Pathogenesis of severe acute respiratory syndrome

Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441–700 of the spike protein (S protein) as the major epitope.

[1]  C. Fraser,et al.  Epidemiological and genetic analysis of severe acute respiratory syndrome , 2004, The Lancet Infectious Diseases.

[2]  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.

[3]  Y. Guan,et al.  Molecular epidemiology of the novel coronavirus that causes severe acute respiratory syndrome , 2004, The Lancet.

[4]  P. Hsueh,et al.  Chronological evolution of IgM, IgA, IgG and neutralisation antibodies after infection with SARS‐associated coronavirus , 2004, Clinical Microbiology and Infection.

[5]  F. Chang,et al.  Plasma proteome of severe acute respiratory syndrome analyzed by two-dimensional gel electrophoresis and mass spectrometry. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[6]  Y. Guan,et al.  Cytokine Responses in Severe Acute Respiratory Syndrome Coronavirus-Infected Macrophages In Vitro: Possible Relevance to Pathogenesis , 2005, Journal of Virology.

[7]  J. Peiris,et al.  Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome , 2003, The Lancet.

[8]  A. Carfi,et al.  Structure of a proteolytically resistant core from the severe acute respiratory syndrome coronavirus S2 fusion protein , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[9]  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.

[10]  X. L. Liu,et al.  Isolation and Characterization of Viruses Related to the SARS Coronavirus from Animals in Southern China , 2003, Science.

[11]  H. Deng,et al.  Neutralizing Antibodies in Patients with Severe Acute Respiratory Syndrome-Associated Coronavirus Infection , 2004, The Journal of Infectious Diseases.

[12]  Christian Drosten,et al.  Characterization of a Novel Coronavirus Associated with Severe Acute Respiratory Syndrome , 2003, Science.

[13]  J. Lepault,et al.  Severe acute respiratory syndrome coronavirus (SARS-CoV) infection inhibition using spike protein heptad repeat-derived peptides. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[14]  J. Sung,et al.  Enteric involvement of severe acute respiratory syndrome-associated coronavirus infection , 2003, Gastroenterology.

[15]  Y. Lau.  SARS: future research and vaccine , 2004, Paediatric Respiratory Reviews.

[16]  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.

[17]  Obi L. Griffith,et al.  The Genome Sequence of the SARS-Associated Coronavirus , 2003, Science.

[18]  Malik Peiris,et al.  Aetiology: Koch's postulates fulfilled for SARS virus , 2003, Nature.

[19]  J. A. Comer,et al.  A novel coronavirus associated with severe acute respiratory syndrome. , 2003, The New England journal of medicine.

[20]  R. Crystal,et al.  Resolution of Primary Severe Acute Respiratory Syndrome-Associated Coronavirus Infection Requires Stat1 , 2004, Journal of Virology.

[21]  B. Murphy,et al.  Contributions of the structural proteins of severe acute respiratory syndrome coronavirus to protective immunity. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[22]  Xiaolei Yin,et al.  Expression cloning of functional receptor used by SARS coronavirus , 2004, Biochemical and Biophysical Research Communications.

[23]  B. Murphy,et al.  An efficient method to make human monoclonal antibodies from memory B cells: potent neutralization of SARS coronavirus , 2004, Nature Medicine.

[24]  Y. Guan,et al.  Coronavirus as a possible cause of severe acute respiratory syndrome , 2003, The Lancet.

[25]  Christophe Fraser,et al.  The Epidemiology of Severe Acute Respiratory Syndrome in the 2003 Hong Kong Epidemic: An Analysis of All 1755 Patients , 2004, Annals of Internal Medicine.

[26]  Ching-Chow Chen,et al.  Induction of IL-8 Release in Lung Cells via Activator Protein-1 by Recombinant Baculovirus Displaying Severe Acute Respiratory Syndrome-Coronavirus Spike Proteins: Identification of Two Functional Regions1 , 2004, The Journal of Immunology.

[27]  J. Loo,et al.  Association of HLA class I with severe acute respiratory syndrome coronavirus infection , 2003, BMC Medical Genetics.

[28]  J. Peiris,et al.  Prolonged disturbances of in vitro cytokine production in patients with severe acute respiratory syndrome (SARS) treated with ribavirin and steroids , 2004, Clinical and experimental immunology.

[29]  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.

[30]  Weifeng Chen,et al.  T-Cell Epitopes in Severe Acute Respiratory Syndrome (SARS) Coronavirus Spike Protein Elicit a Specific T-Cell Immune Response in Patients Who Recover from SARS , 2004, Journal of Virology.

[31]  G. Simmons,et al.  Characterization of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) spike glycoprotein-mediated viral entry , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[32]  J. Sung,et al.  Viral Replication in the Nasopharynx Is Associated with Diarrhea in Patients with Severe Acute Respiratory Syndrome , 2004, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[33]  Yi Guan,et al.  Lung pathology of fatal severe acute respiratory syndrome , 2003, The Lancet.

[34]  John L. Sullivan,et al.  Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus , 2003, Nature.

[35]  J. Sung,et al.  Haematological manifestations in patients with severe acute respiratory syndrome: retrospective analysis , 2003, BMJ : British Medical Journal.

[36]  W. Thomas,et al.  Amino Acids 270 to 510 of the Severe Acute Respiratory Syndrome Coronavirus Spike Protein Are Required for Interaction with Receptor , 2004, Journal of Virology.

[37]  Y. Guan,et al.  The aetiology, origins, and diagnosis of severe acute respiratory syndrome , 2004, The Lancet Infectious Diseases.

[38]  L. Poon,et al.  Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia : a prospective study , 2003 .

[39]  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.

[40]  Andreas Pichlmair,et al.  Inhibition of Beta Interferon Induction by Severe Acute Respiratory Syndrome Coronavirus Suggests a Two-Step Model for Activation of Interferon Regulatory Factor 3 , 2005, Journal of Virology.

[41]  Christian Drosten,et al.  Identification of a novel coronavirus in patients with severe acute respiratory syndrome. , 2003, The New England journal of medicine.

[42]  J. Sung,et al.  Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome , 2004, Clinical and experimental immunology.

[43]  A. Debnath,et al.  Interaction between heptad repeat 1 and 2 regions in spike protein of SARS-associated coronavirus: implications for virus fusogenic mechanism and identification of fusion inhibitors , 2004, The Lancet.

[44]  A. Danchin,et al.  The Severe Acute Respiratory Syndrome , 2003 .

[45]  Renji Reghunathan,et al.  Expression profile of immune response genes in patients with Severe Acute Respiratory Syndrome , 2005, BMC Immunology.

[46]  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.

[47]  Martin L Hibberd,et al.  A human in vitro model system for investigating genome-wide host responses to SARS coronavirus infection , 2004, BMC infectious diseases.

[48]  R. Webster.  Wet markets—a continuing source of severe acute respiratory syndrome and influenza? , 2004, The Lancet.

[49]  K. Kain,et al.  Fatal Severe Acute Respiratory Syndrome Is Associated with Multiorgan Involvement by Coronavirus , 2005, The Journal of infectious diseases.

[50]  D. Hui,et al.  ACE2 Gene Polymorphisms Do Not Affect Outcome of Severe Acute Respiratory Syndrome , 2004, Clinical chemistry.

[51]  J. Xie,et al.  Significant Changes of Peripheral T Lymphocyte Subsets in Patients with Severe Acute Respiratory Syndrome , 2004, The Journal of infectious diseases.

[52]  Wenhui Li,et al.  Potent neutralization of severe acute respiratory syndrome (SARS) coronavirus by a human mAb to S1 protein that blocks receptor association. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[53]  J. Kwang,et al.  Immunological Characterization of the Spike Protein of the Severe Acute Respiratory Syndrome Coronavirus , 2004, Journal of Clinical Microbiology.

[54]  Xiaolei Yin,et al.  Neutralizing antibodies in patients with severe acute respiratory syndrome-associated coronavirus infection. , 2004, The Journal of infectious diseases.

[55]  Kwanyee Leung,et al.  Evasion of antibody neutralization in emerging severe acute respiratory syndrome coronaviruses. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[56]  J. Peiris,et al.  Mannose-Binding Lectin in Severe Acute Respiratory Syndrome Coronavirus Infection , 2005, The Journal of infectious diseases.

[57]  Y. Lau,et al.  Chemokine up-regulation in SARS-coronavirus–infected, monocyte-derived human dendritic cells , 2005, Blood.

[58]  R. Weinstein.  Planning for epidemics--the lessons of SARS. , 2004, The New England journal of medicine.

[59]  Guoping Zhao,et al.  Molecular Evolution of the SARS Coronavirus During the Course of the SARS Epidemic in China , 2004, Science.