Lactate dehydrogenase-elevating virus infection: an experimental model of immune microenvironment modulation.

Lactate dehydrogenase-elevating virus (LDV), a mouse arterivirus, is characterized by a lifelong viremia, despite antiviral innate and adaptative immune response. It induces strong modifications of the host immune microenvironment, including macrophage and natural killer cell activation, secretion of pro-inflammatory cytokines, modulation of T helper cell differentiation and polyclonal activation of B-lymphocytes. This modification of the immune microenvironment results in the protection against some diseases such as allergies, graft-versus-host reaction, experimental autoimmune encephalitis, and growth of some tumors. In contrast, it exacerbates other pathologies such as endotoxin shock and autoantibody-mediated autoimmune diseases. Thus, LDV infection provides an interesting model to understand the consequences of viral infections on pathogenic mechanisms and to define new therapeutic approaches.