Changes in hemopoiesis during the course of acute LCM virus infection in mice.
Although severe hematologic and immunologic disorders occur in several viral infections, insight into the mechanisms by which viruses may affect hemopoietic tissues is poor. The previous demonstration of distinct immunohemopoietic lesions in mice with acute lymphocytic choriomeningitis (LCM) virus infection has led us to investigate the function of hemopoietic precursor cells in the course of this experimental infection. During the first week of infection, there was profound suppression of pluripotential stem cell (CFU) and in vitro colony-forming cell (CFU) compartments, and of 59Fe uptake into hemopoietic tissues. During the same period, we found enhanced activity of colony-stimulating factor, lack of responsiveness to erythropoietin, and appreciable titers of interferon in blood and spleen. After day 10 post infection, there was a striking increase in CFU and 59Fe uptake confined to spleen and blood. Restoration of bone marrow, however, was markedly delayed. With reference to recent studies on interferon, and the findings in mice with persistent LCM virus infection, we suggest that interferon may be the comprehensive suppressor of the hemopoietic precursor cells in the first stage of acute LCM virus infection, and that these cells in the recovery period are directed preferentially into erythropoiesis.
D000208:Acute Disease; D000818:Animals; D001854:Bone Marrow Cells; D003115:Colony-Stimulating Factors / Q000097:blood; D004920:Erythropoiesis; D004921:Erythropoietin / Q000494:pharmacology; D006400:Hematocrit; D006410:Hematopoiesis; D007372:Interferons / Q000096:biosynthesis; D008216:Lymphocytic Choriomeningitis / Q000097:blood*; D008217:Lymphocytic choriomeningitis virus; D051379:Mice; D008809:Mice, Inbred C3H; D013154:Spleen / Q000166:cytology
D003115:Colony-Stimulating Factors; D004921:Erythropoietin; D007372:Interferons