Document Detail


Innate immunity in acute HIV-1 infection.
MedLine Citation:
PMID:  21734567     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: Acute HIV-1 infection (AHI) is composed of the eclipse phase, during which the transmitted virus struggles to avoid eradication and achieve amplification/spread; the expansion phase when virus disseminates and undergoes exponential replication associated with extensive CD4⁺ T-cell destruction; and the containment phase when set-point levels of viremia and immune activation are established. The importance of interactions between HIV-1 and innate responses in determining events throughout AHI is increasingly recognized, and is reviewed here.
RECENT FINDINGS: During the eclipse phase, HIV-1 subverts dendritic cell functions to promote its replication at mucosal sites and employs multiple strategies to minimize control by type 1 interferons. Systemic virus dissemination is associated with widespread activation of innate responses which fuels HIV-1 replication. To minimize the protective effects of innate responses, HIV-1 resists control by natural killer cells and may impair innate regulation of adaptive responses. Innate responses remain chronically activated after HIV-1 containment which is thought to drive HIV-1 pathogenesis.
SUMMARY: Innate responses are pivotal determinants of events at all stages of AHI. Increased understanding of mechanisms involved in innate control of HIV-1 and pathways regulating innate activation during HIV-1 infection could facilitate development of novel approaches to combating this infection.
Authors:
Persephone Borrow
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current opinion in HIV and AIDS     Volume:  6     ISSN:  1746-6318     ISO Abbreviation:  Curr Opin HIV AIDS     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-09     Completed Date:  2011-12-02     Revised Date:  2012-01-26    
Medline Journal Info:
Nlm Unique ID:  101264945     Medline TA:  Curr Opin HIV AIDS     Country:  United States    
Other Details:
Languages:  eng     Pagination:  353-63     Citation Subset:  IM; X    
Affiliation:
Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK. persephone.borrow@ndm.ox.ac.uk
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MeSH Terms
Descriptor/Qualifier:
HIV Infections / immunology*,  virology*
HIV-1 / immunology*,  pathogenicity*
Humans
Immunity, Innate*
Grant Support
ID/Acronym/Agency:
U01 AI067854-06/AI/NIAID NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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