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