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10.1097/COH.0000000000000105 http://scihub22266oqcxt.onion/10.1097/COH.0000000000000105 C4319532!4319532 !25203638     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25203638 &cmd=llinks): Failed to open stream: HTTP request failed! 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Neuropathogenesis of HIV-associated neurocognitive disorders: roles for immune activation, HIV blipping and viral tropism |pdf=|usr=}}{{25203638 }} gab.com Text Neuropathogenesis of HIV-associated neurocognitive disorders: roles for immune activation, HIV blipping and viral tropism JO: Curr Opin HIV AIDS http://www.kidney.de/pget.php?&tw=1&pmid=25203638 #FOAvip PURPOSE OF REVIEW: The purpose of this study is to discuss why HIV-associated neurocognitive disorders (HAND) persist despite apparently effective HIV suppression by highly active antiretroviral therapy (ART). RECENT FINDINGS: As many as 50% of HIV-infected individuals suffer from HAND despite ART suppression of HIV replication to apparently undetectable levels in most treated individuals. Prior to ART, HIV-associated dementia (HAD), the severest form of HAND, affected nearly 20% of infected individuals; HAD now affects only nearly 2% of ART-treated persons, although less severe HAND forms persist. Recent studies link persistent immune activation, inflammation and viral escape/blipping in ART-treated individuals, as well as comorbid conditions, to HIV disease progression and increased HAND risk. Despite sustained HIV suppression in most ART-treated individuals, indicated by routine plasma monitoring and occasional cerebrospinal fluid (CSF) monitoring, 'blips' of HIV replication are often detected with more frequent monitoring, thus challenging the concept of viral suppression. Although the causes of HIV blipping are unclear, CSF HIV blipping associates with neuroinflammation and, possibly, central nervous system (CNS) injury. The current theory that macrophage-tropic HIV strains within the CNS predominate in driving HAND and these associated factors is now also challenged. SUMMARY: Protection of the CNS by ART is incomplete, probably due to combined effects of incomplete HIV suppression, persistent immune activation and host comorbidity factors. Adjunctive therapies to ART are necessary for more effective protection. Twit Text FOAVip Neuropathogenesis of HIV-associated neurocognitive disorders: roles for immune activation, HIV blipping and viral tropism ????Curr Opin HIV AIDS http://www.kidney.de/pget.php?&tw=1&pmid=25203638 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25203638 #FOAvip English Wikipedia <ref>{{Cite pmid|25203638 }}</ref> Neuropathogenesis of HIV-associated neurocognitive disorders: roles for immune activation, HIV blipping and viral tropism #MMPMID25203638 Chen MF ; Gill AJ ; Kolson DL Curr Opin HIV AIDS 2014[Nov]; 9 (6 ): 559-64 PMID25203638 show ga PURPOSE OF REVIEW: The purpose of this study is to discuss why HIV-associated neurocognitive disorders (HAND) persist despite apparently effective HIV suppression by highly active antiretroviral therapy (ART). RECENT FINDINGS: As many as 50% of HIV-infected individuals suffer from HAND despite ART suppression of HIV replication to apparently undetectable levels in most treated individuals. Prior to ART, HIV-associated dementia (HAD), the severest form of HAND, affected nearly 20% of infected individuals; HAD now affects only nearly 2% of ART-treated persons, although less severe HAND forms persist. Recent studies link persistent immune activation, inflammation and viral escape/blipping in ART-treated individuals, as well as comorbid conditions, to HIV disease progression and increased HAND risk. Despite sustained HIV suppression in most ART-treated individuals, indicated by routine plasma monitoring and occasional cerebrospinal fluid (CSF) monitoring, 'blips' of HIV replication are often detected with more frequent monitoring, thus challenging the concept of viral suppression. Although the causes of HIV blipping are unclear, CSF HIV blipping associates with neuroinflammation and, possibly, central nervous system (CNS) injury. The current theory that macrophage-tropic HIV strains within the CNS predominate in driving HAND and these associated factors is now also challenged. SUMMARY: Protection of the CNS by ART is incomplete, probably due to combined effects of incomplete HIV suppression, persistent immune activation and host comorbidity factors. Adjunctive therapies to ART are necessary for more effective protection. |Central Nervous System Diseases/immunology/pathology/*virology [MESH] |Cognition Disorders/immunology/pathology/*virology [MESH] |HIV Infections/immunology/pathology/*virology [MESH] |HIV-1/pathogenicity/*physiology [MESH] |Humans [MESH]Neuropathogenesis of HIV-associated neurocognitive disorders: roles fo(epmc).pdf DeepDyve Pubget Overpricing