Relevant bibliographies by topics / Virus induced diseases

Contents

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

Academic literature on the topic 'Virus induced diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Virus induced diseases"

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Ludewig, Burkhard, Rolf M. Zinkernagel, and Hans Hengartner. "Transgenic Animal Models for Virus-Induced Autoimmune Diseases." Experimental Physiology 85, no. 6 (November 2000): 653–59. http://dx.doi.org/10.1111/j.1469-445x.2000.02093.x.

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Mori, Isamu, Takayuki Komatsu, Kenji Takeuchi, Kazuya Nakakuki, Masakatsu Sudo, and Yoshinobu Kimura. "Viremia induced by influenza virus." Microbial Pathogenesis 19, no. 4 (October 1995): 237–44. http://dx.doi.org/10.1016/s0882-4010(95)90290-2.

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M.G.M. Verjans, Georges, and Arnd Heiligenhaus. "Herpes Simplex Virus-Induced Ocular Diseases: Detrimental Interaction Between Virus and Host." Current Immunology Reviews 7, no. 3 (August 1, 2011): 310–27. http://dx.doi.org/10.2174/157339511796196557.

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Petrishcheva, Olga. "HIV-induced diseases in adults." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 5 (May 1, 2020): 12–19. http://dx.doi.org/10.33920/med-10-2005-02.

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Now, when the coronavirus pandemic has swept the whole world, few people recall that AIDS was called the plague of XX century. Manifestations of acquired immunodeficiency syndrome are the terminal stage of infection of the body with the human immunodeficiency virus, which belongs to retroviruses and leads to the development of secondary immunodeficiency. The first case of HIV infection in an adult was described in 1981 in America. A young homosexual sought help for a fungal infection resistant to treatment in one of the hospitals of San Francisco. Some time after the treatment, pneumonia developed in the young man, from the complications of which he soon died. Human immunodeficiency virus got its name only in 1982, and the disease caused by it began to be called acquired immunodeficiency syndrome. Today there are more than 40 million infected people in the world, 2/3 of whom live in Africa. Nearly 100 million people have been infected with HIV since the beginning of the epidemic, and the number of victims is twice as much as the number of people killed in the World War I. Despite the fact that this infection is not transmitted by airborne droplets, in the household and via contact, the growth rate of this disease continues to shock. So, every day about 5 thousand people in the world become infected with HIV, about 1 million die every year from the complications of this disease. It should be noted that only 71% of infected people know about their status, while all the rest continue to be a potential source of the spread of this terrible infection.
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Rose, John W. "Virus-Induced Demyelination: From Animal Models to Human Diseases." Mayo Clinic Proceedings 67, no. 9 (September 1992): 903–6. http://dx.doi.org/10.1016/s0025-6196(12)60833-7.

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Brault, Charlène, Pierre Levy, and Birke Bartosch. "Hepatitis C Virus-Induced Mitochondrial Dysfunctions." Viruses 5, no. 3 (March 21, 2013): 954–80. http://dx.doi.org/10.3390/v5030954.

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Akkina, Ramesh K., and Kevin P. Raisch. "Intracellular virus-induced polypeptides of pestivirus border disease virus." Virus Research 16, no. 1 (April 1990): 95–105. http://dx.doi.org/10.1016/0168-1702(90)90046-e.

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ABRAMSON, JON S., and J. GARY WHEELER. "Virus-induced neutrophil dysfunction." Pediatric Infectious Disease Journal 13, no. 7 (July 1994): 643–52. http://dx.doi.org/10.1097/00006454-199407000-00012.

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Dakhama, Azzeddine, Young Mok Lee, and Erwin W. Gelfand. "Virus-Induced Airway Dysfunction." Pediatric Infectious Disease Journal 24, Supplement (November 2005): S159—S169. http://dx.doi.org/10.1097/01.inf.0000188155.46381.15.

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Bondada, Megha, Yongxiu Yao, and Venugopal Nair. "Multifunctional miR-155 Pathway in Avian Oncogenic Virus-Induced Neoplastic Diseases." Non-Coding RNA 5, no. 1 (March 13, 2019): 24. http://dx.doi.org/10.3390/ncrna5010024.

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MicroRNAs (miRNAs) are small noncoding RNAs that fine-tune the responses of the cell by modulating the cell transcriptome and gene expression. MicroRNA 155 (miR-155) is a conserved multifunctional miRNA involved in multiple roles including the modulation of the immune responses. When deregulated, miR-155 can also contribute to cancer as has been demonstrated in several human malignancies such as diffuse large B cell lymphoma, chronic lymphocytic leukemia, as well as in Epstein–Barr virus (EBV)-induced B cell transformation. Avian oncogenic viruses such as Marek’s disease virus (MDV), avian leukosis virus (ALV), and reticuloendotheliosis virus (REV) that account for more than 90% of cancers in avian species, also make use of the miR-155 pathway during oncogenesis. While oncogenic retroviruses, such as ALV, activate miR-155 by insertional activation, acutely transforming retroviruses use transduced oncogenes such as v-rel to upregulate miR-155 expression. MDV on the other hand, encodes a functional miR-155 ortholog mdv1-miR-M4, similar to the miR-155 ortholog kshv-miR-K11 present in Kaposi’s sarcoma-associated herpesvirus (KSHV). We have shown that mdv1-miR-M4 is critical for the induction of MDV-induced lymphomas further demonstrating the oncogenic potential of miR-155 pathway in cancers irrespective of the diverse etiology. In this review, we discuss on our current understanding of miR-155 function in virus-induced lymphomas focusing primarily on avian oncogenic viruses.
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Dissertations / Theses on the topic "Virus induced diseases"

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Foster, Rosalinda Gram. "Virus-Host Interactions in the Development of Avian Leukosis Virus-Induced Osteopetrosis: a Dissertation." eScholarship@UMMS, 1993. https://escholarship.umassmed.edu/gsbs_diss/180.

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Avian leukosis virus (ALV)-induced osteopetrosis is a proliferative disorder of the bone affecting the growth and differentiation of osteoblasts. Osteopetrosis is a polyclonal disease in which cells of the bone contain, on average, multiple viral DNA copies. Osteopetrotic bone is also characterized by the accumulation of unintegrated viral DNA, suggesting an atypical life cycle of the virus in the infected osteoblasts. To better understand virus-host interactions in the induction of osteopetrosis by ALVs, infected chick osteoblast cultures and osteopetrotic bone were examined for aspects of the virus life cycle and effects of infection on osteoblast function. Levels of infection and virus expression were compared in cultured osteoblasts and osteopetrotic bone. Osteopetrotic bone contained higher levels of viral DNA and correspondingly higher levels of viral proteins than infected osteoblast cultures, suggesting a higher viral load in the diseased bone. A significant level of mature Gag protein was present in the bone, suggesting the accumulation of mature virus particles in the diseased bone. It is possible that the accumulation of virus could facilitate the high levels of infection observed in the diseased bone. The mechanism by which unintegrated viral DNA persisted in osteopetrotic bone was investigated by examining the susceptibility of infected osteoblasts to superinfection. The results indicated that, in culture, infected osteoblasts were able to establish interference to superinfection. This suggests that the persistence of unintegrated viral DNA in osteopetrotic bone may not result from the continuing infection of productively infected osteoblasts. The effect of virus infection on osteoblast function was examined in the diseased bone and in osteoblast cultures. In infected chickens, osteoblast activity, as evidenced by the expression of osteoblast phenotypic markers, was increased only in chickens developing severe osteopetrosis. In culture, virus infection had no apparent effect on either the proliferation or differentiation of osteoblasts. This indicates that infection was itself not sufficient to perturb osteoblast function. Furthermore, it suggested that additional components of the bone may be required for ALV infection to induce the abnormal activity of osteoblasts observed in osteopetrosis.
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Gould, Keith Geoffrey. "Cytotoxic T cell recognition of the influenza A/PR/8/34 haemagglutinin." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293397.

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Masiri, Jongkit Murphy John F. "The nature of cucumber mosaic virus-induced symptoms in bell pepper (Capsicum annuum L.)." Auburn, Ala., 2009. http://hdl.handle.net/10415/1977.

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Zaver, Himesh, Momani Laith Al, Kalpit Devani, and Chakradhar M. Reddy. "Ledipasvir/sofosbuvir induced nephrotic syndrome: A challenging case of Hepatitis C management." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/80.

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ABSTRACT: Hepatitis C virus (HCV) is associated with various glomerulopathies and nephrotic syndrome. However nephrotic syndrome following treatment is rare. Ledipasvir/sofosbuvir (L/S) has recently come into favor in treating HCV due to its relatively mild side effects compared to the more traditional interferon therapy. To the best of our knowledge, there are no reported cases of nephrotic syndrome following treatment with L/S. We present a case of nephrotic syndrome suspected secondary to L/S in a patient with chronic kidney disease. Increased vigilance when assessing therapeutic options in HCV patients with renal comorbidities can improve patient outcomes. A 63 year-old male patient presented to the hospital with shortness of breath, and a two-week history of bilateral lower extremity edema. Past medical history was significant for liver cirrhosis secondary to Hepatitis C genotype Ia, hepatocellular carcinoma status post liver transplantation 6 months prior to admission and Stage 3b chronic kidney disease with baseline creatinine (Cr) approximately 1.5 mg/dl. Medications included L/S for HCV and tacrolimus and prednisone for post-transplant treatment. Patient’s vitals were stable and physical exam was remarkable for facial swelling, mainly on the eyelids, decreased breath sounds bilaterally, distended abdomen with a fluid wave, and 2-3+ pitting edema up to the knees on lower extremities bilaterally. Laboratory work-up was remarkable for low albumin of 3.0 g/dl, and total protein of 5.6 g/ dl. Creatinine of 1.8 mg/dl was elevated from patient’s baseline. HCV viral load was undetectable and electrolytes, transaminases and the complete blood count were within normal limits. Subsequently, urine protein to creatinine ratio was measured because of generalized swelling and hypoproteinemia, which was found to be significantly high at 8.80, compared to 0.04 one year prior. 24-hour total urine protein was found to be 2065 mg/day. Renal ultrasonography showed no hydronephrosis and was otherwise unremarkable. Renal biopsy however, revealed changes suggestive of membranoproliferative glomerulonephritis (MPGN] most likely secondary to HCV. No immune complexes, lambda/kappa light chains, or cryogloblin were appreciated. Nephrotoxic agents such as diuretics and corticosteroids were held. Tacrolimus trough was appropriate to dose level and was continued along with L/S. As admission progressed the patient’s creatinine continued to get worse and rose up to 4.3 mg/dl with persistent proteinuria. With tacrolimus trough levels within normal limits and given L/S was the most recently initiated drug, L/S was thought to be the culprit and was thus held. The renal function began to improve gradually, and the patient was discharged in stable condition with close follow up. Follow up one month later found creatinine and renal function return to baseline and proteinuria resolved. Our case shows that Ledipasvir/sofosbuvir may possibly be related to nephrotic syndrome in HCV patients. Although further studies are needed to prove the causality our case seeks to raise clinical suspicion and increase vigilance when assessing therapeutic options in HCV patients with renal comorbidities such as chronic kidney disease.
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Wong, Tsz-yeung, and 王子揚. "Molecular characterization of IBDV-induced apoptosis in vitro using cDNA microarrays." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36375998.

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Torok, Valeria Anna. "Biological and molecular variation among isolates of pea seed borne mosaic virus." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09pht686.pdf.

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Corrigendum inserted at the back. Includes bibliographical references (leaves 133-158). Ch. 1. General introduction -- ch. 2. General materials and methods -- ch. 3. Biological characterisation of Australian PSbMV isolates -- ch. 4. Developing nucleic acid based diagnostics for PSbMV -- ch. 5. Detection of PSbMV isolates by RT-PCR and RFLP analysis -- ch. 6. Developing an internal control for PSbMV RT-PCR -- ch. 7. Molecular analysis of the PSbMV VPG -- ch. 8. PSbMV sequence and phylogenetic analysis -- ch. 9. General discussion Sixteen pea seed borne mosaic virus (PSbMV) isolates were collected between 1995 and 1998. These isolates were biologically distinct yet serologically indistinguishable. The conclusion is that PSbMV is widespread and occurs at a low incidence in Australia. Reports sequence information on new isolates of PSbMV which has allowed genomic regions to be identified which distinguish PSbMV pathotypes and isolates; and, to the development of PSbMV nucleic acid hybridisation and RT-PCR assays.
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Magalo, Simone Issaca. "Evaluation of immunity and protection induced in pullets by the V4 oral vaccine against a pneumotropic velogenic Newcastle disease virus (NDV) strain." Diss., University of Pretoria, 2002. http://upetd.up.ac.za/thesis/available/etd-11042005-140706/.

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Yuen, Kit-man, and 阮潔雯. "Comparison of influenza A virus induced apoptosis in human respiratoryepithelial cells: an in vitro and ex vivostudy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47177019.

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Highly pathogenic avian influenza H5N1, which is panzootic in poultry, continues to spread and becomes endemic in Asia, Africa, and Europe. It causes human disease with high fatality (about 60%) and continues to pose a pandemic threat. The pathological lesions associated with human H5N1 disease is Acute Respiratory Distress Syndrome (ARDS). The biological basis underlying the development of ARDS in human H5N1 disease remains controversial. Clinical, animal and in vitro studies suggested that the differences between H5N1 influenza viruss and low pathogenic influenza viruses in regard to viral replication, tissue tropism and cytokine dysregulation may contribute to disease pathogenesis. We previously found delayed onset of apoptosis in influenza H5N1 virus infected human peripheral blood monocyte-derived macrophages. This may allow a longer survival time for the virus in target cells for prolonged viral replication, which may contribute to the pathogenesis of H5N1 disease. As human bronchial and alveolar epithelial cells are target cells of influenza virus, I explored if influenza H5N1 and H1N1 virus infected human respiratory epithelial cells displayed differential apoptotic response and dissected the apoptotic pathways triggered by influenza virus infection. In this study, the apoptotic response in highly pathogenic influenza H5N1 viruses, A/HK/483/97 and A/Vietnam/1203/04, their precursor avian influenza H9N2 virus, A/Quail/HK/G1/97, and seasonal H1N1 virus, A/HK/54/98 infected primary human alveolar and bronchial epithelial cells was compared by TUNEL. A delayed onset of apoptosis in influenza H5N1 viruses and avian H9N2 virus infected alveolar epithelial cells was observed; the pattern was similar in bronchial epithelial cells. Concomitantly, by Western blotting, a delay in caspase 3 activation in H5N1 virus (A/HK/483/97) infected alveolar epithelial cells compared to H1N1 virus (A/HK/54/98) infected cells was shown. Also, influenza H5N1 and H1N1 virus induced apoptosis through both intrinsic and extrinsic pathways in human alveolar epithelial cells. Chemokine IP-10 was differentially up-regulated in influenza H5N1 virus infected alveolar epithelial cells, but its relationship to the delayed onset of apoptosis requires further studies. TRAIL, an upstream signaling molecule of extrinsic apoptotic pathway, mRNA was up-regulated in influenza H5N1 infected alveolar epithelial cells but not in influenza H1N1 infected cells. Using recombinant viruses, I showed that the 627 amino acid residue on PB2 of H5N1 virus and mutation of amino acids on 253 and 591 residues on PB2 of H9N2 virus contribute to the TRAIL upregulation. Immunohistochemical staining of physiologically relevant ex vivo model of human bronchus showed that influenza H5N1 (A/Vietnam/3046/04) and H9N2 (A/Quail/HK/G1/97) virus did not infect human bronchi as well as human H1N1 (A/HK/54/98) virus. Profiling of apoptosis related genes showed that TRAIL tends to be up-regulated in H5N1 virus infected bronchi ex vivo. This study demonstrated the delayed onset of apoptosis by H5N1 virus infected respiratory epithelial cells may be a mean for influenza virus to have prolonged replication within the human respiratory tract and contribute to disease severity. The results generated provide a robust research agenda, yielding critical information that elucidate molecular mechanisms, such as TRAIL up-regulation, that may contribute to the virulence and pathogenesis in human H5N1 disease.
HKU 3 Minute Thesis Award, 2rd Runner-up (2011)
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Pathology
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Master of Philosophy
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Hansmann, Florian Heinrich [Verfasser]. "The pathogenic role of matrix metalloproteinases in a virus-induced mouse model of demyelinating diseases / Florian Heinrich Hansmann." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2012. http://d-nb.info/1024435393/34.

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Poulin, Louise. "Expression differentielle du produit du gene 'src' dans les tumeurs induites par le virus de sarcome aviaire = Differential expression of the 'src' gene product in tumor cells induced by avian sarcoma virus." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74020.

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Books on the topic "Virus induced diseases"

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Sandberg, Kristian. Characterization of the interferon-alpha/beta producing leukocytes and their responses to viral inducers. Uppsala: Sveriges Lantbruksuniversitet, 1991.

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Steven, Specter, Bendinelli Mauro, and Friedman Herman 1931-, eds. Virus-induced immunosuppression. New York: Plenum Press, 1989.

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M, Goldman J., Epstein M. A, and Leukaemia Research Fund, eds. Vaccine intervention against virus-induced tumours. Basingstoke, Hampshire: Macmillan, 1986.

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Vaccine Intervention Against Virus-induced Tumors (Leukaemia & Lymphoma Research). Mcgraw-Hill (Tx), 1986.

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Baker, Carlye Ann. Production and characterization of polyclonal and monoclonal antibodies to three virus-induced proteins of papaya ringspot virus type W. 1989.

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Jackson, Michael Keven. Nucleotide sequence of S reading frame and viral-induced trans-activation of caprine arthritis-encephalitis virus. 1990.

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Knowles, Donald P. Studies of the pathogenesis of viral-induced arthritis and the transcriptional organization of caprine arthritis-encephalitis virus. 1988.

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Norbert, Gilmore, Wainberg Mark A, Medical Research Council (Canada), Canada. National Advisory Committee on AIDS., and Workshop on Viral Mechanisms of Immunosuppression (1984 : Montréal, Quebec), eds. Viral mechanisms of immunosuppression: Proceedings of a workshop. New York: Liss, 1985.

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AIDS: Virus- or Drug Induced? Springer, 2011.

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Peter, Duesberg, ed. AIDS: Virus or drug induced? Dordrecht: Kluwer Academic Publishers, 1996.

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Book chapters on the topic "Virus induced diseases"

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Libbey, Jane E., and Robert S. Fujinami. "Virus-Induced Immunosuppression." In Polymicrobial Diseases, 375–87. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817947.ch19.

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Fraser, R. S. S. "Mechanisms of Induced Resistance to Virus Disease." In Mechanisms of Resistance to Plant Diseases, 373–404. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5145-7_9.

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Erokhina, Tatyana N. "THE USE OF MONOCLONAL ANTIBODIES IN PLANT PROTECTION AND FOR STUDYING VIRUS-INDUCED PATHOGENIC PROCESSES." In Virus Diseases and Crop Biosecurity, 89–99. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/978-1-4020-5298-9_8.

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Hosakote, Yashoda Madaiah, and Kempaiah Rayavara. "Respiratory Syncytial Virus-Induced Oxidative Stress in Lung Pathogenesis." In Oxidative Stress in Lung Diseases, 297–330. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9366-3_13.

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Liebert, Uwe G., and Volker ter Meulen. "Measles Virus Induced Autoimmune Reactions against Brain Antigen." In A Multidisciplinary Approach to Myelin Diseases II, 127–35. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2435-9_13.

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Gibbs, C. J. "Virus Induced Slow Infections of the Central Nervous System." In A Multidisciplinary Approach to Myelin Diseases, 285–302. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-0354-2_24.

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Schneider-Schaulies, Sibylle, and Volker ter Meulen. "Molecular Aspects of Measles-Virus-Induced Central Nervous System Diseases." In Molecular Neurovirology, 419–48. Totowa, NJ: Humana Press, 1992. http://dx.doi.org/10.1007/978-1-4612-0407-7_11.

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Claoué, C., and S. Howie. "Immunological Aspects of Anterior Segment Disease of the Eye Induced by Herpes Simplex Virus." In Immunology of Eye Diseases, 23–40. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2490-1_3.

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Villar, C. J., T. N. Fredrickson, and C. A. Kozak. "Effect of the Gv-1 Locus on Moloney Ecotropic Murine Leukemia Virus Induced Disease in Inbred Wild Mice." In Genetics of Immunological Diseases, 250–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-50059-6_38.

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Ricci, Angela, Silvia Sabbadini, Laura Miozzi, Bruno Mezzetti, and Emanuela Noris. "Host-induced gene silencing and spray-induced gene silencing for crop protection against viruses." In RNAi for plant improvement and protection, 72–85. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789248890.0072.

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Abstract Since the beginning of agriculture, plant virus diseases have been a strong challenge for farming. Following its discovery at the very beginning of the 1990s, the RNA interference (RNAi) mechanism has been widely studied and exploited as an integrative tool to obtain resistance to viruses in several plant species, with high target-sequence specificity. In this chapter, we describe and review the major aspects of host-induced gene silencing (HIGS), as one of the possible plant defence methods, using genetic engineering techniques. In particular, we focus our attention on the use of RNAi-based gene constructs to introduce stable resistance in host plants against viral diseases, by triggering post-transcriptional gene silencing (PTGS). Recently, spray-induced gene silencing (SIGS), consisting of the topical application of small RNA molecules to plants, has been explored as an alternative tool to the stable integration of RNAi-based gene constructs in plants. SIGS has great and innovative potential for crop defence against different plant pathogens and pests and is expected to raise less public and political concern, as it does not alter the genetic structure of the plant.
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Conference papers on the topic "Virus induced diseases"

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Bessis, N., V. Cottard, D. Mulleman, and MC Boissier. "OP0023 Adeno-associated virus encoding for il-4 inhibits collagen-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-2001.948.

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Roos, Raymond P., Katsuhisa Masaki, Yoshifumi Sonobe, and Ghanashyam Ghadge. "TDP-43 PROTEINOPATHY IN THE PATHOGENESIS OF THEILER'S MURINE ENCEPHALOMYELITIS VIRUS INDUCED DISEASES." In Viruses: Discovering Big in Small. TORUS PRESS, 2019. http://dx.doi.org/10.30826/viruses-2019-10.

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Luz, Jeniffer, Scenio De Araujo, Caio Abreu, Juvenal Silva Neto, and Carlos Gulo. "Formation of a cooperation network in Mato Grosso on Machine Learning and Image Analysis: Diagnosis of COVID-19 in X-ray images." In Computer on the Beach. São José: Universidade do Vale do Itajaí, 2021. http://dx.doi.org/10.14210/cotb.v12.p523-524.

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Since the beginning of the COVID-19 outbreak, the scientific communityhas been making efforts in several areas, either by seekingvaccines or improving the early diagnosis of the disease to contributeto the fight against the SARS-CoV-2 virus. The use of X-rayimaging exams becomes an ally in early diagnosis and has been thesubject of research by the medical image processing and analysiscommunity. Although the diagnosis of diseases by image is a consolidatedresearch theme, the proposed approach aims to: a) applystate-of-the-art machine learning techniques in X-ray images forthe COVID-19 diagnosis; b) identify COVID-19 features in imagingexamination; c) to develop an Artificial Intelligence model toreduce the disease diagnosis time; in addition to demonstrating thepotential of the Artificial Intelligence area as an incentive for theformation of critical mass and encouraging research in machinelearning and processing and analysis of medical images in the Stateof Mato Grosso, in Brazil. Initial results were obtained from experimentscarried out with the SVM (Support Vector Machine) classifier,induced on a publicly available image dataset from Kaggle repository.Six attributes suggested by Haralick, calculated on the graylevel co-occurrence matrix, were used to represent the images. Theprediction model was able to achieve 82.5% accuracy in recognizingthe disease. The next stage of the studies includes the study of deeplearning models.
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He, Qin, Rubin Wang, and Xiaochuan Pan. "This paper presents a two-dimensional histogram shifting technique for reversible data hiding algorithm. In order to avoid the distortion drift caused by hiding data into stereo H.264 video, we choose arbitrary embeddable blocks from 4×4 quantized discrete cosine transform luminance blocks which will not affect their adjacent blocks. Two coefficients in each embeddable block are chosen as a hiding coefficient pair. The selected coefficient pairs are classified into different sets on the basis of their values. Data could be hidden according to the set which the value of the coefficient pair belongs to. When the value of one coefficient may be changed by adding or subtracting 1, two data bits could be hidden by using the proposed method, whereas only one data bit could be embedded by employing the conventional histogram shifting. Experiments show that this two-dimensional histogram shifting method can be used to improve the hiding performance." In 10th International Conference on Software Engineering and Applications (SEAS 2021). AIRCC Publishing Corporation, 2021. http://dx.doi.org/10.5121/csit.2021.110205.

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Arc, one virus-like gene, crucial for learning and memory, was dis-covered by researchers in neurological disorders fields, Arc mRNA’s single directed path and allowing protein binding regional restric-tively is a potential investigation on helping shuttle toxic proteins responsible for some diseases related to memory deficiency. Mean time to switching (MTS) is calculated explicitly quantifying the switching process in statistical methods combining Hamiltonian Markov Chain(HMC). The model derived from predator and prey with typeII functional response studies the mechanism of normals with intrin-sic rate of increase and the persisters with the instantaneous discovery rate and converting coefficients. During solving the results, since the numeric method is applied for the 2D approximation of Hamiltonion with intrinsic noise induced switching combining geometric minimum action method. In the application of Hamiltonian Markov Chain, the behavior of the convertion (between mRNA and proteins through 6 states from off to on ) is described with probabilistic conditional logic formula and the final concentration is computed with both Continuous and Discret Time Markov Chain(CTMC/DTMC) through Embedding and Switching Diffusion. The MTS, trajectories and Hamiltonian dynamics demonstrate the practical and robust advantages of our model on interpreting the switching process of genes (IGFs, Hax Arcs and etc.) with respects to memory deficiency in aging process which can be useful in further drug efficiency test and disease curing. Coincidentally, the Hamiltonian is also well used in describing quantum mechanics and convenient for computation with time and position information using quantum bits while in the second model we construct, switching between excitatory and inhibitory neurons, similarity of qubit and neuron is an interesting object as well. Especially with the interactions operated with phase gates, the excitation from the ground state to excitation state is a well analogue to the neuron excitation. Not only on theoretical aspect, the experimental methods in neuron switching model is also inspiring to quantum computing. Most basic one is as stimulate hippocampus can be identical to spontaneous neural excitation(|g>|e>), pi-pulse is utilized to drive the ground state to the higher state. There thus exists prosperous potential to study the transfer between states with our switch models both classical and quantum computationally.
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Sohn, Kyoung Min. "IDDF2019-ABS-0020 Acute cholestatic hepatitis induced by epstein-barr virus infection in an adult." 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.242.

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Ansari, Sana, Imran Shafi, Aiza Ansari, Jamil Ahmad, and Syed Ismail Shah. "Diagnosis of liver disease induced by hepatitis virus using Artificial Neural Networks." In 2011 IEEE 14th International Multitopic Conference (INMIC). IEEE, 2011. http://dx.doi.org/10.1109/inmic.2011.6151515.

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Vlahos, Ross, John Stambas, Grant Drummond, and Stavros Selemidis. "NOX2 OXIDASE AS A THERAPEUTIC TARGET IN INFLUENZA A VIRUS-INDUCED LUNG DISEASE." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6189.

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Shpagina, L., I. Shpagin, O. Kotova, G. Kuznetsova, D. Gerasimenko, and E. Anikina. "Virus-Induced Exacerbations of Occupational Chronic Obstructive Pulmonary Disease in Workers Exposed to Industrial Aerosols." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3055.

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Ansar, M., T. Ivanciuc, A. Casola, and R. P. Garofalo. "Intranasal Administration of Catalase Ameliorates Respiratory Syncytial Virus-Induced Airway Disease Via Modulation of Innate Immune Responses." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5899.

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Kanthou, C., C. Parker, D. E. Huber, P. Stroobant, V. V. Kakkar, N. Pringle, and W. Richardson. "PLATELET-DERIVED GROWTH FACTORA-CHAIN GENE ACTIVATION AND GROWTH FACTOR PRODUCTION BY HUMAN AORTIC SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643751.

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The many contributory factors leading to the development of cardiovascular disease are currently thought to induce a common pathological change involving smooth muscle cells, which migrate from the vessel wall, proliferate,accumulate at the sites of endothelial cell damage, and then secrete connective tissue proteins and lipids which contribute to the plaque which results in the occlusion of the vessel. According to the recently modified hypothesis of Ross (1), a key event in the development of atheroma may be the abnormal release of a number of growth modulatory polypeptides,including platelet-derived growth factor (PDGF), which can potentially originate from platelets, endothelial cells, monocytes or macrophages, and smooth muscle cells themselves.We have isolated smooth muscle cell lines from 25 samples of human aorta, using digestion with collagenase and elastase. With DNA synthesis and Northern blot techniques, we examined them for both the production of PDGF-like proteins, and for the possible activation of the PDGF A-chain and B-chain genes. Severallines secreted a growth factor and were stillviable after culture for 57 days in serum-free medium. Parallel experiments using Northernblot analysis revealed the activation of the PDGF A-chain gene in all lines examined with no detectable B-chain gene transcripts.These data raise the possibility that vascular damage may activate the gene encoding the A-chain of PDGF in adjacent smooth muscle cells. Such cells might then become capable ofautonomous growth, in an analogous manner tocells transformed by Simian Sarcoma Virus, whose sis oncogene encodes the B-chain of PDGF.
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Reports on the topic "Virus induced diseases"

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Loy, Duan S., Lyric C. Bartholomay, and D. L. Hank Harris. Direct Delivery of VP19 Double-Stranded RNA into Litopenaeus vannamei by Reverse Gavage Induces Protection against White Spot Syndrome Virus Disease. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-798.

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