Evidence for polyclonal B cell activation as the mechanism for LCMV-induced autoimmune hemolytic anemia.

A docile substrain of lymphocytic choriomeningitis virus (LCMV) causes a persistent infection in adult C3HeB mice and induces a severe autoimmune hemolytic anemia (AIHA) which is maximal around three weeks post infection (PI). Evaluations of serum immunoglobulin levels of these mice demonstrated grossly elevated IgG2a levels along with increased IgG1 and IgG2b levels, suggesting that these animals also develop polyclonal B cell activation (PBA). Interestingly, LCMV-infected B10.BR mice did not demonstrate a marked hypogammaglobulinemia nor did they experience a severe hemolytic anemia. Although evaluations of the hematocrits indicated that these animals endure a mild anemia 21 days PI, a below normal reticulocyte count until day 18 PI suggests that there was a prolonged suppression in hematopoiesis. It is clear from RBC survival studies that there is not an accelerated rate of RBC elimination, as seen in infected C3H mice, demonstrating that the anemia in B10.BR mice is not due to a hemolytic process. These results imply a correlation between the development of PBA and AIHA, suggesting a cause and effect relationship.