Document Detail


Prothymosin-alpha inhibits HIV-1 via Toll-like receptor 4-mediated type I interferon induction.
MedLine Citation:
PMID:  20479248     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Induction of type I interferons (IFN) is a central feature of innate immune responses to microbial pathogens and is mediated via Toll-like receptor (TLR)-dependent and -independent pathways. Prothymosin-alpha (ProTalpha), a small acidic protein produced and released by CD8(+) T cells, inhibits HIV-1, although the mechanism for its antiviral activity was not known. We demonstrate that exogenous ProTalpha acts as a ligand for TLR4 and stimulates type I IFN production to potently suppress HIV-1 after entry into cells. These activities are induced by native and recombinant ProTalpha, retained by an acidic peptide derived from ProTalpha, and lost in the absence of TLR4. Furthermore, we demonstrate that ProTalpha accounts for some of the soluble postintegration HIV-1 inhibitory activity long ascribed to CD8(+) cells. Thus, a protein produced by CD8(+) T cells of the adaptive immune system can exert potent viral suppressive activity through an innate immune response. Understanding the mechanism of IFN induction by ProTalpha may provide therapeutic leads for IFN-sensitive viruses.
Authors:
Arevik Mosoian; Avelino Teixeira; Colin S Burns; Leif E Sander; G Luca Gusella; Cijiang He; J Magarian Blander; Paul Klotman; Mary E Klotman
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-05-17
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  107     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-10     Completed Date:  2010-06-29     Revised Date:  2010-09-30    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10178-83     Citation Subset:  IM    
Affiliation:
Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. arevik.mosoian@mssm.edu
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Vesicular Transport / immunology
Amino Acid Sequence
Animals
Anti-HIV Agents / immunology,  pharmacology
CD8-Positive T-Lymphocytes / immunology
HIV-1 / drug effects*,  genetics,  immunology,  physiology
Humans
Immunity, Innate / drug effects
Interferon Type I / biosynthesis*,  genetics
Ligands
Macrophages / drug effects,  immunology,  virology
Mice
Mice, Knockout
Molecular Sequence Data
Myeloid Differentiation Factor 88 / immunology
Protein Precursors / genetics,  immunology,  pharmacology*
RNA, Messenger / genetics,  metabolism
Recombinant Proteins / genetics,  immunology,  pharmacology
Sequence Homology, Amino Acid
Thymosin / analogs & derivatives*,  genetics,  immunology,  pharmacology
Toll-Like Receptor 4 / drug effects*,  metabolism*
Tumor Necrosis Factor-alpha / biosynthesis,  genetics
Virus Replication / drug effects
Grant Support
ID/Acronym/Agency:
AI76092-01A1/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Vesicular Transport; 0/Anti-HIV Agents; 0/Interferon Type I; 0/Ligands; 0/MYD88 protein, human; 0/Myeloid Differentiation Factor 88; 0/Protein Precursors; 0/RNA, Messenger; 0/Recombinant Proteins; 0/TICAM1 protein, human; 0/TLR4 protein, human; 0/Toll-Like Receptor 4; 0/Tumor Necrosis Factor-alpha; 0/prothymosin alpha; 61512-21-8/Thymosin
Comments/Corrections

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