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Query: UMLS:C1175175 (SARS)
 19,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe acute respiratory syndrome (SARS) has recently recognized as a new human infectious disease. A novel coronavirus was identified as the causative agent of SARS. This report summarizes the hematological findings in SARS patients and proposes a hypothesis for the pathophysiology of SARS coronavirus related abnormal hematopoiesis. Hematological changes in patients with SARS were common and included lymphopenia (68% - 90% of adults; 100% of children, n = 10), thrombocytopenia (20% - 45% of adults, 50% of children), and leukopenia (20% - 34% of adults, 70% of children). The possible mechanisms of this coronavirus on blood system may include (1) directly infect blood cells and bone marrow stromal cells via CD13 or CD66a; and/or (2) induce auto-antibodies and immune complexes to damage these cells. In addition, lung damage in SARS patients may also play a role on inducing thrombocytopenia by (1) increasing the consumption of platelets/megakaryocytes; and/or (2) reducing the production of platelets in the lungs. Since the most common hematological changes in SARS patients were lymphopenia and immunodeficiency. We postulate that hematopoietic growth factors such as G-CSF, by mobilizing endogenous blood stem cells and endogenous cytokines, could become a hematological treatment for SARS patients, which may enhance the immune system against these virus.
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PMID:The effect of SARS coronavirus on blood system: its clinical findings and the pathophysiologic hypothesis. 1284 98

Severe acute respiratory syndrome (SARS) is a new human infectious disease. The causative agent of SARS is a novel coronavirus (SARS-CoV). This report summarizes the hematological findings in SARS patients and proposes the possible mechanisms of SARS-CoV related abnormal hematopoiesis. Hematological changes in patients with SARS are common and include lymphopenia, thrombocytopenia and occasionally leukopenia. A significant decrease was also observed in peripheral CD4+ and CD8+ T lymphocyte subsets and it was related to onset of SARS. A number of potential mechanisms may be involved. The development of auto-immune antibodies or immune complexes triggered by viral infection may play a major role in inducing lymphopenia and thrombocytopenia. Moreover, SARS-CoV may also directly infect hematopoietic stem/progenitor cells via CD13 or CD66a inducing their growth inhibition and apoptosis. The receptor for group I and III CoV is aminopeptidase N (CD13). CD13 has been identified in human bone marrow CD34+ cells, platelets, megakaryocytes, myeloid cells, and erythroid cells, but not in lymphocytes. The common receptor for group II CoV is CEACAM1a (CD66a). CD66a is an adhesion molecule expressed on bone marrow CD34+ cells, platelets, granulocytes and activated lymphocytes. In addition, glucocorticoids could induce lymphopenia and the use of steroids may account for the decrease of lymphocytes in some SARS patients. The increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative but often overlooked mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions.
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PMID:Hematological findings in SARS patients and possible mechanisms (review). 1525 84

We have recently demonstrated that the severe acute respiratory syndrome coronavirus (SARS-CoV) receptor angiotensin converting enzyme 2 (ACE2) also mediates cellular entry of the newly discovered human coronavirus (hCoV) NL63. Here, we show that expression of DC-SIGN augments NL63 spike (S)-protein-driven infection of susceptible cells, while only expression of ACE2 but not DC-SIGN is sufficient for entry into nonpermissive cells, indicating that ACE2 fulfills the criteria of a bona fide hCoV-NL63 receptor. As for SARS-CoV, murine ACE2 is used less efficiently by NL63-S for entry than human ACE2. In contrast, several amino acid exchanges in human ACE2 which diminish SARS-S-driven entry do not interfere with NL63-S-mediated infection, suggesting that SARS-S and NL63-S might engage human ACE2 differentially. Moreover, we observed that NL63-S-driven entry was less dependent on a low-pH environment and activity of endosomal proteases compared to infection mediated by SARS-S, further suggesting differences in hCoV-NL63 and SARS-CoV cellular entry. NL63-S does not exhibit significant homology to SARS-S but is highly related to the S-protein of hCoV-229E, which enters target cells by engaging CD13. Employing mutagenic analyses, we found that the N-terminal unique domain in NL63-S, which is absent in 229E-S, does not confer binding to ACE2. In contrast, the highly homologous C-terminal parts of the NL63-S1 and 229E-S1 subunits in conjunction with distinct amino acids in the central regions of these proteins confer recognition of ACE2 and CD13, respectively. Therefore, despite the high homology of these sequences, they likely form sufficiently distinct surfaces, thus determining receptor specificity.
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PMID:Highly conserved regions within the spike proteins of human coronaviruses 229E and NL63 determine recognition of their respective cellular receptors. 1691 12