that biases in experimental infection methods led to the misconstruction of a dogma stating that siRNA is the main antiviral pathways in insects, at least in the midgut compartment. And that the use of the pathway products can be successfully used to de-novo assemble previously unknown viruses from the virome. This work indicates that immune modifications in vectors need to be evaluated for changes of vectorial competence to different pathogens. It also opens numerous avenues of research and raises a lot of interesting questions that will need to be investigated in the future
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5

Hauler, Felix. "The ATPase VCP in viral infection and antiviral immunity." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707973.

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Schmitt, Éléonore. "Rôle de DICER dans la pathogénèse aux infections par les Herpesviridae." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ040.

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Dans les organismes multicellulaires, la régulation de l’expression des gènes par les microARNs est un mécanisme essentiel pour le développement cellulaire et l’homéostasie. De plus, le rôle des microARNs a été démontré dans de nombreux processus immunitaires, tels que l’inflammation. Les virus évoluant conjointement avec leurs hôtes, ils ont appris à détourner la machinerie cellulaire pour leur propre bénéfice. Ainsi, des microARNs codés par certains génomes viraux ont été mis en évidence, mais leurs fonctions, ainsi que leurs cibles, restent encore largement inconnues. En utilisant une lignée de souris présentant une mutation hypomorphe pour le gène dicer, caractérisée par une diminution de la production des microARNs, et son hôte naturel, le cytomégalovirus murin, un virus membre de la famille des β-Herpesvirus, nous avons étudié le rôle potentiel des microARNs d’origine cellulaire et virale dans la pathogénèse de ce virus. Lors de l’infection aigüe, nos résultats montrent un rôle dominant et protecteur des microARNs cellulaires, comparé à celui des microARNs viraux, prédits pour être des facteurs de pathogénicité<br>In multicellular organisms, gene expression regulation by microRNAs is an essential mechanism for cell development and homeostasis. Moreover, several immune-related processes, such as inflammation, have been demonstrated to require specific microRNAs. As viruses have coevolved with their host, they have learned to hijack the cellular defenses for their own benefit. Thus microRNAs-encoding genes were also recently discovered in the genome of Herpesviruses, but up to now, the function and the targets of most microRNAs of viral origin are still largely unknown. Using a hypomorphic mouse mutant line, characterized by a diminished production of microRNAs, and the Mouse Cytomegalovirus, a natural pathogen of mice which belongs to the family of β-Herpesviruses, we investigated the potential roles of microRNAs of both cellular and viral origin in the pathogenesis of this virus. Our results point toward a dominant role of cellular microRNAs as protective factors compared to virally-derived microRNAs which are usually predicted to carry pathogenic functions in acute infections
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Md, Bahanur Rahman. "Studies on the antiviral innate immunity factors in animal serum." 京都大学 (Kyoto University), 2002. http://hdl.handle.net/2433/150096.

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要旨には「Studies on the Antiviral Activity of the Normal Animal Serum」とあり<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(薬学)<br>甲第9507号<br>薬博第489号<br>新制||薬||193(附属図書館)<br>UT51-2002-G265<br>京都大学大学院薬学研究科生命薬科学専攻<br>(主査)教授 河合 明彦, 教授 川嵜 敏祐, 教授 市川 厚<br>学位規則第4条第1項該当
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Legrand, Alexandre. "Evolutionary and functional characterization of SAMD9/SAMD9L innate immunity proteins and their involvement in HIV infection." Electronic Thesis or Diss., Lyon, École normale supérieure, 2024. http://www.theses.fr/2024ENSL0055.

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Le VIH, virus responsable de la pandémie de SIDA, trouve son origine dans des transmissions inter-espèces de lentivirus simiens. Comprendre les interactions moléculaires entre le VIH et la cellule hôte est un objectif majeur pour l’avancée de la lutte contre le VIH/SIDA. En particulier, l’identification de nouveaux acteurs de l’immunité innée contre le VIH participe à la compréhension de son adaptation à l’humain, mais aussi renseigne plus largement sur les stratégies antivirales employées par l’hôte. A cet égard, les gènes SAMD9 et SAMD9L apparaissent comme des candidats d’intérêt. Constituant une famille de gènes impliquée dans des maladies génétiques auto-inflammatoires, SAMD9/9L sont également décrits comme antiviraux contre les poxvirus. De plus, SAMD9L a été identifié dans un criblage comme potentiel inhibiteur du VIH. Cependant, leur rôle et implication vis-à-vis du VIH demeurent inconnus. Ces travaux de thèse révèlent que SAMD9 et SAMD9L ont des effets opposés sur la réplication du VIH, au niveau de la synthèse des protéines virales. Alors que SAMD9 favorise la réplication du VIH-1, SAMD9L exerce une action antivirale souche-spécifique contre les VIH-1, VIH-2 et lentivirus simiens SIV. De plus, nous avons identifié un site nucléasique essentiel pour l’activité antivirale de SAMD9L face au VIH. Ce site actif est également déterminant dans l’activité d’inhibition de traduction cellulaire, en particulier des variants délétères de SAMD9/9L impliqués dans des maladies génétiques sévères. De plus, nos analyses évolutives à partir de séquences et de structures prédites montrent la présence de protéines homologues à SAMD9/9L chez les bactéries, qui seraient également impliquées dans l’immunité antivirale. Malgré une potentielle conservation sur des milliards d’années d’évolution, ces gènes évoluent rapidement au niveau génomique et génétique avec des traces typiques de conflits génétiques au sein des mammifères. Grace à des tests fonctionnels complémentaires, nous avons montré que certaines de ces variations au sein des grands singes constitueraient des adaptations aux lentivirus. En conclusion, ce projet caractérise SAMD9 et SAMD9L comme nouveaux facteurs de l’hôte modulant la réplication du VIH et souligne plus largement leur importance dans l’immunité du vivant<br>Human Immunodeficiency Virus (HIV), agent responsible for the AIDS pandemic, originated from interspecies transmissions of simian lentiviruses. Understanding the molecular interactions between HIV and the host cell is a major objective for advancing the fight against HIV/AIDS. In particular, the identification of new players in innate immunity to HIV not only contributes to our understanding of its adaptation to humans, but also provides broader information on the antiviral defense employed by the host. In this regard, the SAMD9 and SAMD9L genes appear as candidates of interest. Constituting a gene family involved in genetic auto-inflammatory diseases, SAMD9/9L are also described as antiviral against poxviruses. Furthermore, SAMD9L was identified in a screen as a potential HIV inhibitor. However, their role and implication regarding HIV remained unknown. This thesis work reveals that SAMD9 and SAMD9L have opposite effects on HIV replication, at the level of viral protein synthesis. While SAMD9 promotes HIV-1 replication, SAMD9L exerts a strain-specific antiviral action against HIV-1, HIV-2, and simian lentiviruses. In addition, we identified a nuclease site essential for the antiviral activity of SAMD9L against HIV. This active site is also decisive in inhibiting cell translation, in particular of deleterious SAMD9/9L variants implicated in severe genetic diseases. Furthermore, our evolutionary analyzes based on sequences and predicted structures show the presence of homologous proteins to SAMD9/9L in bacteria, which would also be involved in antiviral immunity. Despite a potential conservation over billions of years of evolution, these genes are rapidly evolving at the genomic and genetic levels, with typical traces of host-pathogen genetic conflicts within mammals. Thanks to complementary functional assays, we showed that some of these variations within great apes may be adaptations to lentiviruses. In conclusion, this project discovers and characterizes SAMD9 and SAMD9L as host factors modulating HIV replication and more broadly highlights their importance in living immunity
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Sang, Yongming. "Porcine innate antiviral immunity : host defense peptides and toll-like receptors." Diss., Manhattan, Kan. : Kansas State University, 2008. http://hdl.handle.net/2097/960.

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Yen, Pei-Shi. "Transgenic mosquitoes for controlling transmission of arboviruses." Electronic Thesis or Diss., Paris 6, 2017. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2017PA066340.pdf.

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Les arbovirus (virus transmis par des arthropodes) sont à l'origine de maladies humaines telles que la dengue, le chikungunya ou encore le Zika. Le moustique Aedes aegypti, est le vecteur majeur de ces trois arbovirus. La faible efficacité des méthodes de contrôle des populations de moustiques, principalement réalisées au moyen d'insecticides chimiques ouvre un champ de développement de nouvelles approches en lutte antivectorielle. Le moustique, hôte vecteur, contrôle la réplication virale en limitant les réponses immunitaires antivirales. La machinerie RNA interférence (RNAi) est la voie jouant un rôle majeur dans l'immunité antivirale chez le moustique. Alors que le rôle des deux voies, siRNA (" small interfering RNA ") et piRNA (" piwi-interfering RNA "), est de mieux en mieux compris dans les réactions antivirales du vecteur, peu de connaissances sont disponibles à ce jour en ce qui concernent les interactions entre la voie miRNA (" micro RNA ") et les arbovirus. Ainsi, nous proposons une analyse détaillée des mécanismes par lesquels les miARN tentent de réguler la réplication virale chez le moustique. Dans la première partie de la thèse, nous avons effectué une analyse génomique pour identifier les miRNAs pouvant interagir chez Ae. aegypti avec divers lignées/génotypes des virus chikungunya (CHIKV), de dengue (DENV) et de Zika. Avec l'aide d'outils de prédiction faisant appel à divers algorithmes, plusieurs sites de liaison de miARN avec différents lignées/génotypes de chaque arbovirus ont été identifiés. Nous avons ensuite sélectionné les miARN pouvant cibler plus d'un arbovirus et nécessitant un faible seuil d'énergie lors de la formation des complexes entre l'ARNm<br>Mosquito-borne arboviruses cause some of the world’s most devastating diseases and are responsible for recent dengue, chikungunya and Zika pandemics. The yellow-fever mosquito. Aedes aegypti, plays an important role in the transmission of all three viruses. The ineffectiveness of chemical control methods targeting Ae. aegypti makes urgent the need for novel vector-based approaches for controlling these diseases. Mosquitoes control arbovirus replication by triggering immune responses. RNAi machinery is the most significant pathway playing a role on antiviral immunity. Although the role of exogenous siRNA and piRNA pathways in mosquito antiviral immunity is increasingly better understood, there is still little knowledge regarding interactions between the mosquito cellular miRNA pathway and arboviruses. Thus further analysis of mechanisms by which miRNAs may regulate arbovirus replication in mosquitoes is pivotal. In the first part of the thesis, we carried out genomic analysis to identify Ae. aegypti miRNAs that potentially interact with various lineages and genotypes of chikungunya (CHIKV), dengue (DENV) and Zika viruses. By using prediction tools with distinct algorithms, several miRNA binding sites were commonly found within different genotypes/and or lineages of each arbovirus. We further analyzed the miRNAs that could target more than one arbovirus and required a low energy threshold to form miRNA-vRNA (viral RNA) complexes and predicted potential RNA structures using RNAhybrid software. Thus, we predicted miRNA candidates that might participate in regulating arboviral replication in Ae. aegypti. In the second part of the thesis, we developed a miRNA-based approach that results in a dual resistance phenotype in mosquitoes to dengue serotype 3 (DENV-3) and chikungunya (CHIKV) viruses for stopping arboviruses spreading within urban cycles. The target viruses are from two distinct arboviral families and the antiviral mechanism is designed to function through the endogenous miRNA pathway in infected mosquitoes. Ten artificial antiviral 4 miRNAs capable of targeting ~97% of all published strains were designed based on derived consensus sequences of CHIKV and DENV-3. The antiviral miRNA constructs were placed under control of either an Aedes PolyUbiquitin (PUb) or Carboxypeptidase A (AeCPA) gene promoter triggering respectively expression ubiquitously in the transgenic mosquitoes or more locally in the midgut epithelial cells following a blood meal. Challenge experiments using viruses added in blood meals showed subsequent reductions in viral transmission efficiency in the saliva of transgenic mosquitoes as a result of lowered infection rate and dissemination efficiency. Several components of mosquito fitness, including larval development time, larval/pupal mortality, adult lifespan, sex ratio, and male mating competitiveness, were examined: transgenic mosquitoes with the PUb promoter showed minor fitness costs at all developing stages whereas those based on AeCPA exhibited a high fitness cost. Further development of these strains with gene editing tools could make them candidates for releases in population replacement strategies for sustainable control of multiple arbovirus diseases
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Books on the topic "Antiviral immunity"

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Mossman, Karen, ed. Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1.

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Zheng, Chunfu, ed. Antiviral Innate Immunity. Springer US, 2025. http://dx.doi.org/10.1007/978-1-0716-4108-8.

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Symposium in Immunology (5th 1995 Strasbourg, France). Symposium in Immunology V: Antiviral immunity. Springer, 1996.

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Rybkina, Xenia. The landscape and interplay of antiviral immunity mounted against SARS-CoV-2 infection across tissues, age, and disease. [publisher not identified], 2022.

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Harper, D. R. Molecular virology. 2nd ed. Springer, 1998.

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Huber, Christoph, Martha M. Eibl, Ulrich Wahn, and Hans H. Peter. Symposium in Immunology V: Antiviral Immunity. Springer London, Limited, 2012.

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Sambhara, Prakash. Nucleic Acid Sensors and Antiviral Immunity. Taylor & Francis Group, 2012.

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Zheng, Chunfu, Rongtuan Lin, and Junji Xing, eds. Sensing DNA in Antiviral Innate Immunity. Frontier Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-270-0.

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Jiang, Liang, Xiao-Qiang Yu, and Luc Swevers, eds. Novel Insights Into Insect Antiviral Immunity. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-410-7.

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Nucleic Acid Sensors and Antiviral Immunity. Taylor & Francis Group, 2012.

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Book chapters on the topic "Antiviral immunity"

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Vahedi, Fatemeh, Elizabeth C. Giles, and Ali A. Ashkar. "The Application of Humanized Mouse Models for the Study of Human Exclusive Viruses." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_1.

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Pokatayev, Vladislav, and Nan Yan. "Methods of Assessing STING Activation and Trafficking." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_10.

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Zhu, Shiyou, Yuexin Zhou, and Wensheng Wei. "Genome-Wide CRISPR/Cas9 Screening for High-Throughput Functional Genomics in Human Cells." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_11.

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Gall, Bryan J., and Victor R. DeFilippis. "High-Throughput Screening for Identification of Novel Innate Immune Activators." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_12.

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Kim, Yoon Jung, and Tae Hoon Kim. "Chromosome Conformation Capture for Research on Innate Antiviral Immunity." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_13.

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Leiva-Torres, Gabriel A., Nestor Nebesio, and Silvia M. Vidal. "Discovery of Variants Underlying Host Susceptibility to Virus Infection Using Whole-Exome Sequencing." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_14.

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Katzenell, Sarah, Jorge R. Cabrera, Brian J. North, and David A. Leib. "Isolation, Purification, and Culture of Primary Murine Sensory Neurons." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_15.

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Duerr, Claudia U., and Jörg H. Fritz. "Isolation of Group 2 Innate Lymphoid Cells from Mouse Lungs." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_16.

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Wang, Biao, and Mark Loeb. "Epidemiological Methods." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_17.

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Mayer, Alice, Jonathan Maelfait, Anne Bridgeman, and Jan Rehwinkel. "Erratum to: Purification of Cyclic GMP-AMP from Viruses and Measurement of Its Activity in Cell Culture." In Innate Antiviral Immunity. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7237-1_18.

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Conference papers on the topic "Antiviral immunity"

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Johnson, Karyn N. "Wolbachia-insect associations and antiviral immunity." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92696.

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Shin, Dong Ho, Bulent Ozpolat, Andrew G. Gillard, et al. "774 Refocusing on tumors: overcoming antiviral immunity in oncolytic virotherapy." In SITC 39th Annual Meeting (SITC 2024) Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-sitc2024.0774.

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Garziano, M., C. Vanetti, S. Strizzi, et al. "P-112 SARS-CoV-2 natural infection, but not vaccine-induced immunity, elicits cross-reactive immunity to OC43." In Abstracts from the 16° Italian Conference on AIDS and Antiviral Research. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/sextrans-icar-2024.201.

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Cherry, Sara. "UsingDrosophilagenetics to define factors involved in antiviral immunity to human arboviruses." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93824.

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Kornfield, J. M., C. M. Evans, J. Wagner, et al. "Muc5b Mediates Antiviral Immunity and Airway Hyperresponsiveness During Parainfluenza Virus Infection." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6166.

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Hinks, Timothy, Yuqing Long, Michael Edwards, James Porter, and Paul Klenerman. "Mitochondrial antiviral signalling protein (MAVS) triggers innate immunity against bacterial lung infection." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa5319.

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Pavasutthipaisit, S., M. Stoff, M. Ciurkiewicz, et al. "CARD9 signaling enhances antiviral immunity in a mouse model for neurotropic virus infection." In 63. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1712591.

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Bartlett, Nathan W., Louise Slater, Gaetano Caramori, Simon Message, Sebastian L. Johnston, and Michael R. Edwards. "Reduced NF-ºB P65 Expression Inhibits Rhinovirus-Induced Inflammation Without Compromising Antiviral Immunity." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3875.

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Martinez-Nunez, Rocio Teresa, Adam Richardson, Nicole Ponde, et al. "UPF1 and STAU1 modulate rhinovirus pathophysiology contributing to impaired antiviral immunity in asthma." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2324.

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Ghanizada, Muzhda, Sofia Malm Tillgren, Mandy Menzel, et al. "Effect of azithromycin on epithelial antiviral immunity in patients with asthma (AZIMUNE-study)." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.oa1971.

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Reports on the topic "Antiviral immunity"

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วีรกุล, ปราจีน, อัจฉริยา ไศละสูต, คณิศักดิ์ อรวีระกุล, วาสนา ภิญโญชนม์, สุดารัตน์ ดำรงค์วัฒนโภคิน та สันนิภา สุรทัตต์. การวิจัยและการพัฒนาวิธีวินิจฉัย ควบคุมและป้องกันโรคอหิวาต์สุกรในประเทศไทย : รายงานการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย ; สำนักงานคณะกรรมการวิจัยแห่งชาติ, 2002. https://doi.org/10.58837/chula.res.2002.61.

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ชุดโครงการวิจัยนี้ แบ่งการศึกษาออกเป็น 4 โครงการย่อย ซึ่งประกอบด้วย โครงการที่ 1 การศึกษาเปรียบเทียบระดับแอนติบอดีในแม่สุกรที่ได้รับการฉีดวัคซีนโปรแกรม 3 ชนิด และผลกระทบของภูมิคุ้มกันถ่ายทอดจากแม่สู่ลูกในการสร้างภูมิคุ้มกันในลูกสุกรเมื่อได้รับการฉีดวัคซีน โครงการที่ 2 การพัฒนาวิธีการตรวจวินิจฉัยโรคอหิวาต์สุกรและการพัฒนาการตรวจวัดภูมิคุ้มกันชนิดเซลล์ต่อเชื้อไวรัสอหิวาต์สุกร โครงการที่ 3 การศึกษาพัฒนาวิธีผลิตวัคซีนอหิวาต์สุกรชนิดเซลล์เพาะเลี้ยง และโครงการที่ 4 การศึกษาระดับภูมิคุ้มกันถ่ายทอดที่สามารถป้องกันการเกิดอหิวาต์สุกรเมื่อได้รับการฉีดเชื้อพิษอหิวาต์สุกร Chiangmai/98 โครงการที่ 1 การศึกษาสถานภาพของระดับแอนติบอดีในแม่สุกรที่ได้รับการฉีดวัคซีนป้องกันโรคอหิวาต์สุกร 3 โปรแกรมพบว่า ระดับแอนติบอดีในแม่สุกรที่ 1 สัปดาห์หลังคลอดในโปรแกรมที่ได้รับการฉีดวัคซีน 3 สัปดาห์ก่อนคลอดหรือโปรแกรมฉีดพร้อมกันทุกตัวในฟาร์มปีละ 3 ครั้ง ไม่มีความแตกต่างกัน ส่วนแม่สุกรที่ฉีดวัคซีนโปรแกรม 3 สัปดาห์หลังคลอดมีค่าใช้จ่ายของระดับแอนติบอดีต่ำกว่าทั้ง 2 โปรแกรมอย่างมีนัยสำคัญทางสถิติ (p&lt;0.05) ผลการศึกษาระดับภูมิคุ้มกันถ่ายทอดสู่ลูกสุกรที่เกิดจากแม่ที่ได้รับการฉีดวัคซีนทั้ง 3 โปรแกรมเมื่อลูกสุกรอายุ 1 และ 3 สัปดาห์ มีระดับแอนติบอดีที่สอดคล้องกับแอนติบอดีในแม่ การศึกษาผลกระทบของระดับภูมิคุ้มกันถ่ายทอดจากแม่สู่ลูกที่อาจมีผลรบกวนการสร้างภูมิคุ้มกันในลูกสุกรเมื่อฉีดวัคซีน ผลการศึกษาการประเมินประสิทธิภาพของโปรแกรมการฉีดวัคซีนในลูกสุกรครั้งเดียวที่อายุ 3 สัปดาห์หรือ 2 ครั้งที่อายุ 3 และ 5 สัปดาห์ พบว่า วัคซีนให้ความคุ้มโรคได้ แม้ลูกสุกรมีภูมิคุ้มกันถ่ายทอดจากแม่ในระดับที่แตกต่างกัน ณ วันฉีดวัคซีน อย่างไรก็ตามพบว่าภูมิคุ้มกันถ่ายทอดในระดับสูงจะรบกวนการสร้างภูมิคุ้มกันชนิดเซลล์ในลูกสุกรเมื่อฉีดวัคซีน โครงการที่ 2 การตรวจวินิจฉัยโรคอหิวาต์สุกรโดยวิธี reverse transcriptase polymerase chain reaction (RT-PCR) พบว่าเมื่อใช้ primer 324 และ 326 เป็นวิธีที่มีความไวและความจำเพาะสูง สามารถตรวจหาสารพันธุกรรมของเชื้อไวรัสอหิวาต์สุกรที่แยกได้ในประเทศทุก genogroups และให้ผลสอดคล้องกับวิธีการแยกและพิสูจน์เชื้อในเซลล์เพาะเลี้ยง จึงเหมาะสำหรับนำมาใช้ในการวินิจฉัยโรคอหิวาต์สุกรในประเทศ (โครงการที่ 2.1) สำหรับวิธี RT-PCR เพื่อตรวจหาสารพันธุกรรมของไวรัสอหิวาต์สุกรในส่วนของ gp 55 ร่วมกับการใช้เอ็นไซม์จำเพาะ เพื่อแยกไวรัสจากวัคซีนที่แยกได้จากท้องที่ พบว่ามีข้อจำกัดในเรื่องความไว และความจำเพาะ จึงอาจไม่เหมาะสำหรับนำมาใช้ในการวินิจฉัยโรคและแยกแยะชนิดของเชื้อในประเทศ การพัฒนาวิธีการตรวจวัดภูมิคุ้มกันชนิดเซลล์โดยการตรวจหาปริมาณเซลล์ที่สร้างแอนติบอดี (antibody secreting cells) และเซลล์ที่สร้างอินเตอเฟอรอนแกมม่า (IFN[gamma]) ที่จำเพาะต่อเชื้ออหิวาต์สุกรเพื่อใช้เป็นตัวบ่งชี้ระดับ antiviral immunity และใช้ในการประเมินประสิทธิภาพของวัคซีนอหิวาต์สุกร ผลการวิจัยสามารถพัฒนาเทคนิค ELISPOT เพื่อตรวจวัดระดับภูมิคุ้มกันชนิดเซลล์ต่อเชื้ออหิวาต์สุกรได้เป็นผลสำเร็จ (โครงการที่ 2.2) โครงการที่ 3 พัฒนาวิธีผลิตวัคซีนอหิวาต์สุกรเชื้อเป็นเซลล์เพาะเลี้ยงโดยใช้เชื้อไวรัสวัคซีนสเตรน GPE เพาะเลี้ยงในเซลล์ FS-L[subscript 3] พบว่าสามารถนำมาใช้ผลิตเป็นวัคซีนชนิดดูดแห้งที่ได้มาตรฐานทางห้องปฏิบัติการเป็นวัคซีนที่มีความปลอดภัยสูงและให้ความคุ้มครองได้อย่างสมบูรณ์ในสุกรเมื่อฉีดพิษทับวัคซีนที่ผลิตได้มีความเหมาะสมที่จะนำไปผลิตในเชิงอุตสาหกรรมต่อไป โครงการที่ 4 การทดสอบภูมิคุ้มกันถ่ายทอดจากแม่และการฉีดวัคซีนในลูกสุกรต่อไวรัสอหิวาต์สุกร Chiangmai/98 ซึ่งเป็นเชื้อใน genogroup 2.2 พบว่าภูมิคุ้มกันถ่ายทอดมีผลน้อยมากต่อการให้ความคุ้มครองโรคต่อการฉีดพิษทับด้วยเชื้อ genogroup 2.2 นอกจากนั้นภูมิคุ้มกันถ่ายทอดมีผลรบกวนการสร้างภูมิคุ้มกันทั้งชนิดเซลล์และแอนติบอดีอย่างมีนัยสำคัญทางสถิติ (p&lt;0.05) ต่อการฉีดวัคซีน
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Bermingham, Rowena. Virology, immunology, epidemiology and COVID-19: What are experts concerned about? Parliamentary Office of Science and Technology, 2020. http://dx.doi.org/10.58248/hs08.

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Over 1,100 experts have shared with us their concerns about COVID-19 and COVID-impacted areas in the immediate and longer term future. This report outlines concerns about virology, immunology and epidemiology. Experts have concerns about the accurate and thorough recording of who is dying from COVID-19 and what demographic they belong to. They worry that there are gaps in the understanding of how the virus spreads, and how symptoms progress. Experts are also concerned about the potential for additional COVID-19 waves, and the impact of seasonality. They are worried about the long term health impacts of COVID-19 after recovery. There are also concerns about the lack of data on patient and population immunity to the virus. Finally experts worry that the virus could become resistant to antiviral therapies, and that there's a risk of creating other antibiotic resistant infections by using antibiotics improperly.
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Tang, Jiqin, Gong Zhang, Jinxiao Xing, Ying Yu, and Tao Han. Network Meta-analysis of Heat-clearing and Detoxifying Oral Liquid of Chinese Medicines in Treatment of Children’s Hand-foot-mouth Disease:a protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.1.0032.

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Review question / Objective: The type of study was clinical randomized controlled trial (RCT). The object of study is the patients with HFMD. There is no limit to gender and race. In the case of clear diagnosis standard, curative effect judgment standard and consistent baseline treatment, the experimental group was treated with pure oral liquid of traditional Chinese medicine(A: Fuganlin oral liquid, B: huangzhihua oral liquid, C: Lanqin oral liquid, D: antiviral oral liquid, E: Huangqin oral liquid, F: Pudilan oral liquid, G: Shuanghuanglian oral liquid.)and the control group was treated with ribavirin or any oral liquid of traditional Chinese medicine. The data were extracted by two researchers independently, cross checked and reviewed according to the pre-determined tables. The data extraction content is (1) Basic information (including the first author, published journal and year, research topic). (2) Relevant information (including number of cases, total number of cases, gender, age, intervention measures, course of treatment of the experimental group and the control group in the literature). (3) Design type and quality evaluation information of the included literature. (4) Outcome measures (effective rate, healing time of oral ulcer, regression time of hand and foot rash, regression time of fever, adverse reactions.). The seven traditional Chinese medicine oral liquids are comparable in clinical practice, but their actual clinical efficacy is lack of evidence-based basis. Therefore, the purpose of this study is to use the network meta-analysis method to integrate the clinical relevant evidence of direct and indirect comparative relationship, to make quantitative comprehensive statistical analysis and sequencing of different oral liquid of traditional Chinese medicine with the same evidence body for the treatment of the disease, and then to explore the advantages and disadvantages of the efficacy and safety of different oral liquid of traditional Chinese medicine to get the best treatment plan, so as to provide reference value and evidence-based medicine evidence for clinical optimization of drug selection. Condition being studied: Hand foot mouth disease (HFMD) is a common infectious disease in pediatrics caused by a variety of enteroviruses. Its clinical manifestations are mainly characterized by persistent fever, hand foot rash, oral herpes, ulcers, etc. Because it is often found in preschool children, its immune system development is not perfect, so it is very vulnerable to infection by pathogens and epidemic diseases, resulting in rapid progress of the disease. A few patients will also have neurogenic pulmonary edema Meningitis, myocarditis and other serious complications even lead to death, so effectively improve the cure rate, shorten the course of disease, prevent the deterioration of the disease as the focus of the study. In recent years, traditional Chinese medicine has played an important role in the research of antiviral treatment. Many clinical practices have confirmed that oral liquid of traditional Chinese medicine can effectively play the role of antiviral and improve the body's immunity.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, 2010. http://dx.doi.org/10.32747/2010.7592113.bard.

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The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.
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Effects of antimicrobial chemical exposures on influenza vaccination and antiviral immunity (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2021. http://dx.doi.org/10.26616/nioshrd-1018-2021-0.

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