Le SIDA murin comme modèle animal du SIDA

Abstract

The MAIDS (murin AIDS) syndrome is induced by a defective retrovirus. The syndrome starts by the proliferation of infected B cells and affected mice develop lymphadenopathy and splenomegaly. The functions of B cells as well as those of T cells are altered by the infection but CD4+ T cells and normal B cells appear required for development of the disease. The etiologic agent is a defective retrovirus which contains a single open reading frame encoding the Pr60gag protein precursor. This protein is not processed by cleavage but it is myristylated and phosphorylated. Thus, Pr60gag appears entirely responsible for the immunodeficiency syndrome. The MAIDS syndrome progresses even in the absence of viral replication, that is, without infection of new target cells. This virus behaves as an oncogenic virus which induces directly or indirectly a B cell lymphoma. Infected B cells can anergize T cells either by producing a growth factor (cytokine) of by interaction with other cells of the immune system, like CD4+ cells. A classical superantigen effect does not appear to be responsible for the MAIDS pathogenesis. This model suggests that defective viruses and B cell infection might be involved in human AIDS and that viral replication might not be essential for progression of the disease.