摘要：

This chapter focuses on how human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) are proposed to interact with and cross the blood–brain barrier (BBB) and to effect central nervous system (CNS) damage. The CNS as a reservoir of virus and the BBB as a limitation to the eradication of HIV are discussed. Animal and tissue culture models for the study of virus interactions with the BBB are reviewed. HIV infection of the CNS is currently one of the most challenging aspects of HIV-induced disease, despite the recent relative success of highly active antiretroviral therapy. Although HIV-induced pathological changes in the brain have been well documented in the absence of opportunistic infections, the mechanisms of viral entry into the brain are little understood as are the sequelae following virus entry. While HIV has now been clearly shown to infect the CNS, neural elements, including neurons and oligodendrocytes, surprisingly do not appear to be directly infected by virus. The BBB is an anatomical barrier between the general circulation and the brain parenchyma. The BBB is composed of specialized microvascular endothelial cells (MVECs) in contact with astrocytes. The contact between brain MVECs and astrocyte foot processes has been postulated to be critical for the formation of the barrier. Some of the enabling properties of the BBB are limited pinocytotic vesicular transport, the presence of tight junctions among endothelial cells, and a selective permeability to physiological ions.

展开