title: The effect of SARS coronavirus on blood system: its clinical findings and the pathophysiologic hypothesis.
abstract: 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.
authors.affiliation: Department of Paediatrics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China. yang1091@cuhk.edu.hk
authors.forename: Mo
authors.initials: M
authors.lastname: Yang
authors.forename: Kam-Lun E
authors.initials: KL
authors.lastname: Hon
authors.forename: Karen
authors.initials: K
authors.lastname: Li
authors.forename: Tai-Fai
authors.initials: TF
authors.lastname: Fok
authors.forename: Chi-Kong
authors.initials: CK
authors.lastname: Li
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000276:immunology; D000943:Antigens, Differentiation / Q000276:immunology; D018826:CD13 Antigens / Q000276:immunology; D015815:Cell Adhesion Molecules; D002648:Child; D006402:Hematologic Diseases / Q000276:immunology / Q000503:physiopathology; D006410:Hematopoiesis / Q000502:physiology*; D006801:Humans; D045473:Severe acute respiratory syndrome-related coronavirus; D045169:Severe Acute Respiratory Syndrome / Q000276:immunology / Q000503:physiopathology* / Q000821:virology
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; C069847:CD66 antigens; D015815:Cell Adhesion Molecules; D018826:CD13 Antigens