1: Exp Biol Med (Maywood). 2005 Dec;230(11):865-71.

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

El-Azami-El-Idrissi M, Franquin S, Day MJ, Mazza G, Elson CJ, Préat V, Pfau CJ,
Coutelier JP.

Unit of Experimental Medicine, Institute for Cellular and Molecular Pathology,
Université Catholique de Louvain, Bruxelles, Belgium.

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.

PMID: 16339752 [PubMed - indexed for MEDLINE]

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