How the SARS coronavirus causes disease: host or organism?
暂无分享,去创建一个
K. To | N. Tang | A. Lo | Anthony WI Lo | Ka‐Fai To | Nelson LS Tang
[1] W. Hong,et al. Characterization of a Unique Group-Specific Protein (U122) of the Severe Acute Respiratory Syndrome Coronavirus , 2004, Journal of Virology.
[2] S. Asa,et al. Pulmonary pathology of severe acute respiratory syndrome in Toronto , 2005, Modern Pathology.
[3] Obi L. Griffith,et al. The Genome Sequence of the SARS-Associated Coronavirus , 2003, Science.
[4] A. Kanamaru,et al. Common features in the onset of ARDS after administration of granulocyte colony-stimulating factor. , 2002, Chest.
[5] Jens H. Kuhn,et al. Retroviruses Pseudotyped with the Severe Acute Respiratory Syndrome Coronavirus Spike Protein Efficiently Infect Cells Expressing Angiotensin-Converting Enzyme 2 , 2004, Journal of Virology.
[6] W. Hong,et al. The Severe Acute Respiratory Syndrome Coronavirus 3a Protein Up-Regulates Expression of Fibrinogen in Lung Epithelial Cells , 2005, Journal of Virology.
[7] S. Humphries,et al. Genetic polymorphisms associated with susceptibility and outcome in ARDS. , 2002, Chest.
[8] D. Dimitrov,et al. The SARS-CoV S glycoprotein: expression and functional characterization , 2003, Biochemical and Biophysical Research Communications.
[9] Hong Yang,et al. Long-term SARS Coronavirus Excretion from Patient Cohort, China , 2004, Emerging infectious diseases.
[10] John L. Sullivan,et al. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus , 2003, Nature.
[11] K. Subbarao,et al. pH-Dependent Entry of Severe Acute Respiratory Syndrome Coronavirus Is Mediated by the Spike Glycoprotein and Enhanced by Dendritic Cell Transfer through DC-SIGN , 2004, Journal of Virology.
[12] T. Greenough,et al. Efficient Replication of Severe Acute Respiratory Syndrome Coronavirus in Mouse Cells Is Limited by Murine Angiotensin-Converting Enzyme 2 , 2004, Journal of Virology.
[13] R. Chiu,et al. Molecular epidemiology of SARS--from Amoy Gardens to Taiwan. , 2003, The New England journal of medicine.
[14] Larissa B. Thackray,et al. CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[15] W. Marasco,et al. An animal model of SARS produced by infection of Macaca mulatta with SARS coronavirus , 2005, The Journal of pathology.
[16] F. Lai,et al. Acute renal impairment in coronavirus-associated severe acute respiratory syndrome , 2005, Kidney International.
[17] G. Meduri,et al. Infections and the inflammatory response in acute respiratory distress syndrome. , 1997, Chest.
[18] Peter Cameron,et al. A major outbreak of severe acute respiratory syndrome in Hong Kong. , 2003, The New England journal of medicine.
[19] C. Hsiao,et al. Clinicopathology of severe acute respiratory syndrome: an autopsy case report. , 2004, Journal of the Formosan Medical Association = Taiwan yi zhi.
[20] J. Sung,et al. The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells. , 2005, The Journal of general virology.
[21] R. Crystal,et al. Macaque Model for Severe Acute Respiratory Syndrome , 2004, Journal of Virology.
[22] Wenhui Li,et al. A 193-Amino Acid Fragment of the SARS Coronavirus S Protein Efficiently Binds Angiotensin-converting Enzyme 2* , 2004, Journal of Biological Chemistry.
[23] Ching-lung Lai,et al. Temporal patterns of hepatic dysfunction and disease severity in patients with SARS. , 2003, JAMA.
[24] D. Luk,et al. Severe acute respiratory syndrome in children: Experience in a regional hospital in Hong Kong* , 2003, Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies.
[25] C. Wong,et al. Chemokine response in children with SARS , 2005, Archives of Disease in Childhood.
[26] C. Johnston,et al. ACE2, a new regulator of the renin–angiotensin system , 2004, Trends in Endocrinology & Metabolism.
[27] S. Chollet-Martin,et al. Polymorphonuclear neutrophil activation during the acute respiratory distress syndrome , 2000, Intensive Care Medicine.
[28] F. Kirchhoff,et al. LSECtin interacts with filovirus glycoproteins and the spike protein of SARS coronavirus , 2005, Virology.
[29] G. Fey,et al. Susceptibility to SARS coronavirus S protein-driven infection correlates with expression of angiotensin converting enzyme 2 and infection can be blocked by soluble receptor , 2004, Biochemical and Biophysical Research Communications.
[30] V. Chinchilli,et al. Polymorphisms of human SP‐A, SP‐B, and SP‐D genes: association of SP‐B Thr131Ile with ARDS , 2000, Clinical genetics.
[31] Junya Fukuoka,et al. Lung pathology of severe acute respiratory syndrome (SARS): a study of 8 autopsy cases from Singapore , 2003, Human Pathology.
[32] J. Sung,et al. Haematological manifestations in patients with severe acute respiratory syndrome: retrospective analysis , 2003, BMJ : British Medical Journal.
[33] H. Rosenberg,et al. Chemokine regulation of inflammation during acute viral infection , 2003, Current opinion in allergy and clinical immunology.
[34] W. Hong,et al. Overexpression of 7a, a Protein Specifically Encoded by the Severe Acute Respiratory Syndrome Coronavirus, Induces Apoptosis via a Caspase-Dependent Pathway , 2004, Journal of Virology.
[35] C. Hsiao,et al. Identification of a novel protein 3a from severe acute respiratory syndrome coronavirus , 2004, FEBS Letters.
[36] J. Sung,et al. Persistent infection of SARS coronavirus in colonic cells in vitro , 2004, Journal of medical virology.
[37] Qingling Zhang,et al. Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS‐CoV) in SARS patients: implications for pathogenesis and virus transmission pathways , 2004, The Journal of pathology.
[38] Arthur S Slutsky,et al. Angiotensin-converting enzyme 2 protects from severe acute lung failure , 2005, Nature.
[39] Yi Guan,et al. Lung pathology of fatal severe acute respiratory syndrome , 2003, The Lancet.
[40] Kwok-Hung Chan,et al. Severe acute respiratory syndrome coronavirus-like virus in Chinese horseshoe bats. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[41] G. Tse,et al. Tissue and cellular tropism of the coronavirus associated with severe acute respiratory syndrome: an in‐situ hybridization study of fatal cases , 2004, The Journal of pathology.
[42] J. Sung,et al. Early Enhanced Expression of Interferon-Inducible Protein-10 (CXCL-10) and Other Chemokines Predicts Adverse Outcome in Severe Acute Respiratory Syndrome , 2005, Clinical chemistry.
[43] D. Hui,et al. Anti-SARS-CoV IgG response in relation to disease severity of severe acute respiratory syndrome , 2005, Journal of Clinical Virology.
[44] T. Kirikae,et al. Identification of an alternative 5′‐untranslated exon and new polymorphisms of angiotensin‐converting enzyme 2 gene: Lack of association with SARS in the Vietnamese population , 2005, American journal of medical genetics. Part A.
[45] Y. Kooyk,et al. DC-SIGN: escape mechanism for pathogens , 2003, Nature Reviews Immunology.
[46] R. Rappuoli,et al. SARS — beginning to understand a new virus , 2003, Nature Reviews Microbiology.
[47] J. Sung,et al. Enteric involvement of severe acute respiratory syndrome-associated coronavirus infection , 2003, Gastroenterology.
[48] W. Leung,et al. Coronaviral hypothetical and structural proteins were found in the intestinal surface enterocytes and pneumocytes of severe acute respiratory syndrome (SARS) , 2005, Modern Pathology.
[49] S. Moochhala,et al. Chemokines in acute respiratory distress syndrome , 2005, American journal of physiology. Lung cellular and molecular physiology.
[50] Xu Han-You,et al. Acute Respiratory Syndrome (SARS) , 2004 .
[51] Yao-Hsu Yang,et al. Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection , 2005, Journal of medical virology.
[52] M. Burdick,et al. Role of CXCL9/CXCR3 Chemokine Biology during Pathogenesis of Acute Lung Allograft Rejection 1 , 2003, The Journal of Immunology.
[53] Michel Theron,et al. An interferon‐γ‐related cytokine storm in SARS patients† , 2004, Journal of medical virology.
[54] J. Sung,et al. Association of Human-Leukocyte-Antigen Class I (B*0703) and Class II (DRB1*0301) Genotypes with Susceptibility and Resistance to the Development of Severe Acute Respiratory Syndrome , 2004, The Journal of infectious diseases.
[55] Xiaolei Yin,et al. Highly infectious SARS-CoV pseudotyped virus reveals the cell tropism and its correlation with receptor expression , 2004, Biochemical and Biophysical Research Communications.
[56] T. Menges,et al. Plasminogen-activator-inhibitor-1 4G/5G promoter polymorphism and prognosis of severely injured patients , 2001, The Lancet.
[57] G. Navis,et al. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis , 2004, The Journal of pathology.
[58] S. Humphries,et al. Angiotensin converting enzyme insertion/deletion polymorphism is associated with susceptibility and outcome in acute respiratory distress syndrome. , 2002, American journal of respiratory and critical care medicine.
[59] P. Chan,et al. Specific epitopes of the structural and hypothetical proteins elicit variable humoral responses in SARS patients , 2006, Journal of Clinical Pathology.
[60] Michelle M. Packard,et al. Immunohistochemical, in situ hybridization, and ultrastructural localization of SARS-associated coronavirus in lung of a fatal case of severe acute respiratory syndrome in Taiwan , 2005, Human Pathology.
[61] Malik Peiris,et al. Koch's postulates fulfilled for SARS virus , 2003, Nature.
[62] W. Hong,et al. A Novel Severe Acute Respiratory Syndrome Coronavirus Protein, U274, Is Transported to the Cell Surface and Undergoes Endocytosis , 2004, Journal of Virology.
[63] O. Tsang,et al. Absence of association between angiotensin converting enzyme polymorphism and development of adult respiratory distress syndrome in patients with severe acute respiratory syndrome: a case control study , 2005, BMC infectious diseases.
[64] J. Sung,et al. Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome , 2004, Clinical and experimental immunology.
[65] Ching-lung Lai,et al. SARS‐associated viral hepatitis caused by a novel coronavirus: Report of three cases , 2004, Hepatology.
[66] Z. Lang,et al. A clinicopathological study of three cases of severe acute respiratory syndrome (SARS) , 2003, Pathology.
[67] J. Peiris,et al. Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome , 2003, The Lancet.
[68] G. Bellingan. The pulmonary physician in critical care • 6: The pathogenesis of ALI/ARDS , 2002, Thorax.
[69] Albert D. M. E. Osterhaus,et al. SARS virus infection of cats and ferrets , 2003, Nature.
[70] Xin Li,et al. The clinical pathology of severe acute respiratory syndrome (SARS): a report from China , 2003, The Journal of pathology.
[71] A. Cariou,et al. Association between a genomic polymorphism within the CD14 locus and septic shock susceptibility and mortality rate* , 2002, Critical care medicine.
[72] Jun Xu,et al. Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome. , 2005, American journal of respiratory and critical care medicine.
[73] L. Trentin,et al. CXC chemokines IP-10 and mig expression and direct migration of pulmonary CD8+/CXCR3+ T cells in the lungs of patients with HIV infection and T-cell alveolitis. , 2000, American journal of respiratory and critical care medicine.
[74] W. Travis,et al. Analysis of deaths during the severe acute respiratory syndrome (SARS) epidemic in Singapore: challenges in determining a SARS diagnosis. , 2004, Archives of pathology & laboratory medicine.
[75] Y. Lau,et al. Chemokine up-regulation in SARS-coronavirus–infected, monocyte-derived human dendritic cells , 2005, Blood.
[76] W. Hong,et al. The severe acute respiratory syndrome coronavirus 3a is a novel structural protein , 2005, Biochemical and Biophysical Research Communications.
[77] Guoping Zhao,et al. Molecular Evolution of the SARS Coronavirus During the Course of the SARS Epidemic in China , 2004, Science.
[78] J. Villar,et al. Genetic susceptibility to acute lung injury , 2003, Critical care medicine.
[79] C. Ayata,et al. Timing of neurologic deterioration in massive middle cerebral artery infarction: A multicenter review , 2003, Critical care medicine.
[80] Ben Berkhout,et al. Human coronavirus NL63 employs the severe acute respiratory syndrome coronavirus receptor for cellular entry , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[81] K. Kain,et al. Fatal Severe Acute Respiratory Syndrome Is Associated with Multiorgan Involvement by Coronavirus , 2005, The Journal of infectious diseases.
[82] Sung Keun Kang,et al. Molecular evolution of the SARS coronavirus during the course of the SARS epidemic in China. , 2004, Science.
[83] D. Hui,et al. ACE2 Gene Polymorphisms Do Not Affect Outcome of Severe Acute Respiratory Syndrome , 2004, Clinical chemistry.
[84] J. Dennis,et al. Dynamic Changes in Clinical Features and Cytokine/Chemokine Responses in Sars Patients Treated with Interferon Alfacon-1 plus Corticosteroids , 2005, Antiviral therapy.
[85] Christian Drosten,et al. Characterization of a Novel Coronavirus Associated with Severe Acute Respiratory Syndrome , 2003, Science.
[86] N. Nagata,et al. Laboratory and Epidemiology Communications SARS Coronavirus-Infected Cells in Lung Detected by New In Situ Hybridization Technique , 2003 .
[87] R. Sung,et al. Pathology of fatal human infection associated with avian influenza A H5N1 virus , 2001, Journal of medical virology.
[88] J. Sung,et al. Retrospective analysis of liver function derangement in severe acute respiratory syndrome , 2004, The American Journal of Medicine.
[89] Christl A. Donnelly,et al. SARS-CoV Antibody Prevalence in All Hong Kong Patient Contacts , 2004, Emerging infectious diseases.
[90] A. Steinkasserer,et al. DC-SIGN and DC-SIGNR Interact with the Glycoprotein of Marburg Virus and the S Protein of Severe Acute Respiratory Syndrome Coronavirus , 2004, Journal of Virology.
[91] Mark Chappell,et al. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury , 2005, Nature Medicine.
[92] J. Loo,et al. Association of HLA class I with severe acute respiratory syndrome coronavirus infection , 2003, BMC Medical Genetics.
[93] C. Dolea,et al. World Health Organization , 1949, International Organization.
[94] Krishna Shankara Narayanan,et al. Severe Acute Respiratory Syndrome Coronavirus 3a Protein Is a Viral Structural Protein , 2005, Journal of Virology.
[95] D. Dimitrov,et al. A model of the ACE2 structure and function as a SARS-CoV receptor , 2003, Biochemical and Biophysical Research Communications.
[96] J. Chan,et al. The spectrum of pathological changes in severe acute respiratory syndrome (SARS) , 2004, Histopathology.
[97] T. Kirikae,et al. ACE1 polymorphism and progression of SARS , 2004, Biochemical and Biophysical Research Communications.
[98] S. Lai,et al. Treatment of severe acute respiratory syndrome , 2005, European Journal of Clinical Microbiology and Infectious Diseases.
[99] C. Biron,et al. A chemokine-to-cytokine-to-chemokine cascade critical in antiviral defense. , 2000, The Journal of clinical investigation.
[100] K. Wong,et al. Myopathic changes associated with severe acute respiratory syndrome: a postmortem case series. , 2005, Archives of neurology.
[101] J. Sung,et al. Pulmonary pathological features in coronavirus associated severe acute respiratory syndrome (SARS) , 2004, Journal of Clinical Pathology.
[102] Y. Lau,et al. Chemokine upregulation in SARS coronavirus infected human monocyte derived dendritic cells , 2008 .
[103] Tzei-Yi Lin,et al. Detection of Severe Acute Respiratory Syndrome–Associated Coronavirus in Pneumocytes of the Lung , 2004, American journal of clinical pathology.