Relevant bibliographies by topics / Viral disease

Contents

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

Academic literature on the topic 'Viral disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 May 2022

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Journal articles on the topic "Viral disease"

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Severson, Jessica L., and Stephen K. Tyring. "Viral disease update." Current Problems in Dermatology 11, no. 2 (March 1999): 37–70. http://dx.doi.org/10.1016/s1040-0486(99)90007-8.

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Stovin, P. "Viral Heart Disease." Journal of Clinical Pathology 38, no. 3 (March 1, 1985): 358. http://dx.doi.org/10.1136/jcp.38.3.358-b.

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Montague, Terrence J., Gary D. Lopaschuk, and Norman J. Davies. "Viral Heart Disease." Chest 98, no. 1 (July 1990): 190–99. http://dx.doi.org/10.1378/chest.98.1.190.

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Gulbahce, Natali, Han Yan, Marc Vidal, and Albert-Laszlo Barabasi. "Viral Disease Networks." Biophysical Journal 98, no. 3 (January 2010): 196a. http://dx.doi.org/10.1016/j.bpj.2009.12.1040.

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Billiau, A. "Viral heart disease." Antiviral Research 5, no. 1 (February 1985): 63. http://dx.doi.org/10.1016/0166-3542(85)90019-1.

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TAPPER, M. L. "Emerging viral diseases and infectious disease risks." Haemophilia 12, s1 (March 2006): 3–7. http://dx.doi.org/10.1111/j.1365-2516.2006.01194.x.

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Franchini, Genoveffa, Richard F. Ambinder, and Michèle Barry. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation.v2000.1.409.20000409.

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As part of the international outreach of the American Society of Hematology, this review addresses some aspects of the genetics, biology, epidemiology, and clinical relevance of viruses that cause a variety of hematopoietic disorders in human populations. The viruses described here have a different pattern of geographical distribution, and the disease manifestations may vary according to environmental and/or genetic characteristics of the host. Epstein-Barr virus, a linear double-stranded DNA virus (herpesvirus), and the human T-cell leukemia virus, a retrovirus with a single-stranded diploid RNA genome, are associated among other diseases with lymphoma and leukemia/lymphoma, respectively. Both viruses cause a lifelong infection, but only a small percentage of infected individuals develop hematopoietic neoplasms. Epidemiological data suggest that the time of infection may be important in determining disease outcome in both HTLV-I and EBV infection. The pathogenic mechanisms used by these viruses are of most interest since they may recapitulate growth dysregulation steps also occurring in other hematopoietic malignancies.In Section I Dr. Franchini reviews the biology, genetics and diseases associated with HTLV-I and HTLV-II. In Section II, Dr. Ambinder reviews the biology of EBV infection and its relationship to the pathogenesis of Hodgkin's disease and other malignancies.In Section III, Dr. Barry reviews the viral hemorrhagic fevers caused by RNA viruses such as Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae, which can lead to acute syndromes that can be fatal. However, prompt diagnosis is key for patient management as well as for limiting their spread to others. These syndromes have become the focus of public concern and represent not only a clinical challenge, since in most cases no specific antiviral treatment is available, but also a challenge for future basic research on their biology and pathogenesis since little is known at present.
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Franchini, Genoveffa, Richard F. Ambinder, and Michèle Barry. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation.v2000.1.409.409.

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Abstract As part of the international outreach of the American Society of Hematology, this review addresses some aspects of the genetics, biology, epidemiology, and clinical relevance of viruses that cause a variety of hematopoietic disorders in human populations. The viruses described here have a different pattern of geographical distribution, and the disease manifestations may vary according to environmental and/or genetic characteristics of the host. Epstein-Barr virus, a linear double-stranded DNA virus (herpesvirus), and the human T-cell leukemia virus, a retrovirus with a single-stranded diploid RNA genome, are associated among other diseases with lymphoma and leukemia/lymphoma, respectively. Both viruses cause a lifelong infection, but only a small percentage of infected individuals develop hematopoietic neoplasms. Epidemiological data suggest that the time of infection may be important in determining disease outcome in both HTLV-I and EBV infection. The pathogenic mechanisms used by these viruses are of most interest since they may recapitulate growth dysregulation steps also occurring in other hematopoietic malignancies. In Section I Dr. Franchini reviews the biology, genetics and diseases associated with HTLV-I and HTLV-II. In Section II, Dr. Ambinder reviews the biology of EBV infection and its relationship to the pathogenesis of Hodgkin's disease and other malignancies. In Section III, Dr. Barry reviews the viral hemorrhagic fevers caused by RNA viruses such as Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae, which can lead to acute syndromes that can be fatal. However, prompt diagnosis is key for patient management as well as for limiting their spread to others. These syndromes have become the focus of public concern and represent not only a clinical challenge, since in most cases no specific antiviral treatment is available, but also a challenge for future basic research on their biology and pathogenesis since little is known at present.
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Burgart, L. J. "Cholangitis in viral disease." Mayo Clinic Proceedings 73, no. 5 (May 1, 1998): 479–82. http://dx.doi.org/10.4065/73.5.479.

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Liesegang, Thomas J. "Varicella Zoster Viral Disease." Mayo Clinic Proceedings 74, no. 10 (October 1999): 983–98. http://dx.doi.org/10.4065/74.10.983.

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Dissertations / Theses on the topic "Viral disease"

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Gangadharan, Bevin. "Proteomics in viral disease." Thesis, University of Oxford, 2006. http://ora.ox.ac.uk/objects/uuid:c66c53ed-a824-4f99-8f2b-d2bc65a984c7.

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The separation, identification, and characterisation of the proteins present in a tissue or biological sample is called ‘proteomics’. This technique can be used for example to identify biomarkers and investigate signalling pathways. Increasingly, proteomics is being applied to the analysis of virus related samples; here two such examples are described. Presently there is no reliable non-invasive way of assessing liver fibrosis. Here a novel 2D-PAGE based proteomics study was used to identify potential fibrosis biomarkers. Serum from patients with varying degrees of hepatic scarring induced by infection with the hepatitis C virus (HCV) was analysed. Several proteins associated with liver scarring and/or viral infection were identified. The most prominent changes were observed when comparing serum samples from cirrhotic patients with healthy controls: Expression of inter-α-trypsin inhibitor heavy chain H4 fragments, α1 antichymotrypsin, apolipoprotein L1 (Apo L1), prealbumin and albumin was decreased in cirrhotic serum, whereas CD5 antigen like protein (CD5L) and β2 glycoprotein I (β2GPI) increased. In general, α2 macroglobulin (a2M) and immunoglobulin components increased with hepatic fibrosis whereas haptoglobin and complement components (C3, C4 and factor H-related protein 1) decreased. Novel proteins associated with HCV-induced fibrosis include the inter-alpha-trypsin inhibitor heavy chain H4 fragments, complement factor H-related protein 1, CD5L, Apo L1, β2GPI and the increase in thiolester cleaved products of a2M. The relationship between these changes is discussed. One of the accessory genes of the HIV viral genome encodes for the Nef protein. Nef is present in lipid rafts and increases viral replication within infected host cells by binding to a guanine nucleotide exchange factor, Vav. This leads to activation of a GTPase, Cdc42, however, the signalling pathway is poorly understood. 2D-PAGE based proteomics was used to identify differentially expressed raft-associated proteins by comparing T cells in the presence and absence of Nef. A ubiquitin conjugating enzyme UbcH7, which acts in conjugation with c-Cbl, was absent from the rafts of Nef-transfected cells. Vav ubiquitination was also absent from these rafts. In collaboration with Dr. Alison Simmons and Prof. Andrew McMichael the absence of UbcH7 in rafts was found to be caused by β-Pix forming a ternary complex with c-Cbl and activated Cdc42. Vav ubiquitination was restored and viral replication was diminished when β-Pix was knocked down providing a new candidate target for inhibiting HIV replication. This thesis demonstrates the use of proteomics in providing novel information for virus related samples. This influential technology benefits in both biomarker discovery to aid clinicians with early diagnosis of diseased individuals and in the elucidation of novel signalling pathways in infected cells to provide new candidate targets.
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Fleeton, Marina N. "Genetic vaccination against acute viral disease /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3811-3/.

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Leo, Nancy Stefany. "Viral Antibodies and Immunoregulation in Autoimmune Disease." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/271610.

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The link between autoimmune diseases and viral infections has long been under scrutiny, with potential mechanisms including viral persistence and viral transactivation of cellular cytokine promoters coupling the two phenomenon. In this study, the relationship between autoimmune disease and the persistence of non-structural NS1 human parvovirusB19 (B19V) protein in serum from patients with SLE and RA was investigated. The hypothesis was that due to a failure in the viral host’s ability to silence persistent viral protein transcripts, non-structural NS1 protein remains elevated in individuals with autoimmune disease (post-infection) and contributes to exacerbation of the disease. To test this hypothesis, anti-PARVO non-structural NS1 antibodies were detected in the serum of 15 SLE subjects. B-cell hybridomas from a patient with SLE secreting elevated levels of anti-PARVO non-structural NS1 IgG were generated, which secreted stable human IgG mAbs specific to non-structural NS1. Six mAb hybridoma sub-clones were isolated with low binding titers to the full length (FLNS1). The sub-clones, however, demonstrated increased binding activity to the nuclease domain of NS1. Optimization of the mAb screening system will be performed for future research, which will facilitate the purification and characterization of the human anti-PARVO non-structural NS1 mAbs.
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Quinlivan, Mark Lee. "Viral genetic variation in varicella zoster virus disease." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418302.

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Stoppelkamp, Sandra. "New viral and transgenic models of Alzheimer's disease." Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=136906.

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Mutated human genes associated with human neurodegenerative conditions were used to develop both in vitro and in vivo models to study cellular pathology and disease progression. The in vitro models employed adenoviral vectors for the gene delivery into primary rat hippocampal neurones. Introduction of both APP and Tau transgenes reduced neuronal viability, with the latter leading to accelerated toxicity and faster onset of cell death. Time-lapsing imaging analyses revealed apoptosis-like features for APP-positive neurones, while Tau-positive neuronal death appeared more necrotic. Interestingly, a direct correlation between cell death and protein content in the APP-transduced neurones was not confirmed. A comparison between viral gene delivery and electroporation with the same transgenic constructs confirmed the cellular toxicity of APP and Tau but also showed that with a lower amount of transgene expressing cells per culture dish Tau-induced toxicity was no longer as aggressive as with the viral model. Therefore, electroporation may allow single-cell investigations of functional parameters whereas the large amount of transgene-positive neurones in viral transductions allows faster quantification of cell death. These methods complement each other and thus offer in vitro models suitable for mechanistic studies and drug screening. Accordingly, initial testing of inhibitors of Tau aggregation and amyloid formation were found to ameliorate the transgene-induced damage as proof of principle for our novel in vitro models. Further testing revealed caffeine to be a very promising drug candidate in AD treatment, since it improved viability in both APP and Tau transduced neurones. The transgenic PLB1 mouse knock-in model harbours the same mutated APP and Tau genes as the viral models. A triple transgenic line (PLB1Triple) has been generated with additional mutated presenilin 1 for increased APP processing and accelerated pathology. The mRNA expression of both APP and Tau transgenes was stable over the investigated time (6 and 12 months) with about 2 to 3-fold higher APP over Tau mRNA levels. This expression was specific to the forebrain and negligible in the cerebellum and thus targets a brain region that is vulnerable in AD. The model showed progressive accumulation of AD-linked histopathological features as well as memory- and activity-related symptoms. This low transgene expression in conjunction with a progressive phenotype is advantageous over other aggressive animals models for studying early disease-related pathology.
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Agarwal, Kaushik. "Immunogenetic studies in autoimmune and viral liver disease." Thesis, University of Newcastle upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275585.

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Silverstein, Noah J. "Disease Tolerance, Epigenetic Inheritance, and Surviving Pathogenic Viral Infections." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1149.

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Health is often defined in terms of absence of disease or pathological processes, but this is a definition of exclusion and incomplete. For example, SARS-CoV-2 viral load does not reliably predict disease severity, and so individuals must vary in their ability to control inflammation and maintain normal tissue homeostasis. This host defense strategy is called disease tolerance, and better understanding of disease tolerance mechanisms could change the way that we treat disease and work to maintain health. The first project presented in this dissertation found that after accounting for effects of age and sex, innate lymphoid cells (ILCs), but not T cells, were lower in adults and children sick with COVID-19 or MIS-C, independent of lymphopenia. Furthermore, abundance of ILCs, but not of T cells, correlated inversely with disease severity. These blood ILCs were shown to produce amphiregulin, a protein implicated in disease tolerance and tissue homeostasis, and the percentage of amphiregulin-producing ILCs was lower in males. These results suggest that, by promoting disease tolerance, homeostatic ILCs decrease morbidity and mortality associated with SARS-CoV-2 infection, and that lower ILC abundance accounts for increased COVID-19 severity with age and in males. The second project describes a novel mouse model of epigenetic inheritance wherein paternal influenza A virus (IAV) infection results in less severe influenza disease in IAV infected offspring. This offspring phenotype was not attributable to differences in viral load, indicating a possible difference in disease tolerance. Paternal caloric deprivation decreased, and influenza B virus infection increased, offspring influenza disease severity, and in vitro fertilization demonstrated sperm are sufficient to transfer IAV-associated epigenetic inheritance phenotypes. These findings represent a foundation for further work that, by continuing to elucidate the mechanisms of disease tolerance and epigenetic inheritance, could provide novel therapeutic interventions to help promote and maintain health.
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Dovigi, Allan Webster-Cyriaque Jennifer. "HIV salivary gland disease a role for viral infection /." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2005. http://dc.lib.unc.edu/u?/etd,297.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2006.
Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Oral and Maxillofacial Pathology School of Dentistry." Discipline: Oral and Maxillofacial Pathology; Department/School: Dentistry.
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Nitsovych, I. R. "Treatment of polyhydramnios caused by acute respiratory viral disease." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18719.

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Moody, Adrian John. "Mapping genetic resistance to infectious bursal disease." Thesis, University of Reading, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326754.

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Books on the topic "Viral disease"

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Nishioka, K., H. Suzuki, S. Mishiro, and T. Oda, eds. Viral Hepatitis and Liver Disease. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68255-4.

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Greenberg, Stephen. Laboratory diagnosis of viral respiratory disease. Washington, DC: American Society for Microbiology, 1986.

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Dessain, Scott K., ed. Human Antibody Therapeutics for Viral Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72146-8.

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Schultheiß, Heinz-Peter, ed. New Concepts in Viral Heart Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73610-0.

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Council on Community Health, Hospital, Institutional, and Medical Affairs. Ad Hoc Committee on Protocol Development. Patients with hepatic disease. Chicago, Ill: American Dental Association, 1990.

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Chisari, Francis V., and Michael B. A. Oldstone, eds. Transgenic Models of Human Viral and Immunological Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-85208-4.

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J, Zuckerman Arie, ed. Viral hepatitis and liver disease: Proceedings of the International Symposium on Viral Hepatitis and Liver Disease, held at the Barbican Centre, London, May 26-28, 1987. New York: Liss, 1988.

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Viral sex: The nature of AIDS. New York: Oxford University Press, 1997.

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International Symposium on Viral Hepatitis and Liver Disease (9th 1996 Rome, Italy). Viral hepatitis and liver disease: Proceedings of IX Triennial International Symposium on Viral Heptatis and Liver Disease, Rome, Italy, 21-25 April 1996. Edited by Rizzetto Mario. Turin: Edizioni Minerva Medica, 1997.

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Blaine, Hollinger F., Lemon Stanley M, and Margolis Harold, eds. Viral hepatitis and liver disease: Proceedings of the 1990 International Symposium on Viral Hepatitis and Liver Disease : contemporary issues and future prospects. Baltimore: Williams & Wilkins, 1991.

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Book chapters on the topic "Viral disease"

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Farver, Carol, Subha Ghosh, Thomas Gildea, and Charles D. Sturgis. "Viral Infections." In Pulmonary Disease, 295–306. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47598-7_21.

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McManus, Bruce M., Michael Seidman, Karin Klingel, and Honglin Luo. "Viral Heart Disease." In Clinical Virology, 99–113. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819439.ch7.

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Chan, Anthony W. H., Alberto Quaglia, Beate Haugk, and Alastair Burt. "Viral Liver Disease." In Atlas of Liver Pathology, 85–103. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9114-9_6.

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Scoazec, Jean-Yves. "Viral Hepatitis." In Infectious Disease and Parasites, 317–21. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30009-2_1081.

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Adle-Biassette, Homa. "Viral Infections." In Infectious Disease and Parasites, 321–28. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30009-2_1082.

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Nomura, Yasuya, Yasuya Nomura, and Yasuya Nomura. "Viral Diseases." In Morphological Aspects of Inner Ear Disease, 117–46. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54204-9_6.

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Hornig, Mady. "Borna Disease Virus." In Neurotropic Viral Infections, 315–36. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33133-1_13.

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Falsey, Ann R. "Viral Infections." In Infectious Disease in the Aging, 225–42. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1007/978-1-59259-026-1_19.

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Duncan, Coley B., and Ann R. Falsey. "Viral Infections." In Infectious Disease in the Aging, 367–84. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-534-7_23.

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Relich, Ryan F. "Viral Infections." In Atlas of Infectious Disease Pathology, 75–100. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54702-2_3.

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Conference papers on the topic "Viral disease"

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Stengel, R. F., R. Ghigliazza, N. Kulkarni, and O. Laplace. "Optimal control of a viral disease." In Proceedings of American Control Conference. IEEE, 2001. http://dx.doi.org/10.1109/acc.2001.946229.

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MACKENZIE, JOHN S. "EMERGING VIRAL DISEASES: THE ROLE OF WILDLIFE IN DISEASE EMERGENCE." In International Seminar on Nuclear War and Planetary Emergencies 34th Session. WORLD SCIENTIFIC, 2006. http://dx.doi.org/10.1142/9789812773890_0017.

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DAS, NANDA, and SAMARES PA. "EFFECT OF VIRAL DISEASE IN A DIFFUSIVE PLANKTON SYSTEM." In International Symposium on Mathematical and Computational Biology. WORLD SCIENTIFIC, 2015. http://dx.doi.org/10.1142/9789814667944_0006.

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Cheung, Dorothy S., Lauren E. Camarda, Sarah J. Ehlenbach, Desire A. Hunter, and Mitchell H. Grayson. "Neutrophil Subsets In The Development Of Post-Viral Atopic Disease." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2562.

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Saydalieva, Mahruy, Mohiniso Hidirova, and Abrorjon Turgunov. "Analysis of different clinical forms of viral hepatitis B disease." In 2021 International Conference on Information Science and Communications Technologies (ICISCT). IEEE, 2021. http://dx.doi.org/10.1109/icisct52966.2021.9670258.

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Le Roux, Mélina, Gwenola Kervoaze, Laurent Gillet, Muriel Pichavant, and Philippe Gosset. "Induction of IL-20 Cytokines during Viral Exacerbations of Chronic Obstructive Pulmonary Disease." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.yi02.

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Hussain, Akram, and Yuan Luo. "Privacy Aware Contact Tracing by Exploiting Social Networks in Viral Disease Outbreaks." In GLOBECOM 2020 - 2020 IEEE Global Communications Conference. IEEE, 2020. http://dx.doi.org/10.1109/globecom42002.2020.9322077.

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Nguyen, Thi Hiep, Fiona Eyers, Ming Yang, and Paul Foster. "Azithromycin modulates viral-induced asthma exacerbation by targeting the innate immune response." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp217.

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Akarapatima, Keerati, and Tatsanai Sattayaraksa. "IDDF2019-ABS-0097 The relationship between hepatic steatosis and result of viral hepatitis C treatment." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.264.

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Spalluto, Cosma Mirella, Alastair Watson, Christopher Mccrae, Doriana Cellura, Hannah Burke, Danen Cunoosamy, Anna Freeman, et al. "Dynamics of IFN-β responses during respiratory viral infection: insights for therapeutic strategies." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp126.

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Reports on the topic "Viral disease"

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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.

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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.
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Kancheva, Lyudmila, Petar Nikolov, Tsvetelina Velikova, Ivan Valkov, Rossen Nikolov, and Lyudmila Mateva. Soluble CD14 is Associated with Disease Activity and Severity in Chronic Viral Hepatitis C and B. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2018. http://dx.doi.org/10.7546/crabs.2018.06.17.

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Xiao, Yong, Xiaojun Min, and Huixia Xiao. Bacterial and viral infection‐related risk of autoimmune thyroid disease: Meta‐analysis of cohort and case–control studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0051.

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Mawassi, Munir, Adib Rowhani, Deborah A. Golino, Avichai Perl, and Edna Tanne. Rugose Wood Disease of Grapevine, Etiology and Virus Resistance in Transgenic Vines. United States Department of Agriculture, November 2003. http://dx.doi.org/10.32747/2003.7586477.bard.

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Rugose wood is a complex disease of grapevines, which occurs in all growing areas. The disease is spread in the field by vector transmission (mealybugs). At least five elongated-phloem- limited viruses are implicated in the various rugose wood disorders. The most fully characterized of these are Grapevine virus A (GV A) and GVB, members of a newly established genus, the vitivirus. GVC, a putative vitivirus, is much less well characterized than GV A or GVB. The information regarding the role of GVC in the etiology and epidemiology of rugose wood is fragmentary and no sequence data for GVC are available. The proposed research is aimed to study the etiology and epidemiology of rugose wood disease, and to construct genetically engineered virus-resistant grapevines. The objectives of our proposed research were to construct transgenic plants with coat protein gene sequences designed to induce post-transcriptional gene silencing (pTGS); to study the epidemiology and etiology of rugose wood disease by cloning and sequencing of GVC; and surveying of rugose wood- associated viruses in Californian and Israeli vineyards. In an attempt to experimentally define the role of the various genes of GV A, we utilized the infectious clone, inserted mutations in every ORF, and studied the effect on viral replication, gene expression, symptoms and viral movement. We explored the production of viral RNAs in a GV A-infected Nicotiana benthamiana herbaceous host, and characterized one nested set of three 5'-terminal sgRNAs of 5.1, 5.5 and 6.0 kb, and another, of three 3'-terminal sgRNAs of 2.2, 1.8 and 1.0 kb that could serve for expression of ORFs 2-3, respectively. Several GV A constructs have been assembled into pCAMBIA 230 I, a binary vector which is used for Angrobacterium mediated transformation: GV A CP gene; two copies of the GV A CP gene arranged in the same antisense orientation; two copies of the GV A CP gene in which the downstream copy is in an antigens orientation; GV A replicase gene; GV A replicase gene plus the 3' UTR sequence; and the full genome of GV A. Experiments for transformation of N. benthamiana and grapevine cell suspension with these constructs have been initiated. Transgenic N. benthamiana plants that contained the CP gene, the replicase gene and the entire genome of GV A were obtained. For grapevine transformation, we have developed efficient protocols for transformation and successfully grapevine plantlets that contained the CP gene and the replicase genes of GV A were obtained. These plants are still under examination for expression of the trans genes. The construction of transgenic plants with GV A sequences will provide, in the long run, a means to control one of the most prevalent viruses associated with grapevines. Our many attempts to produce a cDNA library from the genome of GVC failed. For surveying of rugose wood associated viruses in California vineyards, samples were collected from different grape growing areas and tested by RT-PCR for GV A, GVB and GVD. The results indicated that some of the samples were infected with multiple viruses, but overall, we found higher incidence of GVB and GV A infection in California vineyards and new introduction varieties, respectively. In this research we also conducted studies to increase our understanding of virus - induced rootstock decline and its importance in vineyard productivity. Our results provided supporting evidence that the rootstock response to virus infection depends on the rootstock genotype and the virus type. In general, rootstocks are differ widely in virus susceptibility. Our data indicated that a virus type or its combination with other viruses was responsible in virus-induced rootstock decline. As the results showed, the growth of the rootstocks were severely affected when the combination of more than one virus was present.
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5

Bercovier, Herve, and Ronald P. Hedrick. Diagnostic, eco-epidemiology and control of KHV, a new viral pathogen of koi and common carp. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7695593.bard.

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Original objectives and revisions-The proposed research included these original objectives: field validation of diagnostic tests (PCR), the development and evaluation of new sensitive tools (LC-PCR/TaqManPCR, antibody detection by ELISA) including their use to study the ecology and the epidemiology of KHV (virus distribution in the environment and native cyprinids) and the carrier status of fish exposed experimentally or naturally to KHV (sites of virus replication and potential persistence or latency). In the course of the study we completed the genome sequence of KHV and developed a DNA array to study the expression of KHV genes in different conditions. Background to the topics-Mass mortality of koi or common carp has been observed in Israel, USA, Europe and Asia. These outbreaks have reduced exports of koi from Israel and have created fear about production, import, and movements of koi and have raised concerns about potential impacts on native cyprinid populations in the U.S.A. Major conclusions-A suite of new diagnostic tools was developed that included 3 PCR assays for detection of KHV DNA in cell culture and fish tissues and an ELISA assay capable of detecting anti-KHV antibodies in the serum of koi and common carp. The TKPCR assay developed during the grant has become an internationally accepted gold standard for detection of viral DNA. Additionally, the ELISA developed for detecting serum anti-KHV antibodies is now in wide use as a major nonlethal screening tool for evaluating virus status of koi and common carp populations. Real time PCR assays have been able to detect viral DNA in the internal organs of survivors of natural and wild type vaccine exposures at 1 and 10³ genome equivalents at 7 months after exposure. In addition, vaccinated fish were able to transmit the virus to naive fish. Potential control utilizing hybrids of goldfish and common carp for production demonstrated they were considerably more resistant than pure common carp or koi to both KHV (CyHV-3). There was no evidence that goldfish or other tested endemic cyprinids species were susceptible to KHV. The complete genomic sequencing of 3 strains from Japan, the USA, and Israel revealed a 295 kbp genome containing a 22 kbp terminal direct repeat encoding clear gene homologs to other fish herpesviruses in the family Herpesviridae. The genome encodes156 unique protein-coding genes, eight of which are duplicated in the terminal repeat. Four to seven genes are fragmented and the loss of these genes may be associated with the high virulence of the virus. Viral gene expression was studies by a newly developed chip which has allowed verification of transcription of most all hypothetical genes (ORFs) as well as their kinetics. Implications, both scientific and agricultural- The results from this study have immediate application for the control and management of KHV. The proposal provides elements key to disease management with improved diagnostic tools. Studies on the ecology of the virus also provide insights into management of the virus at the farms that farmers will be able to apply immediately to reduce risks of infections. Lastly, critical issues that surround present procedures used to create “resistant fish” must be be resolved (e.g. carriers, risks, etc.). Currently stamping out may be effective in eradicating the disease. The emerging disease caused by KHV continues to spread. With the economic importance of koi and carp and the vast international movements of koi for the hobby, this disease has the potential for even further spread. The results from our studies form a critical component of a comprehensive program to curtail this emerging pathogen at the local, regional and international levels.
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6

Schmitt, Virgil L., and Kevin Van Dee. Effects of Cruiser Seed Treatment for Bean Leaf Beetle and Soybean Aphid Management on Soybean Yield and on Incidence of Viral Disease in Eastern Iowa. Ames: Iowa State University, Digital Repository, 2006. http://dx.doi.org/10.31274/farmprogressreports-180814-1091.

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7

Ehrlich, Marcelo, John S. Parker, and Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

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Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizootic Hemorrhagic Disease Virus (EHDV) in Israel, underscore the need for: (i) a better comprehension of the infection process of orbiviruses, (ii) the identification of unique vs. common traits among different orbiviruses, (iii) the development of novel diagnosis and treatment techniques and approaches; all aimed at the achievement of more effective control and treatment measures. It is the context of these broad goals that the present project was carried out. To fulfill our long-term goal of identifying specific viral determinants of virulence, growth, and transmission of the orbiviruses, we proposed to: (i) develop reverse genetics systems for BTV and EHDV2-Ibaraki; and (ii) identify the molecular determinants of the NS3 nonstructural protein related to viroporin/viral egress activities. The first objective was pursued with a two-pronged approach: (i) development of a plasmid-based reverse genetics system for BTV-17, and (ii) development of an "in-vitro" transcription-based reverse genetics system for EHDV2-Ibaraki. Both approaches encountered technical problems that hampered their achievement. However, dissection of the possible causes of the failure to achieve viral spread of EHDV2-Ibaraki, following the transfection of in-vitro transcribed genomic segments of the virus, revealed a novel characteristic of EHDV2-Ibaraki infection: an uncharacteristically low fold increase in titer upon infection of different cell models. To address the function and regulation of NS3 we employed the following approaches: (i) development (together with Anima Cell Metrology) of a novel technique (based on the transfection of fluorescently-labeledtRNAs) that allows for the detection of the levels of synthesis of individual viral proteins (i.e. NS3) in single cells; (ii) development of a siRNA-mediated knockdown approach for the reduction in levels of expression of NS3 in EHDV2-Ibaraki infected cells; (iii) biochemical and microscopy-based analysis of the localization, levels and post-translational modifications of NS3 in infected cells. In addition, we identified the altered regulation and spatial compartmentalization of protein synthesis in cells infected with EHDV2-Ibaraki or the mammalian reovirus. In EHDV2-Ibaraki-infected cells such altered regulation in protein synthesis occurs in the context of a cell stress reponse that includes the induction of apoptosis, autophagy and activation of the stressrelated kinase c-Jun N-terminal Kinase (JNK). Interestingly, inhibition of such stress-related cellular processes diminishes the production of infectious virions, suggesting that EHDV usurps these responses for the benefit of efficient infection. Taken together, while the present project fell short of the generation of novel reverse genetics systems for orbiviruses, the development of novel experimental approaches and techniques, and their employment in the analysis of EHDV-infected cells, yielded novel insights in the interactions of orbiviruses with mammalian cells.
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8

David, Lior, Yaniv Palti, Moshe Kotler, Gideon Hulata, and Eric M. Hallerman. Genetic Basis of Cyprinid Herpes Virus-3 Resistance in Common Carp. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592645.bard.

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The goal of this project was to provide scientific and technical basis for initiating the development of breeding protocols using marker assisted selection for viral disease resistance in common carp. The specific objectives were: 1) Establishing families and characterizing the phenotypic and genetic variation of viral resistance; 2) Measuring the dynamics of immune response and developing a method to measure the long term immune memory; 3) Developing markers and generating a new genetic linkage map, which will enable initial QTL mapping; and, 4) Identifying genetic linkage of markers and candidate genes (like MHC and TLRs) with resistance to CyHV-3. The common carp is an important farmed freshwater fish species in the world. Edible carp is second only to tilapia in Israeli aquaculture production and ornamental carp (koi) is an important product in both the US and Israel. Carp industries worldwide have recently suffered enormous economic damage due to a viral disease caused by Cyprinid herpes virus 3 (CyHV-3). Aside from preventative measures, a sustainable solution to this problem will be to establish a genetic improvement program of the resistance of fish to the pathogen. The aims of the project was to take the necessary first steps towards that. The differences in survival rates after infection with CyHV-3 virus among 20 families from six types of crosses between three carp lines (two commercial lines and one wild-type carp) revealed that the wild-type carp and its crosses had a much-improved survival over the crosses of the commercial lines themselves. These crosses set the starting point for breeding of commercial strains with improved resistance. Resistant fish had lower antibody titer against the virus suggesting that resistance might depend more on the innate immunity. A set of 500 microsateliite markers was developed and the markers are currently being used for generating a genetic linkage map for carp and for identifying disease resistance QTL. Fourteen candidate immune genes, some of which were duplicated, were cloned from the carp and SNP markers were identified in them. The expression of these genes varied between tissues and suggested functional divergence of some duplicated genes. Initial association between CyHV-3 resistance and one of the genes was found when SNP alleles in these genes were tested for their segregation between susceptible and resistant progeny. The results of this project have implications to the development of viral resistant commercial carp strains and effective immunization against this aggressive disease. The genetic and immunological knowledge accumulated in this project will not only promote carp and koi production but will also contribute to a broader understanding of fish immunogenetics.
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9

Tignor, Gregory H. Drug Development against Viral Diseases. Fort Belvoir, VA: Defense Technical Information Center, February 1987. http://dx.doi.org/10.21236/ada201949.

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10

Citovsky, Vitaly, and Yedidya Gafni. Nuclear Import of the Tomato Yellow Curl Leaf Virus in Tomato Plants. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568765.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. In Israel the disease is well known and has an economic significance. In recent years viral symptoms were found in countries of the "New World" and since 1997, in Florida. Surprisingly, little is known about the molecular mechanisms of TYLCV interaction with the host plant cells. This proposal was aimed at expanding our understanding of the molecular mechanisms by which TYLCV enters the host cell nucleus. The main objective was to elucidate the TYLCV protein(s) involved in transport of the viral genomic DNA into the host cell nucleus. This goal was best served by collaboration between our laboratories one of which (V.C.) was already investigating the nuclear import of the T-DNA ofAgrobacterium tumefaciens, and the other (Y.G.) was studying the effect of TYLCV capsid protein (CP) in transgenic plants, hypothesizing its involvement in the viral nuclear entry. Three years of our collaborative work have provided signifcant data that strongly support our original hypothesis of the involvement of TYLCtr CP in viral nuclear import. Furthermore, our results have laid a foundation to study fundamental, but as yet practically unresolved, questions about the role ofthe host cell factors in the nuclear import of geminiviruses within their host plant. As a result, this research may lead to development of new approaches for plant protection based on control of TYLCV import to the host plant cell nucleus.
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