We describe three children infected by the human immunodeficiency virus (HIV 1), and one child suffering from familial mucocutaneous candidiasis, who all had multiple, fusiform subarachnoid intracranial aneurysms. Because infectious causative agents were never detected at the level of the lesions, a classical "mycotic" origin of these aneurysms seemed unlikely. Despite the fact that these aneurysms have the same angiographic appearance, they have different etiologies (immune and infectious). These data open the discussion on the reciprocal role of an infectious or immune initial trigger acting on a vascular (endothelial) target. The specificities of the target in terms of location and response enhance specific topographic characteristics (phenotypes) of the cerebral vasculature.