TY - JOUR
T1 - Neurobiological aspects of human immunodeficiency virus infection
T2 - Neurotoxic mechanisms
AU - Nath, Avindra
AU - Geiger, Jonathan
N1 - Funding Information:
The authors thank Kevin Coombs, Melina Jones and David Simpson for helpful comments. This work was supported by funds obtained from the National Health Research Development Program and the Medical Research Council of Canada.
PY - 1998/1
Y1 - 1998/1
N2 - Dementia due to human immunodeficiency virus (HIV) infection is the commonest cause of dementia in children, young adults and middle-aged people. Its incidence continues to rise despite the use of newer antiretroviral agents. The study of the pathogenesis of HIV dementia has lead to the discovery of novel mechanisms of neural dysfunction and toxicity, and holds promise for further discovery of new molecules and pathways involved in maintaining cerebral function and enabling dysfunction. New to the field of neurovirology is the emerging concept that proteins that are part of the virus may themselves be neurotoxic by virtue of their abilities to be either directly toxic to brain cells or may, through their actions on glial cells or macrophages, release neurotoxic products coded by the host genome. These mechanisms have been demonstrated for HIV-1 and accordingly we propose a new term, virotoxins, to describe such actions. This review provides an in-depth analysis of the pathophysiological mechanisms by which these vital and cellular products affected by HIV virotoxins cause neural dysfunction.
AB - Dementia due to human immunodeficiency virus (HIV) infection is the commonest cause of dementia in children, young adults and middle-aged people. Its incidence continues to rise despite the use of newer antiretroviral agents. The study of the pathogenesis of HIV dementia has lead to the discovery of novel mechanisms of neural dysfunction and toxicity, and holds promise for further discovery of new molecules and pathways involved in maintaining cerebral function and enabling dysfunction. New to the field of neurovirology is the emerging concept that proteins that are part of the virus may themselves be neurotoxic by virtue of their abilities to be either directly toxic to brain cells or may, through their actions on glial cells or macrophages, release neurotoxic products coded by the host genome. These mechanisms have been demonstrated for HIV-1 and accordingly we propose a new term, virotoxins, to describe such actions. This review provides an in-depth analysis of the pathophysiological mechanisms by which these vital and cellular products affected by HIV virotoxins cause neural dysfunction.
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U2 - 10.1016/S0301-0082(97)00053-1
DO - 10.1016/S0301-0082(97)00053-1
M3 - Article
C2 - 9460791
AN - SCOPUS:0031974964
SN - 0301-0082
VL - 54
SP - 19
EP - 33
JO - Progress in Neurobiology
JF - Progress in Neurobiology
IS - 1
ER -