Distinct host-dependent pathogenic mechanisms leading to a similar clinical anemia after infection with lymphocytic choriomeningitis virus.

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.