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ORIGINAL RESEARCH ARTICLE

Distinct Host-Dependent Pathogenic Mechanisms Leading to a Similar Clinical Anemia After Infection with Lymphocytic Choriomeningitis Virus

Mohammed El-Azami-El-Idrissi^*,2, Stéphanie Franquin^*,3, Michael J. Day, Graziella Mazza, Christopher J. Elson, Véronique Préat, Charles J. Pfau and Jean-Paul Coutelier^*,1

^* Unit of Experimental Medicine, Institute for Cellular and Molecular Pathology, and Unit of Pharmaceutical Technology, Université Catholique de Louvain, 1200 Bruxelles, Belgium; Department of Pathology & Microbiology, University of Bristol, Bristol BS18 7DU, United Kingdom; and Department of Biology, Rensselaer Polytechnic Institute, Troy, NY 12181

To whom requests for reprints should be addressed at ¹ Unit of Experimental Medicine, UCL-MEXP 7430, Avenue Hippocrate 74, B-1200 Bruxelles, Belgium. E-mail: coutelier{at}mexp.ucl.ac.be

The Docile strain of lymphocytic choriomeningitis virus (LCMV) induces anemia in a number of inbred strains of mice, including C3HeB/FeJ and CBA/Ht animals. A difference in the kinetics of anemia and in compensatory reticulocytosis suggested that impaired erythropoiesis was the major pathogenic mechanism involved in CBA/Ht mice, but not in C3HeB/FeJ mice. In both mouse strains an antierythrocyte autoantibody production that depended on the presence of functional CD4+ T lymphocytes was observed. Although depletion of T helper lymphocytes prevented anemia in C3HeB/FeJ mice, this treatment largely failed to inhibit the development of the disease in CBA/Ht animals. This observation indicated that the antierythrocyte autoimmune response induced by the infection was at least partly responsible for the anemia of C3HeB/FeJ mice, but not of CBA/Ht mice. Erythrophagocytosis was enhanced in both mouse strains after LCMV infection, but did not appear to be a major cause of anemia. These data clearly indicate that similar disease profiles induced by the same virus in two different host strains can be the result of distinctly different mechanisms.

Key Words: anemia • lymphocytic choriomeningitis virus • antierythrocyte autoantibody • phagocytosis • reticulocytosis