Inhibition of MAIDS by GSH-replenishing molecules. (A) LP-BM5 infection is characterized by several immune dysfunctions, including splenomegaly and lymphadenopathy (1–4), and GSH deficiency, which favors a Th2 immune response as well as an alternatively activated macrophage phenotype, distinguished by the expression of the genetic markers Fizz1, Ym1, and Arg1. (B) The inhibitory effect of I-152 on MAIDS can be considered the result of two mechanisms of action: on the one hand, it can directly hamper viral replication; on the other hand, it can inhibit and stimulate Th2 and Th1 cytokine production, respectively, reestablishing a balanced Th1/Th2 immune response.