Preface [ Focus on NeuroAIDS ]

Millions of individuals worldwide have been infected with the human immunodeficiency virus (HIV) and developed the disease known as acquired immunodeficiency syndrome (AIDS). Untreated, the infection can lead to dissolution of both the immunological and central neurological systems. A fraction of the world population of HIV-infected individuals is receiving medications that diminish the peripheral viral burden, but it remains unclear whether drug inaccessibility to the brain and the inability to eliminate existing virus will, in the long-term, lead to increased neurological complications. Preliminary findings indicate that neurological pathologies will remain a consequence of HIV infection. HIV is a lentivirus, a subgroup of retroviruses that uniformly cause CNS disease. Part of this issue of Current HIV Research is focused on our present scientific understanding of neuroAIDS. Nunn provides an overview of neuroAIDS with respect to the scientific and clinical questions being addressed and the present day status of neuroAIDS in the global HIV epidemic [1]. Bell et al. provide an introduction to the component structures and cells of the brain and an overview of their involvement in HIV-induced pathologies [2] and Banks et al. summarize the major role that the blood brain barrier (BBB) plays in establishing and maintaining virus within the CNS and the consequential dysfunction [3]. Dunfee et al. discuss neurotropism of HIV and the dynamic interactions between the evolving virus and the macrophage/microglial brain cells [4]. Ciborowski and Gendelman discuss the central role of mononuclear phagocytes in the development of HIVassociated dementia (HAD) and describe approaches to define the molecular events and biomarkers for HAD [5]. Neurological diseases and productive lentiviral replication in the CNS occur in both rodent and primate macrophages. Zink et al. describe the characterized members of the lentiviral genus that infect varied animals, their similarities and differences and how they may serve as models for understanding HIV infection [6]. Kaul and Lipton describe the complex cellular interplay that potentially contributes to neuronal death in association with HIV-1 disease and discuss recent and prospective approaches for therapy and prevention of HAD [7]. Lastly, Schwartz and Major [8] compare the clinical syndromes of AIDS-dementia complex (ADC) in adults and HIV-associated progressive encephalopathy (PE) in pediatric patients, and they discuss the potential role of neural progenitors in HIV-mediated brain disease. As co-editors of this issue of Current HIV Research, we are very grateful for the time and effort that all of the authors and coauthors have committed to each review article. Furthermore, we hope that the reader will be stimulated by this collection of insightful review articles. REFERENCES [1] Nunn MF. (2006). NeuroAIDS: A Neuroscience Problem with Global Impact. Current HIV Research. 4:245-247. [2] Bell JE, Anthony IC, Simmonds P. (2006). Impact of HIV on Regional & Cellular Organisation of the Brain. Current HIV Research. 4: 249-257. [3] Banks WA, Ercal N, Price TO. (2006). The Blood-Brain Barrier in NeuroAIDS. Current HIV Research. 4: 259-266. [4] Dunfee R, Thomas E, Gorry PR, Wang J, Ancuta P, Gabuzda D. (2006). Mechanisms of HIV-1 Neurotropism. Current HIV Research. 4: 267-278. [5] Ciborowski P, Gendelman HE. (2006). Human Immunodeficiency Virus-Mononuclear Phagocyte Interactions: Emerging Avenues of Biomarker Discovery, Modes of Viral Persistence and Disease Pathogenesis. Current HIV Research. 4: 279-291. [6] Zink MC, Laast VA, Helke KL, Brice AK, Barber SA, Clements JE, Mankowski JL. (2006). From Mice to Macaques - Animal Models of HIV Nervous System Disease. Current HIV Research. 4: 293-305. [7] Kaul M, Lipton SA. (2006). Mechanisms of Neuronal Injury and Death in HIV-1 Associated Dementia. Current HIV Research. 4: 307-318. [8] Schwartz L, Major EO. (2006). Neural Progenitors and HIV-1- Associated Central Nervous System Disease in Adults and Children. Current HIV Research. 4: 319-327.