Disease relevance of Severe Acute Respiratory Syndrome

• Unexpectedly, ACE2 also serves as the cellular entry point for the severe acute respiratory syndrome (SARS) virus and the enzyme is therefore a prime target for pharmacological intervention on several disease fronts [1].
• During the recent global outbreak of severe acute respiratory syndrome (SARS), thousands of patients received treatments of uncertain efficacy and known toxicity such as ribavirin and corticosteroids [2].
• Retroviruses pseudotyped with the severe acute respiratory syndrome coronavirus spike protein efficiently infect cells expressing angiotensin-converting enzyme 2 [3].
• SARS (severe acute respiratory syndrome) appeared as the first emerging infectious disease of this century [4].
• Nosocomial acquisition of methicillin-resistant Staphylococcus aureus during an outbreak of severe acute respiratory syndrome [5].

High impact information on Severe Acute Respiratory Syndrome

• Replication of severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) requires proteolytic processing of the replicase polyprotein by two viral cysteine proteases, a chymotrypsin-like protease (3CLpro) and a papain-like protease (PLpro) [6].
• Severe acute respiratory syndrome (SARS) S protein production in plants: development of recombinant vaccine [7].
• Inhibitors of cathepsin L prevent severe acute respiratory syndrome coronavirus entry [8].
• CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus [9].
• Potent neutralization of severe acute respiratory syndrome (SARS) coronavirus by a human mAb to S1 protein that blocks receptor association [10].

Chemical compound and disease context of Severe Acute Respiratory Syndrome

• Angiotensin-converting enzyme-2 (ACE2) is a critical regulator of heart function and a cellular receptor for the causative agent of severe-acute respiratory syndrome (SARS), SARS-CoV (coronavirus) [11].
• Corresponding tyrosine residues are present in the cytoplasmic tails of the S proteins of other animal CoV but not in the tail portion of the S protein of severe acute respiratory syndrome (SARS)-CoV [12].
• Modulation of the immune response to the severe acute respiratory syndrome spike glycoprotein by gene-based and inactivated virus immunization [13].
• Stable benzotriazole esters as mechanism-based inactivators of the severe acute respiratory syndrome 3CL protease [14].
• Nitric oxide inhibits the replication cycle of severe acute respiratory syndrome coronavirus [15].

Biological context of Severe Acute Respiratory Syndrome

• Exploring the pathogenesis of severe acute respiratory syndrome (SARS): the tissue distribution of the coronavirus (SARS-CoV) and its putative receptor, angiotensin-converting enzyme 2 (ACE2) [16].
• Antibody response of patients with severe acute respiratory syndrome (SARS) targets the viral nucleocapsid [17].
• The severe acute respiratory syndrome coronavirus (SARS-CoV) membrane protein is an abundant virion protein, and its interaction with the nucleocapsid protein is crucial for viral assembly and morphogenesis [18].
• This issue, coupled with recent outbreaks of illnesses that pose a direct risk to ICU staff (such as SARS [severe acute respiratory syndrome]), has led to renewed emphasis on infection control measures and practitioners in the ICU [19].

Anatomical context of Severe Acute Respiratory Syndrome

• Altered p38 mitogen-activated protein kinase expression in different leukocytes with increment of immunosuppressive mediators in patients with severe acute respiratory syndrome [20].
• B-cell responses in patients who have recovered from severe acute respiratory syndrome target a dominant site in the S2 domain of the surface spike glycoprotein [21].
• Intracellular localization of the severe acute respiratory syndrome coronavirus nucleocapsid protein: absence of nucleolar accumulation during infection and after expression as a recombinant protein in vero cells [22].
• Detection and monitoring of SARS coronavirus in the plasma and peripheral blood lymphocytes of patients with severe acute respiratory syndrome [23].
• Longitudinal alteration of circulating dendritic cell subsets and its correlation with steroid treatment in patients with severe acute respiratory syndrome [24].

Gene context of Severe Acute Respiratory Syndrome

• Early enhanced expression of interferon-inducible protein-10 (CXCL-10) and other chemokines predicts adverse outcome in severe acute respiratory syndrome [25].
• Elevated plasma tissue-type plasminogen activator (t-PA) and soluble thrombomodulin in patients suffering from severe acute respiratory syndrome (SARS) as a possible index for prognosis and treatment strategy [26].
• Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome [27].
• Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection [28].
• Function of HAb18G/CD147 in invasion of host cells by severe acute respiratory syndrome coronavirus [29].

Analytical, diagnostic and therapeutic context of Severe Acute Respiratory Syndrome

• Protein chip array profiling analysis in patients with severe acute respiratory syndrome identified serum amyloid a protein as a biomarker potentially useful in monitoring the extent of pneumonia [30].
• Diagnosis of severe acute respiratory syndrome (SARS) by detection of SARS coronavirus nucleocapsid antibodies in an antigen-capturing enzyme-linked immunosorbent assay [31].
• Sensitive and specific monoclonal antibody-based capture enzyme immunoassay for detection of nucleocapsid antigen in sera from patients with severe acute respiratory syndrome [32].
• A seroepidemiologic study was conducted in North China in 2003 to determine the neutralizing antibody titer of severe acute respiratory syndrome (SARS) convalescent sera [33].
• The serological response profile of severe acute respiratory syndrome (SARS) coronavirus (CoV) infection was defined by neutralization tests and subclass-specific immunofluorescent (IF) tests using serial sera from 20 patients [34].

References