Document Detail

Neuropathogenesis of HIV-1 infection: interactions between interleukin-1 and transforming growth factor-beta 1.
MedLine Citation:
PMID:  9106229     Owner:  NLM     Status:  MEDLINE    
Cytokines are widely considered to function as major mediators of neuropathogenesis of HIV-1 infection. This view is based on a large amount of data obtained in vitro, in animal models and in human brain tissue obtained postmortem. Evidence for the involvement of interleukin-1 and transforming growth factor-beta 1, summarized here, indicates that these cytokines likely control HIV-1 expression in the brain and astrocytosis, the two hallmarks of brain in AIDS patients. Although the data do not reveal the precise time course of molecular and cellular changes in vivo, they strongly suggest a complex pattern of interactions whose ordering in time determines when and where HIV-1 is expressed in the brain. Further kinetic data are therefore urgently needed to shed light on the heterogeneity of HIV-1 expression in the brain.
L Vitković
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Molecular psychiatry     Volume:  2     ISSN:  1359-4184     ISO Abbreviation:  Mol. Psychiatry     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-07-30     Completed Date:  1997-07-30     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9607835     Medline TA:  Mol Psychiatry     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  111-2     Citation Subset:  IM; X    
Division of Neuroscience and Behavioral Science, National Institute of Mental Health, National Institutes of Health, Rockville, MD 20857, USA.
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MeSH Terms
AIDS Dementia Complex / physiopathology
Astrocytes / secretion,  virology
HIV Infections / complications,  physiopathology*
HIV-1* / physiology
Interleukin-1 / physiology*
Nervous System Diseases / etiology,  physiopathology*
Transforming Growth Factor beta / physiology*
Virus Replication
Reg. No./Substance:
0/Interleukin-1; 0/Transforming Growth Factor beta

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