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http://purl.uniprot.org/citations/23575248http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23575248http://www.w3.org/2000/01/rdf-schema#comment"

Background

HIV-1 entry into target lymphocytes requires the activity of actin adaptors that stabilize and reorganize cortical F-actin, like moesin and filamin-A. These alterations are necessary for the redistribution of CD4-CXCR4/CCR5 to one pole of the cell, a process that increases the probability of HIV-1 Envelope (Env)-CD4/co-receptor interactions and that generates the tension at the plasma membrane necessary to potentiate fusion pore formation, thereby favouring early HIV-1 infection. However, it remains unclear whether the dynamic processing of F-actin and the amount of cortical actin available during the initial virus-cell contact are required to such events.

Results

Here we show that gelsolin restructures cortical F-actin during HIV-1 Env-gp120-mediated signalling, without affecting cell-surface expression of receptors or viral co-receptor signalling. Remarkably, efficient HIV-1 Env-mediated membrane fusion and infection of permissive lymphocytes were impaired when gelsolin was either overexpressed or silenced, which led to a loss or gain of cortical actin, respectively. Indeed, HIV-1 Env-gp120-induced F-actin reorganization and viral receptor capping were impaired under these experimental conditions. Moreover, gelsolin knockdown promoted HIV-1 Env-gp120-mediated aberrant pseudopodia formation. These perturbed-actin events are responsible for the inhibition of early HIV-1 infection.

Conclusions

For the first time we provide evidence that through its severing of cortical actin, and by controlling the amount of actin available for reorganization during HIV-1 Env-mediated viral fusion, entry and infection, gelsolin can constitute a barrier that restricts HIV-1 infection of CD4+ lymphocytes in a pre-fusion step. These findings provide important insights into the complex molecular and actin-associated dynamics events that underlie early viral infection. Thus, we propose that gelsolin is a new factor that can limit HIV-1 infection acting at a pre-fusion step, and accordingly, cell-signals that regulate gelsolin expression and/or its actin-severing activity may be crucial to combat HIV-1 infection."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.org/dc/terms/identifier"doi:10.1186/1742-4690-10-39"xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Zipeto D."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Ziglio S."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Barroso-Gonzalez J."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Garcia-Exposito L."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Valenzuela-Fernandez A."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Machado J.D."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"Valera M.S."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/author"de Armas-Rillo L."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/name"Retrovirology"xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/pages"39"xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/title"Gelsolin activity controls efficient early HIV-1 infection."xsd:string
http://purl.uniprot.org/citations/23575248http://purl.uniprot.org/core/volume"10"xsd:string
http://purl.uniprot.org/citations/23575248http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23575248
http://purl.uniprot.org/citations/23575248http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23575248
http://purl.uniprot.org/uniprot/P04578#attribution-6989D850A076CE19C85E85EB969AD820http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23575248
http://purl.uniprot.org/uniprot/P06396#attribution-49D588FD0EB240382DB4A4F1E7835342http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23575248
http://purl.uniprot.org/uniprot/P06396#attribution-6737DC76DA2263E8015D63E523E86B9Fhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23575248
http://purl.uniprot.org/uniprot/P06396#attribution-6989D850A076CE19C85E85EB969AD820http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23575248
http://purl.uniprot.org/uniprot/#_A0A0A0MS51-mappedCitation-23575248http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23575248
http://purl.uniprot.org/uniprot/#_A0A0A0MT01-mappedCitation-23575248http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23575248
http://purl.uniprot.org/uniprot/#_A0A384MEF1-mappedCitation-23575248http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23575248
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