Neuroprotection by the caspase-1 inhibitor Ac-YVAD-(acyloxy)mk in experimental neuroAIDS is independent from IL-1β generation

Dear Editor,

The human immunodeficiency virus type-1 (HIV-1) coat protein, gp120, has been implicated in the progression of central nervous system (CNS) damage caused by HIV-1 infection (see Corasaniti et al.¹). Intracerebral (i.c.v.) injection of gp120 in adult rats causes neuropathological alterations, such as microglial cell activation, enhanced expression of the proinflammatory cytokine IL-1β and selective neuronal apoptosis in the brain neocortex which resemble those reported in HIV encephalitis (see Corasaniti et al¹). In particular, expression of neuronal damage in the rat brain neocortex by gp120 is preceded by microglial cell activation and by an early (at 6 and 24 h from i.c.v. injection of a single dose of gp120) enhancement of IL-1β expression with more enhanced expression detectable after 7 days of treatment (see Corasaniti et al¹). IL-1β is synthesised as an inactive 31 kDa precursor molecule (pro-IL-1β) that is processed by caspase-1 (formerly referred to as interleukin-1 converting enzyme, ICE), to yield the mature, 17 kDa biologically active form of the cytokine.²

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