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dc.contributor.authorMartin C., Leyton L., Hott M., Arancibia Y., Spichiger C., McNiven M.A., Concha M.I., Burgos P.V., Otth C.es_CL
dc.contributor.authorCourt, Felipe A. [Centro de Biología Integrativa, Facultad de Ciencias, Universidad Mayor, Chile]es_CL
dc.date.accessioned2020-08-12T14:11:55Z
dc.date.accessioned2020-08-12T18:13:27Z
dc.date.available2020-08-12T14:11:55Z
dc.date.available2020-08-12T18:13:27Z
dc.date.issued2017es_CL
dc.identifier.citationMartin, C., Leyton, L., Hott, M., Arancibia, Y., Spichiger, C., McNiven, M. A., ... & Otth, C. (2017). Herpes simplex virus type 1 neuronal infection perturbs golgi apparatus integrity through activation of Src tyrosine kinase and Dyn-2 GTPase. Frontiers in cellular and infection microbiology, 7, 371.es_CL
dc.identifier.issn2235-2988es_CL
dc.identifier.urihttps://www.frontiersin.org/articles/10.3389/fcimb.2017.00371/fulles_CL
dc.identifier.urihttps://dx.doi.org/10.3389%2Ffcimb.2017.00371es_CL
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572415/pdf/fcimb-07-00371.pdfes_CL
dc.identifier.urihttp://repositorio.umayor.cl/xmlui/handle/sibum/6928
dc.description.abstractHerpes simplex virus type 1 (HSV-1) is a ubiquitous pathogen that establishes a latent persistent neuronal infection in humans. The pathogenic effects of repeated viral reactivation in infected neurons are still unknown. Several studies have reported that during HSV-1 epithelial infection, the virus couldmodulate diverse cell signaling pathways remodeling the Golgi apparatus (GA) membranes, but the molecular mechanisms implicated, and the functional consequences to neurons is currently unknown. Here we report that infection of primary neuronal cultures with HSV-1 triggers Src tyrosine kinase activation and subsequent phosphorylation of Dynamin 2 GTPase, two players with a role in GA integrity maintenance. Immunofluorescence analyses showed that HSV-1 productive neuronal infection caused a scattered and fragmented distribution of the GA through the cytoplasm, contrasting with the uniform perinuclear distribution pattern observed in control cells. In addition, transmission electron microscopy revealed swollen cisternae and disorganized stacks in HSV-1 infected neurons compared to control cells. Interestingly, PP2, a selective inhibitor for Src-family kinases markedly reduced these morphological alterations of the GA induced by HSV-1 infection strongly supporting the possible involvement of Src tyrosine kinase. Finally, we showed that HSV-1 tegument protein VP11/12 is necessary but not sufficient to induce Dyn2 phosphorylation. Altogether, these results show that HSV-1 neuronal infection triggers activation of Src tyrosine kinase, phosphorylation of Dynamin 2 GTPase, and perturbation of GA integrity. These findings suggest a possible neuropathogenic mechanism triggered by HSV-1 infection, which could involve dysfunction of the secretory system in neurons and central nervous system.es_CL
dc.description.sponsorshipThese studies were funded by grants: FONDECYT REGULAR 1150574, FONDECYT 1070377, Ring Initiative ACT1109 and CONICYT 24121539, CISNe-UACh and DID-UACh. We thank Dr. Gonzalo Mardones for antibodies support and critical reading of the manuscript.es_CL
dc.format.extentRevisión
dc.language.isoenes_CL
dc.publisherFrontiers Media S.A.es_CL
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceFrontiers in Cellular and Infection Microbiology, 2017. 7(AUG), ART. N° 371
dc.titleHerpes simplex virus type 1 neuronal infection perturbs golgi apparatus integrity through activation of src tyrosine kinase and Dyn-2 GTPasees_CL
dc.typeArtículo o paperes_CL
umayor.facultadFacultad de Ciencias
umayor.indizadorCOT
umayor.politicas.sherpa/romeoEsta revista tiene licencia Creative Commons BYes_CL
umayor.indexadoWOSes_CL
umayor.indexadoSCOPUSes_CL
dc.identifier.doiDOI: 10.3389%2Ffcimb.2017.00371es_CL]
umayor.indicadores.wos-(cuartil)Q2es_CL
umayor.indicadores.scopus-(scimago-sjr)0.,63es_CL


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