Relevant bibliographies by topics / Adenovirus diseases

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Adenovirus diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Adenovirus diseases.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Adenovirus diseases"

1

Watanabe, Maki, Yuya Nishikawaji, Hirotaka Kawakami, and Ken-ichiro Kosai. "Adenovirus Biology, Recombinant Adenovirus, and Adenovirus Usage in Gene Therapy." Viruses 13, no. 12 (December 14, 2021): 2502. http://dx.doi.org/10.3390/v13122502.

Full text
Abstract:
Gene therapy is currently in the public spotlight. Several gene therapy products, including oncolytic virus (OV), which predominantly replicates in and kills cancer cells, and COVID-19 vaccines have recently been commercialized. Recombinant adenoviruses, including replication-defective adenoviral vector and conditionally replicating adenovirus (CRA; oncolytic adenovirus), have been extensively studied and used in clinical trials for cancer and vaccines. Here, we review the biology of wild-type adenoviruses, the methodological principle for constructing recombinant adenoviruses, therapeutic applications of recombinant adenoviruses, and new technologies in pluripotent stem cell (PSC)-based regenerative medicine. Moreover, this article describes the technology platform for efficient construction of diverse “CRAs that can specifically target tumors with multiple factors” (m-CRAs). This technology allows for modification of four parts in the adenoviral E1 region and the subsequent insertion of a therapeutic gene and promoter to enhance cancer-specific viral replication (i.e., safety) as well as therapeutic effects. The screening study using the m-CRA technology successfully identified survivin-responsive m-CRA (Surv.m-CRA) as among the best m-CRAs, and clinical trials of Surv.m-CRA are underway for patients with cancer. This article also describes new recombinant adenovirus-based technologies for solving issues in PSC-based regenerative medicine.
APA, Harvard, Vancouver, ISO, and other styles
2

Ageeva, M. R., and S. B. Yatsyshina. "UNDERESTIMATED INFECTION - ON THE QUESTION OF THE HUMAN ADENOVIRUS PATHOGENICITY FACTORS." Problems of Virology, Russian journal 64, no. 2 (April 20, 2019): 53–62. http://dx.doi.org/10.18821/0507-4088-2019-64-2-53-62.

Full text
Abstract:
Human adenoviruses cause different organ infections of varying severity, from asymptomatic to severe cases with lethal outcome, that are registered everywhere. Detailed and focused study of factors predisposing to a severe course of infection is required. The literature contains information indicating the association of severe adenoviral respiratory diseases with certain types of adenovirus, primarily type 7. This review highlights the possible causes of increased pathogenicity of some types of adenovirus and their association with severe forms of infection. Pathogenicity factors include the ability of adenovirus to bind the specific cellular receptors, the formation of subviral particles, the interaction with blood proteins, in particular the coagulation factor X, as well as the features of the early genes E1A, E1B, E3, E4. In addition, the severity of the disease may be affected by the presence or absence of pre-existing antibodies specific to certain types of adenoviruses. Chronic diseases or immunosuppression also increase the risk of severe adenovirus infection. The information presented in this review may elucidate the pathogenesis of adenovirus infection, and help to develop new features for prevention and treatment.
APA, Harvard, Vancouver, ISO, and other styles
3

Nikitenko, N. A., T. Speiseder, E. Lam, P. M. Rubtsov, Kh D. Tonaeva, S. A. Borzenok, T. Dobner, and V. S. Prassolov. "Regulation of Human Adenovirus Replication by RNA Interference." Acta Naturae 7, no. 3 (September 15, 2015): 100–107. http://dx.doi.org/10.32607/20758251-2015-7-3-100-107.

Full text
Abstract:
Adenoviruses cause a wide variety of human infectious diseases. Adenoviral conjunctivitis and epidemic keratoconjunctivitis are commonly associated with human species D adenoviruses. Currently, there is no sufficient or appropriate treatment to counteract these adenovirus infections. Thus, there is an urgent need for new etiology-directed therapies with selective activity against human adenoviruses. To address this problem, the adenoviral early genes E1A and E2B (viral DNA polymerase) seem to be promising targets. Here, we propose an effective approach to downregulate the replication of human species D adenoviruses by means of RNA interference. We generated E1A expressing model cell lines enabling fast evaluation of the RNA interference potential. Small interfering RNAs complementary to the E1A mRNA sequences of human species D adenoviruses mediate significant suppression of the E1A expression in model cells. Furthermore, we observed a strong downregulation of replication of human adenoviruses type D8 and D37 by small hairpin RNAs complementary to the E1A or E2B mRNA sequences in primary human limbal cells. We believe that our results will contribute to the development of efficient anti-adenoviral therapy.
APA, Harvard, Vancouver, ISO, and other styles
4

Zhu, Jiangao, Xiaopei Huang, and Yiping Yang. "Innate Immune Response to Adenoviral Vectors Is Mediated by both Toll-Like Receptor-Dependent and -Independent Pathways." Journal of Virology 81, no. 7 (January 17, 2007): 3170–80. http://dx.doi.org/10.1128/jvi.02192-06.

Full text
Abstract:
ABSTRACT Recombinant adenoviral vectors have been widely used for gene therapy applications and as vaccine vehicles for treating infectious diseases such as human immunodeficiency virus disease. The innate immune response to adenoviruses represents the most significant hurdle in clinical application of adenoviral vectors for gene therapy, but it is an attractive feature for vaccine development. How adenovirus activates innate immunity remains largely unknown. Here we showed that adenovirus elicited innate immune response through the induction of high levels of type I interferons (IFNs) by both plasmacytoid dendritic cells (pDCs) and non-pDCs such as conventional DCs and macrophages. The innate immune recognition of adenovirus by pDCs was mediated by Toll-like receptor 9 (TLR9) and was dependent on MyD88, whereas that by non-pDCs was TLR independent through cytosolic sensing of adenoviral DNA. Furthermore, type I IFNs were pivotal in innate and adaptive immune responses to adenovirus in vivo, and type I IFN blockade diminished immune responses, resulting in more stable transgene expression and reduction of inflammation. These findings indicate that adenovirus activates innate immunity by its DNA through TLR-dependent and -independent pathways in a cell type-specific fashion, and they highlight a critical role for type I IFNs in innate and adaptive immune responses to adenoviral vectors. Our results that suggest strategies to interfere with type I IFN pathway may improve the outcome of adenovirus-mediated gene therapy, whereas approaches to activate the type I IFN pathway may enhance vaccine potency.
APA, Harvard, Vancouver, ISO, and other styles
5

Liu, Minli, Lefang Jiang, Weihua Cao, Jianguo Wu, and Xulin Chen. "Identification of Inhibitors and Drug Targets for Human Adenovirus Infections." Viruses 14, no. 5 (May 4, 2022): 959. http://dx.doi.org/10.3390/v14050959.

Full text
Abstract:
Adenoviruses can cause infections in people of all ages at all seasons of the year. Adenovirus infections cause mild to severe illnesses. Children, immunocompromised patients, or those with existing respiratory or cardiac disease are at higher risk. Unfortunately, there are no commercial drugs or vaccines available on the market for adenovirus infections. Therefore, there is an urgent need to discover new antiviral drugs or drug targets for adenovirus infections. To identify potential antiviral agents for adenovirus infections, we screened a drug library containing 2138 compounds, most of which are drugs with known targets and past phase I clinical trials. On a cell-based assay, we identified 131 hits that inhibit adenoviruses type 3 and 5. A secondary screen confirmed the antiviral effects of 59 inhibitors that inhibit the replication of adenoviruses type 3 or 5. Most of the inhibitors target heat shock protein, protein tyrosine kinase, the mTOR signaling pathway, and other host factors, suggesting that these host factors may be essential for replicating adenoviruses. Through this study, the newly identified adenovirus inhibitors may provide a start point for developing new antiviral drugs to treat adenovirus infections. Further validation of the identified drug targets can help the development of new therapeutics against adenovirus infections.
APA, Harvard, Vancouver, ISO, and other styles
6

Kulanayake, Shermila, and Suresh K. Tikoo. "Adenovirus Core Proteins: Structure and Function." Viruses 13, no. 3 (February 28, 2021): 388. http://dx.doi.org/10.3390/v13030388.

Full text
Abstract:
Adenoviruses have served as a model for investigating viral-cell interactions and discovering different cellular processes, such as RNA splicing and DNA replication. In addition, the development and evaluation of adenoviruses as the viral vectors for vaccination and gene therapy has led to detailed investigations about adenovirus biology, including the structure and function of the adenovirus encoded proteins. While the determination of the structure and function of the viral capsid proteins in adenovirus biology has been the subject of numerous reports, the last few years have seen increased interest in elucidating the structure and function of the adenovirus core proteins. Here, we provide a review of research about the structure and function of the adenovirus core proteins in adenovirus biology.
APA, Harvard, Vancouver, ISO, and other styles
7

Perkins, Laura E. Leigh, Raymond P. Campagnoli, Barry G. Harmon, Christopher R. Gregory, W. L. Steffens, Ken Latimer, Susan Clubb, and Maria Crane. "Detection and Confirmation of Reptilian Adenovirus Infection by in Situ Hybridization." Journal of Veterinary Diagnostic Investigation 13, no. 4 (July 2001): 365–68. http://dx.doi.org/10.1177/104063870101300418.

Full text
Abstract:
Adenovirus infections are documented in at least 12 different species of reptiles. In contrast to their mammalian and avian counterparts reptilian adenoviruses are not well characterized as to their pathogenic potential and their ability to cause primary disease. In the diagnostic setting, fresh tissues are often not available for virus isolation, and the confirmation of reptilian adenovirus infections is dependent largely upon electron microscopy for the identification of intranuclear viral inclusions associated with histopathologic changes. The diagnosis of adenovirus infection in 2 different species of snake was confirmed by the application of DNA in situ hybridization. Using an aviadenovirus specific oligoprobe, adenoviral DNA was observed in the nuclei of hepatocytes, Kupffer cells, endothelial cells, and enterocytes. Electron microscopy of the liver confirmed the presence of intranuclear viral particles morphologically consistent with an adenovirus. DNA in situ hybridization on formalin-fixed tissues can serve as a suitable alternative to electron microscopy in the diagnosis of reptilian adenovirus infections. Both affected snakes had other concurrent diseases, suggesting that the adenovirus may not have been the primary pathogen.
APA, Harvard, Vancouver, ISO, and other styles
8

Rajaiya, Jaya, Amrita Saha, Ashrafali M. Ismail, Xiaohong Zhou, Ting Su, and James Chodosh. "Adenovirus and the Cornea: More Than Meets the Eye." Viruses 13, no. 2 (February 13, 2021): 293. http://dx.doi.org/10.3390/v13020293.

Full text
Abstract:
Human adenoviruses cause disease at multiple mucosal sites, including the respiratory, gastrointestinal, and genitourinary tracts, and are common agents of conjunctivitis. One site of infection that has received sparse attention is the cornea, a transparent tissue and the window of the eye. While most adenovirus infections are self-limited, corneal inflammation (keratitis) due to adenovirus can persist or recur for months to years after infection, leading to reduced vision, discomfort, and light sensitivity. Topical corticosteroids effectively suppress late adenovirus keratitis but are associated with vision-threatening side effects. In this short review, we summarize current knowledge on infection of the cornea by adenoviruses, including corneal epithelial cell receptors and determinants of corneal tropism. We briefly discuss mechanisms of stromal keratitis due to adenovirus infection, and review an emerging therapy to mitigate adenovirus corneal infections based on evolving knowledge of corneal epithelial receptor usage.
APA, Harvard, Vancouver, ISO, and other styles
9

Guo, Xiaojuan, Yangyang Sun, Juan Chen, Xiaohui Zou, Wenzhe Hou, Wenjie Tan, Tao Hung, and Zhuozhuang Lu. "Restriction-Assembly: A Solution to Construct Novel Adenovirus Vector." Viruses 14, no. 3 (March 6, 2022): 546. http://dx.doi.org/10.3390/v14030546.

Full text
Abstract:
Gene therapy and vaccine development need more novel adenovirus vectors. Here, we attempt to provide strategies to construct adenovirus vectors based on restriction-assembly for researchers with little experience in this field. Restriction-assembly is a combined method of restriction digestion and Gibson assembly, by which the major part of the obtained plasmid comes from digested DNA fragments instead of PCR products. We demonstrated the capability of restriction-assembly in manipulating the genome of simian adenovirus 1 (SAdV-1) in this study. A PCR product of the plasmid backbone was combined with SAdV-1 genomic DNA to construct an infectious clone, plasmid pKSAV1, by Gibson assembly. Restriction-assembly was performed repeatedly in the steps of intermediate plasmid isolation, modification, and restoration. The generated adenoviral plasmid was linearized by restriction enzyme digestion and transfected into packaging 293 cells to rescue E3-deleted replication-competent SAdV1XE3-CGA virus. Interestingly, SAdV1XE3-CGA could propagate in human chronic myelogenous leukemia K562 cells. The E1 region was similarly modified to generate E1/E3-deleted replication-defective virus SAdV1-EG. SAdV1-EG had a moderate gene transfer ability to adherent mammalian cells, and it could efficiently transduce suspension cells when compared with the human adenovirus 5 control vector. Restriction-assembly is easy to use and can be performed without special experimental materials and instruments. It is highly effective with verifiable outcomes at each step. More importantly, restriction-assembly makes the established vector system modifiable, upgradable and under sustainable development, and it can serve as the instructive method or strategy for the synthetic biology of adenoviruses.
APA, Harvard, Vancouver, ISO, and other styles
10

Blanchette, Paola, and Jose G. Teodoro. "A Renaissance for Oncolytic Adenoviruses?" Viruses 15, no. 2 (January 26, 2023): 358. http://dx.doi.org/10.3390/v15020358.

Full text
Abstract:
In the 1990s, adenovirus became one of the first virus types to be genetically engineered to selectively destroy cancer cells. In the intervening years, the field of “oncolytic viruses” has slowly progressed and culminated in 2015 with the FDA approval of Talimogene laherparepvec, a genetically engineered herpesvirus, for the treatment of metastatic melanoma. Despite the slower progress in translating oncolytic adenovirus to the clinic, interest in the virus remains strong. Among all the clinical trials currently using viral oncolytic agents, the largest proportion of these are using recombinant adenovirus. Many trials are currently underway to use oncolytic virus in combination with immune checkpoint inhibitors (ICIs), and early results using oncolytic adenovirus in this manner are starting to show promise. Many of the existing strategies to engineer adenoviruses were designed to enhance selective tumor cell replication without much regard to interactions with the immune system. Adenovirus possesses a wide range of viral factors to attenuate both innate anti-viral pathways and immune cell killing. In this review, we summarize the strategies of oncolytic adenoviruses currently in clinical trials, and speculate how the mutational backgrounds of these viruses may impact upon the efficacy of these agents in oncolytic and immunotherapy. Despite decades of research on human adenoviruses, the interactions that these viruses have with the immune system remains one of the most understudied aspects of the virus and needs to be improved to rationally design the next generation of engineered viruses.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Adenovirus diseases"

1

Arnall, Jennifer K. "Susceptibily of colostrum-deprived lambs and lambs receiving colostrum to the cervid adenovirus that causes hemorrhagic disease in deer." Laramie, Wyo. : University of Wyoming, 2007. http://proquest.umi.com/pqdweb?did=1495962561&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Campbell, Hamish George, and n/a. "The functions of p53 during an adenovirus infection." University of Otago. Dunedin School of Medicine, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080411.115504.

Full text
Abstract:
p53 is a pivotal tumour suppressor in mammalian cells. It protects the integrity of a number of cellular pathways, preventing the malignant transformation of cells. There is however perhaps nothing more efficient at disrupting cellular pathways than a virus. Viruses infiltrate cells commandeering the normal growth and survival pathways for their narcissistic needs. While the association between viral infections and the induction of p53 has long been recognised, there is controversy surrounding the ultimate role of p53 during a virus infection. The classical model of p53 in an adenovirus infection is that p53 is a formidable obstacle which needs to be overcome. Adenoviruses overcome p53 by degrading the protein and removing its ability to transactivate its target genes. However the degradation is not immediate and there is increasing evidence which would suggest p53 is actually beneficial to an adenovirus infection. In the introductory chapter, I review what is known about p53 and virus infections. What emerges from this review is the sheer number of interactions that occur between viruses and p53, indicating its importance in an infection. Additionally it shows that adenoviruses are not the only virus shown to benefit from the presence of p53. What beneficial role p53 may be fulfilling in an adenovirus infection is unclear. The experiments reported in this thesis investigate the functions of p53 in an adenovirus infection. In Chapter Three, immunoblots on a panel of adenovirus infected cells reveal that p53 levels do not correlate with the level of the classical p53 target proteins. This indicates that p53 is disconnected from its target genes during an infection. Promoter/reporter assays carried out on infected cells show that adenovirus can directly regulate p53 target genes independently of p53. In Chapter Five, I show this regulation is dependent on E1a, with transient transfection of E1a resulting in the marked activation of p53 target promoters. E1a mediated transactivation appears to be reliant on the largest splice variant of E1a (E1a-289R) and the presence of pRB. Electrophoresis mobility shift assays reveal that the transcription factor Sp1 is involved. In Chapter Four, p53 transcription in an adenovirus infection was directly assayed by using an artificial p53 consensus response element. The results show that p53 is unable to activate its consensus response element during an infection. However, I show that p53 is transcriptionally competent in an infection, and is able to transactivate a mutant derivative of the p53 consensus sequence. This shows that p53 is not only transcriptional competent but has a gain-of-function in an infection. This gain-of-function requires E1a, and appears not to be due to a change in the DNA binding affinity of p53. The data in this thesis show that adenoviruses not only appear to inhibit and control the normal transcriptional profile of p53 but appear to modify p53, giving it a new transcriptional profile. This provides a possible mechanism by which p53 could aid an adenovirus infection.
APA, Harvard, Vancouver, ISO, and other styles
3

Dahl, Noelle Parisi. "Effect of pre-existing adenovirus neutralizing antibody on vector infectivity and transgene expression." Click here for download, 2010. http://proquest.umi.com.ps2.villanova.edu/pqdweb?did=2013968771&sid=1&Fmt=2&clientId=3260&RQT=309&VName=PQD.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tai, Yunlin 1962. "Functional studies on the coxsackie and adenovirus receptor (CAR) in skeletal muscle cells." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31548.

Full text
Abstract:
CAR (for C&barbelow;oxsackievirus and A&barbelow;denovirus R&barbelow;eceptor) is a novel member of the Ig superfamily, which has recently been identified as a high affinity receptor for both Coxsackievirus and certain adenovirus (AV) serotypes. Virus bound by CAR is believed to be passed to integrins which bind an RGD (Arg-Gly-Asp) sequence in the viral penton base protein and act as secondary receptors responsible for virus internalization.
Recent studies have shown that, in integrin-expressing cells, CAR-mediated AV uptake does not require the cytoplasmic (CP) domain of CAR, presumably because virus bound to the CAR extracellular (EC) domain can be passed to integrins for subsequent internalization. It has however also been reported that CAR can directly mediate AV uptake in the absence of penton base RGD-alphav integrin interactions. I therefore attempted to determine whether the CP domain of CAR is required for CAR-mediated AV uptake in cells which do not express integrins, or in which integrin function has been blocked by RGD-containing peptide.
As CAR is the primary AV receptor and integrins are secondary AV receptors I investigated the possibility that these proteins associate in a functional complex in the cell membrane. (Abstract shortened by UMI.)
APA, Harvard, Vancouver, ISO, and other styles
5

Segerman, Anna. "Adenovirus species B: receptors, tropism and hematopoietic cells." Doctoral thesis, Umeå : Klinisk mikrobiologi, Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-303.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Rauma-Pinola, T. (Tanja). "Adenovirus endocytosis and adenoviral gene transfer in cardiovascular and dermatologic disease models." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514274342.

Full text
Abstract:
Abstract Adenoviral gene transfer is a valuable tool in molecular biology research. In order to be an efficient and safe vector, adenovirus structure and infection mechanism as well as molecular biology of the used transgene need to be well studied. The aim of this study was to evaluate the role of adenovirus as a gene transfer vector from several perspectives. Adenovirus uses receptor-mediated endocytosis in order to enter the target cell. The effect of Rab5 GTPase on adenovirus entry and gene transfer efficiency was examined first. Next, adenovirus was used as an investigatory tool in the cardiovascular research, focused on clarifying the role of adrenomedullin (AM) in heart and vascular remodeling. Finally, a model of adenoviral gene transfer into skin fibroblasts was used. The role of Rab5 GTPase in the adenovirus endocytosis was examined in HeLa cells using Cy3-labeled adenovirus, and gene transfer efficiency using β-galactosidase encoding adenovirus. Rab5 increased both adenovirus uptake and gene transfer, whereas dominant negative Rab5S34N decreased both endocytosis and gene transfer. The data indicate that Rab5 is needed in mediating the adenovirus uptake into the target cell. In the rat heart, adenovirus-mediated AM gene transfer transiently improved systolic function both in vivo and in vitro. AM caused activation of translocation of protein kinases C ε and δ, whereas phosphorylation of p38 mitogen activated protein kinase was decreased in the left ventricle. AM significantly attenuated the development of angiotensin II-induced cardiac hypertrophy. In rats with myocardial infarction, AM enhanced dilatation of left ventricle and thinning of anterior wall. The role of AM in neointima formation was evaluated in rat artery after endothelial injury. Intravascular AM gene transfer decreased neointimal growth and increased neointimal myofibroblasts apoptosis. These results show that AM regulates left ventricular systolic function and remodeling in the heart, and plays a role in pathological vascular remodeling. Adenovirus-mediated lysyl hydroxylase (LH) gene transfer into skin fibroblasts of type VI Ehlers-Danlos syndrome patient and rat skin increased functional LH production, elevated LH activity, and human LH mRNA production both in vitro and in vivo. LH gene replacement therapy may thus lead to possibilities to improve skin wound healing in Ehlers-Danlos syndrome patients.
APA, Harvard, Vancouver, ISO, and other styles
7

Forbes, Emily K. "Enhancing the efficacy of viral vector blood-stage malaria vaccines." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:a51e20cd-dfdb-45fe-9fe0-7231c77afe1f.

Full text
Abstract:
Replication-deficient adenovirus (Ad) and modified vaccinia virus Ankara (MVA) vectors expressing single Plasmodium falciparum antigens can induce potent T cell and antibody responses and have entered clinical testing using a heterologous prime-boost immunisation approach (Ad_MVA). This thesis describes a number of pre-clinical approaches aimed at enhancing the efficacy of these viral vectored vaccines targeting the blood-stage of malaria. First, the development of a highly efficacious malaria vaccine is likely to require a multi-antigen and/or multi-stage subunit vaccine. The utility of an Ad_MVA immunisation regime combining vaccines expressing the 42kDa C-terminus of the blood- stage antigen merozoite surface protein 1 (MSP142) and the pre-erythrocytic antigen circumsporozoite protein (CSP) in the P. yoelii mouse model was investigated. It was found that vaccine co- administration leads to maintained antibody responses and efficacy against blood-stage infection, but reduced secondary CD8+ T cell responses and efficacy against liver-stage infection. CD8+ T cell interference can be minimised by co-administering the MVA vaccines at separate sites, resulting in enhanced liver-stage efficacy. The mechanisms of CD8+ T cell interference were explored. Second, Ad_MVA regimes expressing blood-stage antigens that can protect against P. chabaudi and P. yoelii blood-stage infection were tested against P. berghei, but did not confer protection. Similarly, IgG from rabbits immunised against P. falciparum MSP1 (PfMSP1) could not protect mice from a chimeric P. berghei parasite expressing PfMSP1. Third, two molecular adjuvants, the C4bp α-chain oligomerisation domain (IMX108/313) and the Fc fragment of murine IgG2a, were tested for their ability to enhance immunogenicity of recombinant adenoviruses when fused at the C-terminus of a blood-stage antigen. IMX108/313 was found to adjuvant T cell responses of small (< 80kDa) antigens and this was associated with antigen oligomerisation. However, the Fc fragment did not adjuvant responses. Finally, it was found that using a strong early promoter to drive antigen expression enhances the immunogenicity of single administration MVA vaccines, but that this did not enhance post-boost immunogenicity in an Ad_MVA regime.
APA, Harvard, Vancouver, ISO, and other styles
8

Loustalot, Fabien. "Study of CAR membrane dynamics in adenovirus infection and CAR endogenous role in healthy and diseased brain." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT029.

Full text
Abstract:
Les pathogènes neurotropiques représentent une banque d’outils biologique afin de cibler spécifiquement le système nerveux central (SNC), pour son étude mais aussi dans l’optique d’une thérapie. Parmi eux, l’adénovirus canin de type 2 (CAV-2) est un vecteur prometteur pour cibler le SNC. CAR a été principalement étudié en tant que récepteur viral. Cependant, plusieurs études montrent que CAR est essentiel dans le développement du cœur ainsi que du système lymphatique. De manière intéressante, CAR est fortement exprimé pendant le développement du SNC, suggérant un rôle dans l’établissement des réseaux neuronaux. Dans ce travail, nous avons confirmé que CAR est lié aux mécanismes d’endocytoses et au trafic intracellulaire. L’endocytose de CAR est ligand dépendant. La partie intracellulaire de CAR régule son endocytose. Nos données suggèrent que CAR est l’unique récepteur pour CAV-2. Le présent travail de recherche montre aussi que CAR ne semble pas participer à la formation du SNC. En revanche, au niveau du SNC mature, CAR est impliqué dans la plasticité synaptique, dans la neurogénèse adulte et participe à l’homéostasie des synapses, mécanismes impliqués dans les processus mnésiques
The coxsackievirus and adenovirus receptor (CAR) is a single-pass transmembrane protein belonging to the CTX subfamily of the immunoglobulin superfamily. CAR has been extensively studied as a viral receptor for coxsackie B viruses and some adenoviruses (AdVs). CAR is essential for the development of the cardiovascular and lymphatic system. Interestingly, CAR is highly expressed in the developing brain and has been hypothesized to regulate the establishment of the neuronal networks. In my PhD work, I showed that CAR can be link to the endocytic pathways and intracellular trafficking. CAR endocytosis is ligand-dependent and is regulated by CAR intracellular domain (ICD), suggesting strongly that CAR is most likely the unique receptor for canine adenovirus type 2 (CAV-2). Moreover, we demonstrated that CAR depletion in the developing brain did not significantly perturb brain development. In the healthy adult brain, CAR is relatively abundant and we demonstrated that CAR loss of function affected hippocampal plasticity, adult neurogenesis and synapse homeostasis, which affect cognition
APA, Harvard, Vancouver, ISO, and other styles
9

Chen, Chen. "Evaluation of the coxsackievirus and adenovirus receptor (CAR) as a therapeutic target in cardiac disease." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15980.

Full text
Abstract:
Der Coxsackievirus- und Adenovirusrezeptor (CAR) ist ein Typ I Transmembran-protein, das an der Adsorption von Viren und der Aufrechterhaltung von Zell-Zellkontakten beteiligt ist. Coxsackievirus B3 (CVB3) Infektionen sind eine häufige Ursache für akute Myokarditis, die bei Patienten häufig zu chronischer Kardiomyopathie bis zur Herzinsuffizienz führen können. CAR ist für die Aufnahme von Viren in unterschiedliche Zelltypen verantwortlich und damit ein potentielles Ziel bei der Therapie und Prävention von CVB3-Infektionen. Der komplette Knockout von CAR ist embryonal letal. Die betroffenen Embryonen zeigten Missbildungen des Herzens. Weiterhin konnte eine reduzierte Expression von Connexinen im Knockout beobachtet werden – ein mögliches Zeichen gestörter interzellulärer Kommunikation. In konditionellen CAR Knockout Tieren führte die Infektion mit CVB3 im Gegensatz zu CVB3-infizierten Wildtyp Kontrolltieren zu keinen pathologischen Veränderungen oder eine Erhöhung von Entzündungsmarkern. Die kontraktile Funktion des CVB3-infizierten Knockout Herzen war erhalten. Um mögliche unerwünschte Konsequenzen aus dem Verlust von CAR zu untersuchen, wurde eine umfassende kardiale Phänotypisierung durchgeführt, die AV-block im Knockout-Herzen zeigte. Der zugrunde liegende Mechanismus betrifft die Interaktion von Tight- und Gap-Junctions mit veränderter Expression und Lokalisierung von Connexinen, sowie die interzelluläre Kommunikation zwischen CAR-Knockout Kardiomyzeten. CAR ist essentiell für eine normale Embryonalentwicklung und kardiale Funktion. Das CAR-Knockout-Modell bietet einerseits den ersten genetischen Hinweis für eine Rolle von CAR als Virusrezeptor in vivo und belegt andererseits die Relevanz von direkter Virus-vermittelter Symptomatik gegenüber einer sekundären autoimmun- Komponente in CVB3-induzierten Herzerkrankungen. Damit ist CAR ein potentielles therapeutisches Target in der Prävention und Behandlung von viraler Myokarditis.
The coxsackievirus and adenovirus receptor (CAR) is a type I transmembrane protein involved in virus uptake and the maintenance of cell-cell contacts. Coxsackievirus B3 (CVB3) infections are frequent causes of human acute myocarditis, often resulting in chronic cardiomyopathy that may progress into terminal heart failure. The coxsackievirus and adenovirus receptor (CAR) is involved in virus uptake into various cell types and has therefore been suggested as a therapeutic target to prevent or treat CVB3 induced diseases. The complete CAR-knockout was embryonic lethal at midgestation with cardiac malformation. Connexin expression was decreased in the knockout, suggesting an abnormal cell-cell communication secondary to the loss of CAR. The role of CAR in murine viral myocarditis was investigated using the inducible CAR-knockout infected with CVB3. Unlike control animals exposed to CVB3, the cardiac inducible knockout mice did not exhibit structural changes such following CVB3 infection, or increased production of markers of inflammation, and severe contractile dysfunction. To evaluate possible adverse effects that might result from CAR deficiency, we implemented a detailed cardiac phenotyping protocol and found that CAR deficient animals developed AV nodal block. The underlying mechanism relates to the crosstalk of tight and gap junctions with altered expression and localization of connexins that affect the communication between CAR knockout cardiomyocytes. Thus, CAR is essential for embryonic development and normal cardiac function. The CAR-knockout does not only provide the first genetic evidence to establish CAR as the CVB3 receptor in vivo, but furthermore demonstrates the relevance of direct virus-mediated pathology versus a secondary autoimmune component in CVB3 induced heart disease. Our data suggest that CAR is a suitable target to help prevent and treat viral myocarditis.
APA, Harvard, Vancouver, ISO, and other styles
10

Kelly, Christabel. "Novel adenoviral vectored vaccines and the implications of viral diversity in therapeutic strategies against Hepatitis C Virus infection." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:8991c349-7096-4643-ae6a-2e36902c8056.

Full text
Abstract:
Hepatitis C virus (HCV) is a major global pathogen estimated to infect over 170 million people worldwide. A recent study has shown that vaccination with adenoviral vectors, based on rare human and simian serotypes encoding the non-structural (NS) proteins of HCV, induces highly potent, multi-specific and durable T cell responses in healthy human volunteers. In this thesis I assess the safety and immunogenicity of these vaccines (ChAd3–NSmut and Ad6-NSmut), for the first time in HCV infected patients. This work also explores whether vaccine-induced T cell responses target in vivo circulating HCV antigens and common naturally occurring epitope variants. Patients with treatment naive chronic genotype 1 HCV infection were vaccinated (i.m.) with ChAd3-NSmut and Ad6-NSmut in a heterologous prime boost schedule, either with or without current IFN and ribavirin (IFN/RBV). Epitope-specific T cell responses were defined by fine mapping using HCV peptides. Circulating viral genomic sequence was determined in vaccinated patients at baseline and at any point of viral relapse. Cross-reactivity of vaccine-induced T cell responses was determined in T cell assays, using peptides corresponding to both circulating host virus and common population HCV epitope variants. An in vitro dendritic cell /T cell priming model was used to identify possible candidates for a cross-reactive vaccine immunogen at the most immunodominant epitope, NS31406. 33 patients were vaccinated. Vaccination was well tolerated. At the highest vaccine dose (2.5 x 1010vp) vaccine-induced T cell responses were detectable in 11/20 patients receiving concurrent IFN/RBV and 2/4 patients receiving vaccination alone. In total 14 antigenic targets were identified, 2 of which have not previously been described. However, T cell responses were of lower magnitude and more narrowly focused than those observed in healthy volunteers vaccinated with the same regimen. Analysis of viral sequence showed that in many cases vaccine-induced T cells did not target the circulating virus. At the most immunodominant epitope (NS31406), T cells induced by vaccination failed to target common circulating genotype 1 HCV variants. An in vitro model suggested that in order to target all genotype 1 sequences at this epitope, it would be necessary to insert both a genotype 1a and 1b version of this epitope into a vaccine immunogen. Vaccination with adenoviral vectors induces T cell responses in patients with chronic HCV infection, however immune responses are attenuated compared with healthy volunteers. Ultimately a successful therapeutic or prophylactic vaccine strategy will rely on inducing responses that target conserved or cross-reactive epitopes.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Adenovirus diseases"

1

István, Nász. Az adenovírusok pathológiai jelentősége és molekuláris szerkezete: Akadémiai székfoglaló, 1986. február 20. Budapest: Akadémiai Kiadó, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

1933-, Doerfler Walter, and Böhm P, eds. The Molecular repertoire of adenoviruses. Berlin: Springer-Verlag, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Tabery, Helena M. Adenovirus epithelial keratitis and Thygeson's superficial punctate keratitis: In vivo morphology in the human cornea. Heidelberg: Springer, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

S, Di͡a︡chenko N., Smirnov V. V, Instytut mikrobiolohiï i virusolohiï im. D.K. Zabolotnoho., and Semmelweis Orvostudományi Egyetem. Mikrobiológiai Intézet., eds. Adenovirus, kletka, organizm. Kiev: Nauk. dumka, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Berger, Stephen, and Inc Gideon Informatics. Adenovirus Infection: Global Status. Gideon Informatics, Incorporated, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Berger, Stephen, and Inc Gideon Informatics. Adenovirus Infection: Global Status. Gideon Informatics, Incorporated, 2021.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

M, Wold William S., and Tollefson Ann E, eds. Adenovirus methods and protocols. 2nd ed. Totowa, N.J: Humana Press, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Babar, Shakeel. Characterization of adenovirus isolated from sheep in Oregon. 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

William S. M. Wold (Editor) and Ann E. Tollefson (Editor), eds. Adenovirus Methods And Protocols: Adenoviruses, Ad Vectors, Quantitation, And Animal Models (Methods in Molecular Medicine). 2nd ed. Humana Press, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Doerfler, Walter, and Petra Böhm. Molecular Repertoire of Adenoviruses III: Biology and Pathogenesis. Springer London, Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Adenovirus diseases"

1

La Rosa, G., and E. Suffredini. "Adenovirus." In Handbook of Foodborne Diseases, 13–24. Boca Raton : Taylor & Francis, [2019] | Series: Food microbiology series | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2018. http://dx.doi.org/10.1201/b22030-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Decaro, Nicola, Canio Buonavoglia, Kevin Eatwell, Károly Erdélyi, and J. Paul Duff. "Adenovirus Infections." In Infectious Diseases of Wild Mammals and Birds in Europe, 210–18. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118342442.ch14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Cesaro, Simone, Silvio Ragozzino, and Nina Khanna. "Polyomavirus, Adenovirus, and Viral Respiratory Diseases." In Hematologic Malignancies, 191–219. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-57317-1_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Doerfler, Walter. "Discoveries in Molecular Genetics with the Adenovirus 12 System: Integration of Viral DNA and Epigenetic Consequences." In Epigenetics of Infectious Diseases, 47–63. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55021-3_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Müller, Claudia, Timothy A. Blenkinsop, Jeffrey H. Stern, and Silvia C. Finnemann. "Efficiency of Membrane Protein Expression Following Infection with Recombinant Adenovirus of Polarized Non-Transformed Human Retinal Pigment Epithelial Cells." In Retinal Degenerative Diseases, 731–37. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_97.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Friedman, Allan D., and Sean O. McKenna. "Adenoviruses." In The Neurological Manifestations of Pediatric Infectious Diseases and Immunodeficiency Syndromes, 127–33. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-391-2_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kagnoff, M. F. "Celiac Disease: Adenovirus and Alpha Gliadin." In Current Topics in Microbiology and Immunology, 67–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74594-2_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Dieleman, L. A., A. S. Peña, H. van Doorninck, M. L. Mearin, W. van Duijn, and C. B. H. W. Lamers. "Negative Humoral Response to Adenovirus 12 in Coeliac Disease." In Coeliac Disease, 191. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-015-7943-8_37.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Wadell, G. "Adenoviridae: The Adenoviruses." In Laboratory Diagnosis of Infectious Diseases Principles and Practice, 284–300. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3900-0_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Brunetti-Pierri, Nicola, and Philip Ng. "Helper-dependent adenoviral vectors." In Gene Therapy for Autoimmune and Inflammatory Diseases, 193–207. Basel: Springer Basel, 2010. http://dx.doi.org/10.1007/978-3-0346-0165-8_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Adenovirus diseases"

1

Jorgensen, C., F. Apparailly, C. Bouquet, V. Millet, D. Noel, P. Yeh, and J. Sany. "THU0076 Adenovirus mediated gene transfer of urokinase plasminogen inhibitor inhibits angiogenesis in experimental arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.953.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Dudler, J., R. Salvi, N. Busso, V. Chobaz-Péclat, and A. So. "OP0033 Systemic adenovirus mediated gene therapy using a chimeric soluble il-1 receptor type ii ?igg protein reduces acute inflammation in antigen-induced arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.818.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Gounis, Matthew J., Baruch B. Lieber, Keith A. Webster, Bernard J. Wasserlauf, Howard M. Prentice, and Ajay K. Wakhloo. "Angiographic Quantification of Angiogenesis." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43196.

Full text
Abstract:
Therapeutic angiogenesis is the attempt to increase vascular density by means of an exogenously administered proangiogenic agent and offers a potential treatment for diseases associated with tissue ischemia. Vascular endothelial growth factor (VEGF) expressed by gene therapy has been shown to be a potent stimulator of angiogenesis and to improve the function of ischemic tissues in patients [Isner, 1998]. Unregulated gene therapy is disconcerting since there is no assurance that the treatment will target the ischemic territory. A new regulated adeno-associated viral vector expressing VEGF165 that is conditionally silenced has been developed by one of the authors (KAW). The transgene expression is regulated by silencing the genes in the absence of the disease and at the same time having strong and local activation in the presence of the disease. The purpose of this work is to establish protocols and techniques to quantify the efficacy of therapeutic angiogenesis. The initial phase of this research involves assessment of angiogenesis using an unregulated, adenoviral vector that is encoded to express VEGF165. Using the rabbit hind limb ischemia model, angiography was performed on animals that were given the proangiogenic treatment and on a sham group, in which phosphate buffered saline (PBS) was injected. Angiographic contrast intensity curves were obtained, modeled, and the optimized model parameters provided insight into flow characteristics within the targeted vascular bed. In the second phase of the project the conditionally silent vector will be employed using the developed protocols and methods of the first phase to afford comparisons with the previous groups.
APA, Harvard, Vancouver, ISO, and other styles
4

Hadi, Azzawi Mustafa, Israa Hashim Saadoon, and Wirya Ahmed Tofiq. "Rate of Adenovirus Infection in Patients with End Stage Renal Disease in Kirkuk Governorate." In 1st International Ninevah Conference on Medical Sciences (INCMS 2021). Paris, France: Atlantis Press, 2021. http://dx.doi.org/10.2991/ahsr.k.211012.009.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Schett, G., S. Hayer, M. Tohidast-Akrad, Q. Xu, G. Kollias, G. Steiner, and J. Smolen. "FRI0074 Adenoviral-based overexpression of timp-1 reduces tissue damage in the joints of tnf-a-transgenic mice." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1203.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Gunay, Melih, Evgin Goceri, and Taner Danisman. "Automated Detection of Adenoviral Conjunctivitis Disease from Facial Images using Machine Learning." In 2015 IEEE 14th International Conference on Machine Learning and Applications (ICMLA). IEEE, 2015. http://dx.doi.org/10.1109/icmla.2015.232.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Van de Loo, FA, AC Bakker, LA Joosten, V. Krasnykh, DT Curiel, and WB Van den Berg. "THU0048 Addition of the rgd motif in the fibre knob of an adenoviral vector improved the transfection efficiency and when used for overexpression of il-1ra resulted in a more effective inhibition of arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.845.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Demirci, T., I. Laniado, C. Alviar, D. Pradhan, and R. Postelnicu. "Severe Adenovirus Acute Respiratory Distress Syndrome (ARDS) Requiring Veno-Venous Extracorporeal Membrane Oxygenation (VV-ECMO) in the Era of Coronavirus Disease 2019 (COVID-19): A Case Report." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1665.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Adenovirus diseases"

1

Grubman, Marvin J., Yehuda Stram, Peter W. Mason, and Hagai Yadin. Development of an Empty Viral Capsid Vaccine against Foot and Mouth Disease. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570568.bard.

Full text
Abstract:
Foot-and-mouth disease (FMD), a highly infectious viral disease of cloven-hoofed animals, is economically the most important disease of domestic animals. Although inactivated FMD vaccines have been succesfully used as part of comprehensive eradication programs in Western Europe, there are a number of concerns about their safety. In this proposal, we have attempted to develop a new generation of FMD vaccines that addresses these concerns. Specifically we have cloned the region of the viral genome coding for the structural proteins and the proteinase responsible for processing of the structural protein precursor into both a DNA vector and a replication-deficient human adenovirus. We have demonstrated the induction of an FMDV-specific immune response and a neutralizing antibody response with the DNA vectors in mice, but preliminary potency and efficacy studies in swine are variable. However, the adenovirus vector induces a significant and long-lived neutralizing antibody response in mice and most importantly a neutralizing and protective response in swine. These results suggest that the empty capsid approach is a potential alternative to the current vaccination strategy.
APA, Harvard, Vancouver, ISO, and other styles
2

Kolavic, Shellie, Jose Sanchez, Leonard Binn, Marcela Echavarria, and Bruce Innis. Acute Respiratory Disease and Adenovirus Infection Among U.S Army Basic Trainees At Ft. Jackson, South Carolina 1998. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada381351.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Adenovirus diseases' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography