Similarly, Nutman (130) and Santiago and Nutman (153) have mapped the evolution of a typical immune response to helminths, from the initiation of infection at mucosal surfaces, when a broad and robust inflammation, primarily mediated by effector Th1, Th2, and Th17 CD4+ cells, attempts to abort the infection; if unsuccessful, a period of weeks or months following, during subacute or latent infection is characterized by a more limited or focused Th2 reaction, primarily mediated by Th2 CD4+ cells, IL-4, IL-5, and eosinophils, which together minimize parasitic load. This evidence concerns the gene CD4 and disease arising from reactivation of latent virus.