CD4 and HIV-1 infection: Recent explanations about the pathogenesis of these disorders suggest that not only the decline in CD4+ T cell counts [6], but also the shift into a Th2 cytokine profile [7], the molecular mimicry [8] and the over-expression of superantigens/xenobiotics [9], play a decisive role in the development of dermatological lesions in the context of HIV-1 infection.