Caracterización molecular de la respuesta inmune innata inducida por interferón-β frente a herpes simplex virus tipo 1 en cultivos primarios de ganglio trigeminal murino

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dc.contributor.advisorCastellanos, Jaime
dc.contributor.advisorPrada-Arismendy, Jeanette
dc.contributor.authorLow Calle, Ana María
dc.contributor.orcidCastellanos, Jaime [0000-0003-1596-8383]
dc.date.accessioned2021-02-23T17:12:21Z
dc.date.available2021-02-23T17:12:21Z
dc.date.issued2021
dc.description.abstractEl virus Herpes simplex tipo 1 (HSV-1) es el principal causante de infecciones virales en la mucosa oral y regiones periorales. Esta infección es seguida por la diseminación del virus a neuronas sensoriales del ganglio trigeminal donde establece una infección latente de por vida. Se ha descrito que la respuesta inmune es importante para el control de la infección por HSV-1 y para el establecimiento de infecciones en el ganglio trigeminal. Sin embargo, no se conoce totalmente el papel de la respuesta inmune innata, en especial la de los Interferones (IFNs), frente al HSV-1 en el ganglio trigeminal. Por esto, se propuso indagar el papel del IFN-β ante a la infección por HSV1 en cultivos primarios de ganglio trigeminal de ratón. Así como evidenciar la expresión de genes inducidos por IFN en estas células tras la infección por HSV-1 y tras el tratamiento con IFN. Al mismo tiempo, evaluar la activación de la cascada de señalización Jak-Stat activada por IFN-β en cultivos de GT infectados con HSV-1. Se evidenció que el IFN-β tiene un efecto antiviral frente al HSV-1 en cultivos primarios de GT murino, causando una inhibición transcripcional de los 3 tipos de genes virales del ciclo lítico del virus, disminuyendo la producción de partículas virales y evitando la muerte celular por el virus. Adicionalmente la infección con HSV-1 incrementó los transcritos de Oligoadenilato sintetasa-1a y Rnasa L. El tratamiento con IFN-β causó la sobre-expresión de los genes de la Proteína kinasa R y Oligoadenilato sintetasa-1a; indicando que la actividad antiviral del IFN-β puede estar mediada por estas moléculas. Además, la infección disminuyó significativamente los niveles constitutivos del gen de la Proteína kinasa R, que participa en la inhibición traduccional mediada por IFN. Lo cual podría indicar que en el ganglio trigeminal ocurre un mecanismo nuevo de evasión viral al IFN, que hasta el momento no había sido descrito. Asimismo, la infección por HSV-1 causó la inducción del gen del Supresor de Señalización de Citoquinas-3 relacionado con el apagamiento de la señal del IFN-β, pero esta inducción disminuyó con el pre-tratamiento con IFN-β. Finalmente se evidenció que la infección con HSV-1 inhibió parcialmente la activación de la cascada de señalización Jak-Stat inducida por IFN-β, lo cual también podría representar un nuevo mecanismo de evasión viral que ocurre en el GT durante la etapa de infección aguda. Estos mecanismos virales de regulación de la respuesta inducida por IFN, que no han sido reportados previamente en ganglio trigeminal, podrían permitirle al HSV-1 establecer infecciones agudas de forma más eficiente, al contrarrestar parcialmente la respuesta inmune innata mediada por IFN-β en el GT y favorecer la instauración de la latencia.spa
dc.description.abstractenglishHerpes simplex virus type 1 (HSV-1) is the main pathogen that causes viral infections in oral mucosa and perioral regions. This is followed by viral diffusion through the sensory neurons in trigeminal ganglion, where it establishes life-long latent infections. It has been described that immune response is important to control HSV-1 infections and estalishment of latency. However, it is not well known completely, the role of innate immune response, especially the role mediated by Interferons (IFNs), against HSV-1 infections in trigeminal ganglia. For all these, we aimed to dig into the IFN-β role against HSV-1 infection in mice trigeminal ganglion primary cultures. To evaluate IFN stimulated gene expression, in these cells after HSV-1 infection or IFN-β treatment. Besides, we aim to evaluate activation of IFN-β Jak-Stat signal transduction in trigeminal ganglion cultures after HSV-1 infection. It was observed that IFN-β exerts an antiviral effect against HSV-1 in trigeminal ganglion cultures that causes transcripcional inhibition of viral lytic genes decreasing virions production and impairing cell death induced by viral infection. Additionally, HSV-1 infection increased Oligoadenylate synthetase-1a y Rnase L mRNA; and IFN-β treatment caused Oligoadenylate synthetase-1a and Protein kinase R induction, which implies that IFN-β antiviral activity may occur through these molecules. Besides infection significantly decreased constitutive levels Protein kinase R gene, that causes translational inhibition after IFN treatment. This could suggest that in trigeminal ganglia, a viral evasion mechanism exists that has not been described previously. Furthermore, HSV-1 infection caused Suppresor of Cytokine signalling-3 gene upregulation, which is related to IFN negative feedback. But this induction decreased after IFN-β pre-treatment. Finally HSV-1 infection partially inhibited IFN Jak-Stat pathway after infection. This also could be a novel viral evasion mechanism that occurs in trigeminal ganglion during acute herpes infection. These viral mechanisms of immune regulation to IFN allow the virus to establish acute infections more efficiently, by partially counteracting IFN-β innate immune response in trigeminal ganglia favoring viral latency establishment.eng
dc.description.degreelevelMaestríaspa
dc.description.degreenameMagíster en Ciencias Básicas Biomédicasspa
dc.format.mimetypeapplication/pdf
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlrepourl:https://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/5423
dc.language.isospa
dc.publisher.facultyFacultad de Medicinaspa
dc.publisher.grantorUniversidad El Bosquespa
dc.publisher.programMaestría en Ciencias Básicas Biomédicasspa
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dc.relation.referencesYoshimura A, Naka T, Kubo M. 2007. SOCS proteins, cytokine signalling and immune regulation. Nat Rev Immunol. 7: 454-465.spa
dc.relation.referencesZhou A, Hassel BA, Silverman RH. 1993. Expression cloning of 2-5A-dependent RNAase: a uniquely regulated mediator of interferon action. Cell. 72: 753-765.spa
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightshttps://purl.org/coar/access_right/c_abf2
dc.rights.creativecommons2011
dc.rights.localAcceso abiertospa
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.decsAntígenos de respuesta inmunespa
dc.subject.decsHerpes simplespa
dc.subject.decsGanglio del trigéminospa
dc.subject.nlmW 50
dc.titleCaracterización molecular de la respuesta inmune innata inducida por interferón-β frente a herpes simplex virus tipo 1 en cultivos primarios de ganglio trigeminal murinospa
dc.type.coarhttps://purl.org/coar/resource_type/c_bdcc
dc.type.coarversionhttps://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.driverinfo:eu-repo/semantics/masterThesis
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersion
dc.type.localTesis/Trabajo de grado - Monografía - Maestríaspa

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Maestría en Ciencias Básicas Biomédicas