Early after primary infection of human immunodeficiency virus (HIV), the HIV virus invades the central nervous system resulting in motor and cognitive dysfunction ranging from mild impairment to frank dementia. Chronic HIV infection can result in neurodegenerative disease, overall termed neuroAIDS. HIV infection leads to neuronal dysfunction and neurodegeneration via the activation of brain macrophages/microglia, the presence of viral proteins, and/or inflammatory factors generated in response to viral infection as well as alterations in glia and the blood-brain barrier. Although HIV does not productively infect neurons, neuronal injury and loss play a central role in the neurological decline and HIV-associated neuropathology. Early in the AIDS epidemic, patients exhibited high viral loads and elevated markers of immune activation as well as neurological dysfunction in cognition, motor performance, and behavior. Despite successful reduction of viral burden using antiretroviral therapies, the persistence of a milder less severe form of HIV-associated neurocognitive disorder (HAND) remains. The presence of several risk factors has been associated with the development of HAND, which include host factors, HIV disease and viral factors, comorbidity factors, as well as CNS penetrance and toxicity of cART. As HAND has been associated with increased mortality, decreased quality of life, and poor adherence to treatment, even this milder form of HIV-associated neurocognitive impairment is clinically relevant. This chapter on NeuroAIDS highlights the progression in the field and our current understanding of HIV infection of the CNS, HIV-induced neurodegeneration, and HAND pathogenesis.
- Blood-brain barrier
- HIV-associated neurocognitive disorders
ASJC Scopus subject areas