請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/78709完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 林宜玲 | |
| dc.contributor.author | Katy Rue-hsin Chang | en |
| dc.contributor.author | 張儒心 | zh_TW |
| dc.date.accessioned | 2021-07-11T15:13:45Z | - |
| dc.date.available | 2024-08-28 | |
| dc.date.copyright | 2019-08-28 | |
| dc.date.issued | 2019 | |
| dc.date.submitted | 2019-07-31 | |
| dc.identifier.citation | 1. Stanelle-Bertram, S., et al., Male offspring born to mildly ZIKV-infected mice are at risk of developing neurocognitive disorders in adulthood. Nat Microbiol, 2018. 3(10): p. 1161-1174.
2. Petersen, L.R., et al., Zika Virus. N Engl J Med, 2016. 374(16): p. 1552-63. 3. Shan, C., et al., An Infectious cDNA Clone of Zika Virus to Study Viral Virulence, Mosquito Transmission, and Antiviral Inhibitors. Cell Host & Microbe, 2016. 19(6): p. 891-900. 4. Lanciotti, R.S., et al., Genetic and serologic properties of Zika virus associated with an epidemic, Yap State, Micronesia, 2007. Emerging infectious diseases, 2008. 14(8): p. 1232-1239. 5. Duffy, M.R., et al., Zika Virus Outbreak on Yap Island, Federated States of Micronesia. New England Journal of Medicine, 2009. 360(24): p. 2536-2543. 6. Musso, D., E.J. Nilles, and V.M. Cao-Lormeau, Rapid spread of emerging Zika virus in the Pacific area. Clinical Microbiology and Infection, 2014. 20(10): p. O595-O596. 7. WHO, Situation report. Zika virus microcephaly Guillain-Barré syndrome. 2017. 8. Heukelbach, J., et al., Zika virus outbreak in Brazil. J Infect Dev Ctries, 2016. 10(2): p. 116-20. 9. de Oliveira, W.K., et al., Infection-related microcephaly after the 2015 and 2016 Zika virus outbreaks in Brazil: a surveillance-based analysis. The Lancet, 2017. 390(10097): p. 861-870. 10. Centers for Disease Control and Prevention, C. 2019 June 6, 2019; Available from: https://www.cdc.gov/zika/reporting/2019-case-counts.html. 11. Lo, D. and B. Park, Modeling the spread of the Zika virus using topological data analysis. PLoS One, 2018. 13(2): p. e0192120. 12. O'Reilly, K.M., et al., Projecting the end of the Zika virus epidemic in Latin America: a modelling analysis. BMC medicine, 2018. 16(1): p. 180-180. 13. Foy, B.D., et al., Probable non-vector-borne transmission of Zika virus, Colorado, USA. Emerg Infect Dis, 2011. 17(5): p. 880-2. 14. Nicastri, E., et al., Persistent detection of Zika virus RNA in semen for six months after symptom onset in a traveller returning from Haiti to Italy, February 2016. Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin, 2016. 21(32): p. 30314. 15. Musso, D., et al., Potential for Zika virus transmission through blood transfusion demonstrated during an outbreak in French Polynesia, November 2013 to February 2014. Euro Surveill, 2014. 19(14). 16. Gallian, P., et al., Zika virus in asymptomatic blood donors in Martinique. Blood, 2017. 129(2): p. 263-266. 17. Blohm, G.M., et al., Evidence for Mother-to-Child Transmission of Zika Virus Through Breast Milk. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2018. 66(7): p. 1120-1121. 18. Calvet, G., et al., Detection and sequencing of Zika virus from amniotic fluid of fetuses with microcephaly in Brazil: a case study. The Lancet Infectious Diseases, 2016. 16(6): p. 653-660. 19. Boyer, S., et al., An overview of mosquito vectors of Zika virus. Microbes and Infection, 2018. 20(11): p. 646-660. 20. Diallo, D., et al., Zika Virus Emergence in Mosquitoes in Southeastern Senegal, 2011. PLOS ONE, 2014. 9(10): p. e109442. 21. Ferreira-de-Brito, A., et al., First detection of natural infection of Aedes aegypti with Zika virus in Brazil and throughout South America. Mem Inst Oswaldo Cruz, 2016. 111(10): p. 655-658. 22. Kraemer, M.U.G., et al., The global distribution of the arbovirus vectors Aedes aegypti and Ae. albopictus. eLife, 2015. 4: p. e08347. 23. World Health Organization, W.P.E.S., Guidelines for efficacy testing of spatial repellents. 2013. 24. Achee, N.L., et al., Alternative strategies for mosquito-borne arbovirus control. PLOS Neglected Tropical Diseases, 2019. 13(1): p. e0006822. 25. Musso, D., E.J. Nilles, and V.M. Cao-Lormeau, Rapid spread of emerging Zika virus in the Pacific area. Clin Microbiol Infect, 2014. 20(10): p. O595-6. 26. Cardoso, C.W., et al., Outbreak of Exanthematous Illness Associated with Zika, Chikungunya, and Dengue Viruses, Salvador, Brazil. Emerg Infect Dis, 2015. 21(12): p. 2274-6. 27. Oehler, E., et al., Zika virus infection complicated by Guillain-Barre syndrome--case report, French Polynesia, December 2013. Euro Surveill, 2014. 19(9). 28. de Araujo, T.V.B., et al., Association between microcephaly, Zika virus infection, and other risk factors in Brazil: final report of a case-control study. Lancet Infect Dis, 2018. 18(3): p. 328-336. 29. Kikuti, M., et al., Congenital brain abnormalities during a Zika virus epidemic in Salvador, Brazil, April 2015 to July 2016. Euro Surveill, 2018. 23(45). 30. Mlakar, J., et al., Zika Virus Associated with Microcephaly. N Engl J Med, 2016. 374(10): p. 951-8. 31. Ventura, C.V., et al., Zika virus in Brazil and macular atrophy in a child with microcephaly. The Lancet, 2016. 387(10015): p. 228. 32. de Fatima Vasco Aragao, M., et al., Clinical features and neuroimaging (CT and MRI) findings in presumed Zika virus related congenital infection and microcephaly: retrospective case series study. BMJ, 2016. 353: p. i1901. 33. Pena, L.J., et al., In vitro and in vivo models for studying Zika virus biology. Journal of General Virology, 2018. 99(12): p. 1529-1550. 34. Miner, J.J. and M.S. Diamond, Zika Virus Pathogenesis and Tissue Tropism. Cell Host Microbe, 2017. 21(2): p. 134-142. 35. Matusali, G., et al., Zika virus infects human testicular tissue and germ cells. The Journal of Clinical Investigation, 2018. 128(10): p. 4697-4710. 36. Tang, H., et al., Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. Cell stem cell, 2016. 18(5): p. 587-590. 37. Li, C., et al., Zika Virus Disrupts Neural Progenitor Development and Leads to Microcephaly in Mice. Cell Stem Cell, 2016. 19(1): p. 120-126. 38. Li, H., et al., Zika Virus Infects Neural Progenitors in the Adult Mouse Brain and Alters Proliferation. Cell stem cell, 2016. 19(5): p. 593-598. 39. Hamel, R., et al., Biology of Zika Virus Infection in Human Skin Cells. Journal of Virology, 2015. 89(17): p. 8880-8896. 40. Nowakowski, Tomasz J., et al., Expression Analysis Highlights AXL as a Candidate Zika Virus Entry Receptor in Neural Stem Cells. Cell Stem Cell, 2016. 18(5): p. 591-596. 41. Retallack, H., et al., Zika virus cell tropism in the developing human brain and inhibition by azithromycin. Proceedings of the National Academy of Sciences, 2016. 113(50): p. 14408-14413. 42. Rausch, K., et al., Screening Bioactives Reveals Nanchangmycin as a Broad Spectrum Antiviral Active against Zika Virus. Cell Reports, 2017. 18(3): p. 804-815. 43. Fernando, S., et al., An Approach for Zika Virus Inhibition Using Homology Structure of the Envelope Protein. Molecular Biotechnology, 2016. 58(12): p. 801-806. 44. Munjal, A., et al., Advances in Developing Therapies to Combat Zika Virus: Current Knowledge and Future Perspectives. Frontiers in microbiology, 2017. 8: p. 1469-1469. 45. Bhatia, H.K., et al., Sofosbuvir: A novel treatment option for chronic hepatitis C infection. Journal of pharmacology & pharmacotherapeutics, 2014. 5(4): p. 278-284. 46. Sacramento, C.Q., et al., The clinically approved antiviral drug sofosbuvir inhibits Zika virus replication. Scientific Reports, 2017. 7: p. 40920. 47. Sierra, A., et al., The 'Big-Bang' for modern glial biology: Translation and comments on Pio del Rio-Hortega 1919 series of papers on microglia. Glia, 2016. 64(11): p. 1801-40. 48. Michell-Robinson, M.A., et al., Roles of microglia in brain development, tissue maintenance and repair. Brain, 2015. 138(Pt 5): p. 1138-59. 49. Derecki, N.C., et al., Microglia as a critical player in both developmental and late-life CNS pathologies. Acta Neuropathol, 2014. 128(3): p. 333-45. 50. Furube, E., et al., Brain Region-dependent Heterogeneity and Dose-dependent Difference in Transient Microglia Population Increase during Lipopolysaccharide-induced Inflammation. Scientific reports, 2018. 8(1): p. 2203-2203. 51. Town, T., V. Nikolic, and J. Tan, The microglial 'activation' continuum: from innate to adaptive responses. Journal of Neuroinflammation, 2005. 2(1): p. 24. 52. Zotova, E., et al., Inflammatory components in human Alzheimer’s disease and after active amyloid-β42 immunization. Brain, 2013. 136(9): p. 2677-2696. 53. de Haas, A.H., et al., Neuronal chemokines: versatile messengers in central nervous system cell interaction. Molecular neurobiology, 2007. 36(2): p. 137-151. 54. Frost, J.L. and D.P. Schafer, Microglia: Architects of the Developing Nervous System. Trends in cell biology, 2016. 26(8): p. 587-597. 55. Colonna, M. and O. Butovsky, Microglia Function in the Central Nervous System During Health and Neurodegeneration. Annu Rev Immunol, 2017. 35: p. 441-468. 56. Smith, J.A., et al., Role of pro-inflammatory cytokines released from microglia in neurodegenerative diseases. Brain Research Bulletin, 2012. 87(1): p. 10-20. 57. Martinez, F.O. and S. Gordon, The M1 and M2 paradigm of macrophage activation: time for reassessment. F1000prime reports, 2014. 6: p. 13-13. 58. Ransohoff, R.M., A polarizing question: do M1 and M2 microglia exist? Nature Neuroscience, 2016. 19: p. 987. 59. Negash, A.A., et al., IL-1β Production through the NLRP3 Inflammasome by Hepatic Macrophages Links Hepatitis C Virus Infection with Liver Inflammation and Disease. PLOS Pathogens, 2013. 9(4): p. e1003330. 60. Tang, Y. and W. Le, Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases. Molecular Neurobiology, 2016. 53(2): p. 1181-1194. 61. Colton, C.A., Heterogeneity of microglial activation in the innate immune response in the brain. Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2009. 4(4): p. 399-418. 62. Ponomarev, E.D., et al., CNS-Derived Interleukin-4 Is Essential for the Regulation of Autoimmune Inflammation and Induces a State of Alternative Activation in Microglial Cells. The Journal of Neuroscience, 2007. 27(40): p. 10714-10721. 63. Hu, X., et al., Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia. Stroke, 2012. 43(11): p. 3063-70. 64. Yang, M.-S., et al., Interleukin-13 and -4 induce death of activated microglia. Glia, 2002. 38(4): p. 273-280. 65. Chen, Z., D. Zhong, and G. Li, The role of microglia in viral encephalitis: a review. Journal of Neuroinflammation, 2019. 16(1): p. 76. 66. Quick, E.D., et al., Activation of intrinsic immune responses and microglial phagocytosis in an ex vivo spinal cord slice culture model of West Nile virus infection. Journal of virology, 2014. 88(22): p. 13005-13014. 67. Rock, R.B., et al., Role of microglia in central nervous system infections. Clinical microbiology reviews, 2004. 17(4): p. 942-964. 68. Polazzi, E. and A. Contestabile, Reciprocal interactions between microglia and neurons: from survival to neuropathology. Rev Neurosci, 2002. 13(3): p. 221-42. 69. Block, M.L., L. Zecca, and J.-S. Hong, Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nature Reviews Neuroscience, 2007. 8: p. 57. 70. Agbulos, D.S., et al., Zika Virus: Quantification, Propagation, Detection, and Storage. Curr Protoc Microbiol, 2016. 43: p. 15d.4.1-15d.4.16. 71. Lin, Y.L., et al., Study of Dengue virus infection in SCID mice engrafted with human K562 cells. J Virol, 1998. 72(12): p. 9729-37. 72. Chen, L.K., et al., Persistence of Japanese encephalitis virus is associated with abnormal expression of the nonstructural protein NS1 in host cells. Virology, 1996. 217(1): p. 220-9. 73. Barba-Spaeth, G., et al., Structural basis of potent Zika-dengue virus antibody cross-neutralization. Nature, 2016. 536(7614): p. 48-53. 74. Bagga, S. and M.J. Bouchard, Cell cycle regulation during viral infection. Methods Mol Biol, 2014. 1170: p. 165-227. 75. Walker, D.G. and L.-F. Lue, Immune phenotypes of microglia in human neurodegenerative disease: challenges to detecting microglial polarization in human brains. Alzheimer's research & therapy, 2015. 7(1): p. 56-56. 76. Badie, B., et al., Interferon-γ Induces Apoptosis and Augments the Expression of Fas and Fas Ligand by Microglia in Vitro. Experimental Neurology, 2000. 162(2): p. 290-296. 77. Savli, H., et al., Gene network and canonical pathway analysis in prostate cancer: a microarray study. Experimental & molecular medicine, 2008. 40(2): p. 176-185. 78. Krämer, A., et al., Causal analysis approaches in Ingenuity Pathway Analysis. Bioinformatics (Oxford, England), 2014. 30(4): p. 523-530. 79. Socodato, R., et al., Genetic ablation of RhoA in adult microglia causes synapse and neuronal loss. bioRxiv, 2017: p. 218107. 80. Kim, S.H., C.J. Smith, and L.J. Van Eldik, Importance of MAPK pathways for microglial pro-inflammatory cytokine IL-1β production. Neurobiology of Aging, 2004. 25(4): p. 431-439. 81. Ji, R.-R. and M.R. Suter, p38 MAPK, microglial signaling, and neuropathic pain. Molecular pain, 2007. 3: p. 33-33. 82. Light, A.R., et al., Purinergic receptors activating rapid intracellular Ca increases in microglia. Neuron Glia Biol, 2006. 2(2): p. 125-138. 83. Inoue, K., The function of microglia through purinergic receptors: neuropathic pain and cytokine release. Pharmacol Ther, 2006. 109(1-2): p. 210-26. 84. Van Steenwinckel, J., et al., Loss of the Wnt/β-catenin pathway in microglia of the developing brain drives pro-inflammatory activation leading to white matter injury. bioRxiv, 2018: p. 334359. 85. Brault, V., et al., Inactivation of the (β)-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development. Development, 2001. 128(8): p. 1253-1264. 86. Quintanilla, R.A., E. Utreras, and F.A. Cabezas-Opazo, Role of PPAR gamma in the Differentiation and Function of Neurons. PPAR Res, 2014. 2014: p. 768594. 87. Schafer, D.P. and B. Stevens, Microglia Function in Central Nervous System Development and Plasticity. Cold Spring Harbor Perspectives in Biology, 2015. 7(10). 88. Lum, F.M., et al., Zika Virus Infects Human Fetal Brain Microglia and Induces Inflammation. Clin Infect Dis, 2017. 64(7): p. 914-920. 89. Liu, J., et al., Interplay between human microglia and neural stem/progenitor cells in an allogeneic co-culture model. J Cell Mol Med, 2013. 17(11): p. 1434-43. 90. Homem, C.C.F., M. Repic, and J.A. Knoblich, Proliferation control in neural stem and progenitor cells. Nature reviews. Neuroscience, 2015. 16(11): p. 647-659. 91. Gieryng, A., et al., Immune microenvironment of experimental rat C6 gliomas resembles human glioblastomas. Scientific Reports, 2017. 7(1): p. 17556. 92. Elkabes, S., E. DiCicco-Bloom, and I. Black, Brain microglia/macrophages express neurotrophins that selectively regulate microglial proliferation and function. The Journal of Neuroscience, 1996. 16(8): p. 2508-2521. 93. Zhong, P., et al., Cell-to-cell transmission of viruses. Current opinion in virology, 2013. 3(1): p. 44-50. 94. Igakura, T., et al., Spread of HTLV-I Between Lymphocytes by Virus-Induced Polarization of the Cytoskeleton. Science, 2003. 299(5613): p. 1713-1716. 95. Smith, G.A., S.P. Gross, and L.W. Enquist, Herpesviruses use bidirectional fast-axonal transport to spread in sensory neurons. Proceedings of the National Academy of Sciences, 2001. 98(6): p. 3466-3470. 96. Pais-Correia, A.M., et al., Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses. Nat Med, 2010. 16(1): p. 83-9. 97. Ch'ng, T.H. and L.W. Enquist, Neuron-to-Cell Spread of Pseudorabies Virus in a Compartmented Neuronal Culture System. Journal of Virology, 2005. 79(17): p. 10875-10889. 98. Sherer, N.M., et al., Retroviruses can establish filopodial bridges for efficient cell-to-cell transmission. Nature Cell Biology, 2007. 9(3): p. 310-315. 99. Abela, I.A., et al., Cell-cell transmission enables HIV-1 to evade inhibition by potent CD4bs directed antibodies. PLoS Pathog, 2012. 8(4): p. e1002634. 100. Chen, P., et al., Predominant Mode of Human Immunodeficiency Virus Transfer between T Cells Is Mediated by Sustained Env-Dependent Neutralization-Resistant Virological Synapses. Journal of Virology, 2007. 81(22): p. 12582-12595. 101. Ganesh, L., et al., Infection of Specific Dendritic Cells by CCR5-Tropic Human Immunodeficiency Virus Type 1 Promotes Cell-Mediated Transmission of Virus Resistant to Broadly Neutralizing Antibodies. Journal of Virology, 2004. 78(21): p. 11980-11987. 102. Mothes, W., et al., Virus Cell-to-Cell Transmission. Journal of Virology, 2010. 84(17): p. 8360-8368. 103. Lehmann, M.J., et al., Actin- and myosin-driven movement of viruses along filopodia precedes their entry into cells. The Journal of cell biology, 2005. 170(2): p. 317-325. 104. Monje, M.L., H. Toda, and T.D. Palmer, Inflammatory Blockade Restores Adult Hippocampal Neurogenesis. Science, 2003. 302(5651): p. 1760-1765. 105. Vallieres, L., et al., Reduced hippocampal neurogenesis in adult transgenic mice with chronic astrocytic production of interleukin-6. J Neurosci, 2002. 22(2): p. 486-92. 106. Garber, C., et al., T cells promote microglia-mediated synaptic elimination and cognitive dysfunction during recovery from neuropathogenic flaviviruses. Nature Neuroscience, 2019. 107. Alirezaei, M., W.B. Kiosses, and H.S. Fox, Decreased neuronal autophagy in HIV dementia: a mechanism of indirect neurotoxicity. Autophagy, 2008. 4(7): p. 963-6. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/78709 | - |
| dc.description.abstract | Zika virus (ZIKV) is a flavivirus and mostly causes mild symptoms in humans. The recent ZIKV outbreak in Brazil during 2015 to 2016 raised public concerns, since neurological malfunction such as Guillain-Barré syndrome and microcephaly were linked to ZIKV infection. Microglia, the resident immune cells in the central nervous system, was shown to be ZIKV’s target. In this thesis study, we aim to elucidate the roles of microglia in ZIKV infection by using human microglial cells (HMC3) and neuroblastoma cells (BE(2)-C). Results showed that HMC3 cells were more susceptible to ZIKV infection than BE(2)-C cells, and virus titer increased earlier than that from BE(2)-C cells. Also, ZIKV infection could activate microglia cells. In studies of interplay between the two cells, co-culture with HMC3 cells increased BE(2)-C cell growth, whereas the promotion of BE(2)-C cell growth was decreased when infected with ZIKV. Moreover, ZIKV can be transmitted to BE(2)-C cells through a cell-cell-contact manner when co-cultured with microglia cells, demonstrated by transwell assay and antibody neutralization assay. In addition, through mRNA screening, we suggested ZIKV infection activated the neuroinflammation signaling pathway in HMC3 cells and may lead the cells to a pro-inflammatory neurotoxic state (M1). | en |
| dc.description.provenance | Made available in DSpace on 2021-07-11T15:13:45Z (GMT). No. of bitstreams: 1 ntu-108-R06445117-1.pdf: 2206769 bytes, checksum: 3621e6abc545106623e744d791b062bb (MD5) Previous issue date: 2019 | en |
| dc.description.tableofcontents | Abstract I
中文摘要 II Introduction 1 ZIKA Virus 1 Microglia 6 Thesis background and motivation 8 Materials and Methods 10 Results 15 HMC3 cells were more susceptible to ZIKV infection than BE(2)-C cells. 15 ZIKV infection activated HMC3 cells. 17 ZIKV infection reduced the promotion of BE(2)-C cell proliferation by HMC3 cells. 17 ZIKV infection repressed the migration ability of HMC3 cells. 18 ZIKV infected HMC3 cells can transmit ZIKV through cell-cell contact. 19 ZIKV infection of HMC3 cells induced inflammatory responses. 21 Discussion 24 References 29 Figures 37 | |
| dc.language.iso | en | |
| dc.subject | 微膠細胞 | zh_TW |
| dc.subject | 茲卡病毒 | zh_TW |
| dc.subject | microglia | en |
| dc.subject | Zika virus | en |
| dc.title | 茲卡病毒對微膠細胞之影響 | zh_TW |
| dc.title | To study the responses of microglia to Zika virus infection | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 107-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 陳儀莊,陶秘華,周申如 | |
| dc.subject.keyword | 茲卡病毒,微膠細胞, | zh_TW |
| dc.subject.keyword | Zika virus,microglia, | en |
| dc.relation.page | 51 | |
| dc.identifier.doi | 10.6342/NTU201901952 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2019-07-31 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| dc.date.embargo-lift | 2024-08-28 | - |
| 顯示於系所單位： | 微生物學科所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-108-R06445117-1.pdf 未授權公開取用 | 2.16 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。