Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)

Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have...
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Gespeichert in:

Autor*in:	Rao, Vasudev R [verfasserIn] Ruiz, Arthur P Prasad, Vinayaka R

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Lipoprotein Receptor Related Protein Brain Endothelial Cell Human Brain Microvascular Endothelial Cell Asymptomatic Neurocognitive Impairment Mild Neurocognitive Disorder

Anmerkung:	© Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: AIDS research and therapy - London : BioMed Central, 2004, 11(2014), 1 vom: 19. Mai
Übergeordnetes Werk:	volume:11 ; year:2014 ; number:1 ; day:19 ; month:05

Links:	Volltext

DOI / URN:	10.1186/1742-6405-11-13

Katalog-ID:	SPR029203287

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allfields	10.1186/1742-6405-11-13 doi (DE-627)SPR029203287 (SPR)1742-6405-11-13-e DE-627 ger DE-627 rakwb eng Rao, Vasudev R verfasserin aut Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. Lipoprotein Receptor Related Protein (dpeaa)DE-He213 Brain Endothelial Cell (dpeaa)DE-He213 Human Brain Microvascular Endothelial Cell (dpeaa)DE-He213 Asymptomatic Neurocognitive Impairment (dpeaa)DE-He213 Mild Neurocognitive Disorder (dpeaa)DE-He213 Ruiz, Arthur P aut Prasad, Vinayaka R aut Enthalten in AIDS research and therapy London : BioMed Central, 2004 11(2014), 1 vom: 19. Mai (DE-627)477528538 (DE-600)2173450-1 1742-6405 nnns volume:11 year:2014 number:1 day:19 month:05 https://dx.doi.org/10.1186/1742-6405-11-13 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2014 1 19 05
spelling	10.1186/1742-6405-11-13 doi (DE-627)SPR029203287 (SPR)1742-6405-11-13-e DE-627 ger DE-627 rakwb eng Rao, Vasudev R verfasserin aut Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. Lipoprotein Receptor Related Protein (dpeaa)DE-He213 Brain Endothelial Cell (dpeaa)DE-He213 Human Brain Microvascular Endothelial Cell (dpeaa)DE-He213 Asymptomatic Neurocognitive Impairment (dpeaa)DE-He213 Mild Neurocognitive Disorder (dpeaa)DE-He213 Ruiz, Arthur P aut Prasad, Vinayaka R aut Enthalten in AIDS research and therapy London : BioMed Central, 2004 11(2014), 1 vom: 19. Mai (DE-627)477528538 (DE-600)2173450-1 1742-6405 nnns volume:11 year:2014 number:1 day:19 month:05 https://dx.doi.org/10.1186/1742-6405-11-13 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2014 1 19 05
allfields_unstemmed	10.1186/1742-6405-11-13 doi (DE-627)SPR029203287 (SPR)1742-6405-11-13-e DE-627 ger DE-627 rakwb eng Rao, Vasudev R verfasserin aut Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. Lipoprotein Receptor Related Protein (dpeaa)DE-He213 Brain Endothelial Cell (dpeaa)DE-He213 Human Brain Microvascular Endothelial Cell (dpeaa)DE-He213 Asymptomatic Neurocognitive Impairment (dpeaa)DE-He213 Mild Neurocognitive Disorder (dpeaa)DE-He213 Ruiz, Arthur P aut Prasad, Vinayaka R aut Enthalten in AIDS research and therapy London : BioMed Central, 2004 11(2014), 1 vom: 19. Mai (DE-627)477528538 (DE-600)2173450-1 1742-6405 nnns volume:11 year:2014 number:1 day:19 month:05 https://dx.doi.org/10.1186/1742-6405-11-13 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2014 1 19 05
allfieldsGer	10.1186/1742-6405-11-13 doi (DE-627)SPR029203287 (SPR)1742-6405-11-13-e DE-627 ger DE-627 rakwb eng Rao, Vasudev R verfasserin aut Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. Lipoprotein Receptor Related Protein (dpeaa)DE-He213 Brain Endothelial Cell (dpeaa)DE-He213 Human Brain Microvascular Endothelial Cell (dpeaa)DE-He213 Asymptomatic Neurocognitive Impairment (dpeaa)DE-He213 Mild Neurocognitive Disorder (dpeaa)DE-He213 Ruiz, Arthur P aut Prasad, Vinayaka R aut Enthalten in AIDS research and therapy London : BioMed Central, 2004 11(2014), 1 vom: 19. Mai (DE-627)477528538 (DE-600)2173450-1 1742-6405 nnns volume:11 year:2014 number:1 day:19 month:05 https://dx.doi.org/10.1186/1742-6405-11-13 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2014 1 19 05
allfieldsSound	10.1186/1742-6405-11-13 doi (DE-627)SPR029203287 (SPR)1742-6405-11-13-e DE-627 ger DE-627 rakwb eng Rao, Vasudev R verfasserin aut Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND) 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. Lipoprotein Receptor Related Protein (dpeaa)DE-He213 Brain Endothelial Cell (dpeaa)DE-He213 Human Brain Microvascular Endothelial Cell (dpeaa)DE-He213 Asymptomatic Neurocognitive Impairment (dpeaa)DE-He213 Mild Neurocognitive Disorder (dpeaa)DE-He213 Ruiz, Arthur P aut Prasad, Vinayaka R aut Enthalten in AIDS research and therapy London : BioMed Central, 2004 11(2014), 1 vom: 19. Mai (DE-627)477528538 (DE-600)2173450-1 1742-6405 nnns volume:11 year:2014 number:1 day:19 month:05 https://dx.doi.org/10.1186/1742-6405-11-13 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2014 1 19 05
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author	Rao, Vasudev R
spellingShingle	Rao, Vasudev R misc Lipoprotein Receptor Related Protein misc Brain Endothelial Cell misc Human Brain Microvascular Endothelial Cell misc Asymptomatic Neurocognitive Impairment misc Mild Neurocognitive Disorder Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)
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topic_title	Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND) Lipoprotein Receptor Related Protein (dpeaa)DE-He213 Brain Endothelial Cell (dpeaa)DE-He213 Human Brain Microvascular Endothelial Cell (dpeaa)DE-He213 Asymptomatic Neurocognitive Impairment (dpeaa)DE-He213 Mild Neurocognitive Disorder (dpeaa)DE-He213
topic	misc Lipoprotein Receptor Related Protein misc Brain Endothelial Cell misc Human Brain Microvascular Endothelial Cell misc Asymptomatic Neurocognitive Impairment misc Mild Neurocognitive Disorder
topic_unstemmed	misc Lipoprotein Receptor Related Protein misc Brain Endothelial Cell misc Human Brain Microvascular Endothelial Cell misc Asymptomatic Neurocognitive Impairment misc Mild Neurocognitive Disorder
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title	Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)
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title_full	Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)
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title_sort	viral and cellular factors underlying neuropathogenesis in hiv associated neurocognitive disorders (hand)
title_auth	Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)
abstract	Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Abstract As the HIV-1 epidemic enters its fourth decade, HIV-1 associated neurological disorders (HAND) continue to be a major concern in the infected population, despite the widespread use of anti-retroviral therapy. Advancing age and increased life expectancy of the HIV-1 infected population have been shown to increase the risk of cognitive dysfunction. Over the past 10 years, there has been a significant progress in our understanding of the mechanisms and the risk factors involved in the development of HAND. Key events that lead up to neuronal damage in HIV-1 infected individuals can be categorized based on the interaction of HIV-1 with the various cell types, including but not limited to macrophages, brain endothelial cells, microglia, astrocytes and the neurons. This review attempts to decipher these interactions, beginning with HIV-1 infection of macrophages and ultimately resulting in the release of neurotoxic viral and host products. These include: interaction with endothelial cells, resulting in the impairment of the blood brain barrier; interaction with the astrocytes, leading to metabolic and neurotransmitter imbalance; interactions with resident immune cells in the brain, leading to release of toxic cytokines and chemokines. We also review the mechanisms underlying neuronal damage caused by the factors mentioned above. We have attempted to bring together recent findings in these areas to help appreciate the viral and host factors that bring about neurological dysfunction. In addition, we review host factors and viral genotypic differences that affect phenotypic pathological outcomes, as well as recent advances in treatment options to specifically address the neurotoxic mechanisms in play. © Rao et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)
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Viral and cellular factors underlying neuropathogenesis in HIV associated neurocognitive disorders (HAND)

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