dc.creatorOjeda, Diego Sebastian
dc.creatorLopez, Juan Jose
dc.creatorSede, Mariano Miguel
dc.creatorLopez, Ester Maria
dc.creatorBerria, Maria Isabel
dc.creatorQuarleri, Jorge Fabian
dc.date.accessioned2017-05-26T20:25:00Z
dc.date.accessioned2018-11-06T15:26:05Z
dc.date.available2017-05-26T20:25:00Z
dc.date.available2018-11-06T15:26:05Z
dc.date.created2017-05-26T20:25:00Z
dc.date.issued2014-02
dc.identifierOjeda, Diego Sebastian; Lopez, Juan Jose; Sede, Mariano Miguel; Lopez, Ester Maria; Berria, Maria Isabel; et al.; Increased in vitro glial fibrillary acidic protein expression, telomerase activity, and telomere length after productive human immunodeficiency virus-1 infection in murine astrocytes; Wiley; Journal of Neuroscience Research; 92; 2; 2-2014; 267-274
dc.identifier0360-4012
dc.identifierhttp://hdl.handle.net/11336/17005
dc.identifier1097-4547
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1897086
dc.description.abstractAlthough HIV-associated neurocognitive disorders (HAND) result from injury and loss of neurons, productive infection routinely takes place in cells of macrophage lineage. In such a complex context, astrocytosis induced by local chemokines/cytokines is one of the hallmarks of HIV neuropathology. Whether this sustained astrocyte activation is able to alter telomere-aging process is unknown. We hypothesized that interaction of HIV with astrocytes may impact astrocyte telomerase activity (TA) and telomere length in a scenario of astrocytic activation measured by expression of glial fibrillary acidic protein (GFAP). To test this hypothesis, cultured murine astrocytes were challenged with pseudotyped HIV/vesicular stomatitis virus (HIV/VSV) to circumvent the absence of viral receptors; and GFAP, telomerase activity, and telomere length were quantified. As an early and transient event after HIV infection, both TA activity and telomere length were significantly augmented (P < 0.001). Later, a strong negative correlation (−0.8616, P < 0.0001) between virus production and telomerase activity was demonstrated. Once HIV production had reached a peak (7 dpi), the TA decreased, showing levels similar to those of noninfected cells. In contrast, the astrocyte became activated, exhibiting significantly increased levels of GFAP expression directly related to the level of HIV/VSV replication (P < 0.0001). Our results suggest that HIV-infected astrocytes exhibit early disturbance in their cellular functions, such as telomerase activity and telomere length, that may attenuate cell proliferation and enhance the astrocyte dysregulation, contributing to HIV neuropathogenesis. Understanding the mechanisms involved in HIV-mediated persistence by altering the telomere-related aging processes could aid in the development of therapeutic modalities for neurological complications of HIV infection.
dc.languageeng
dc.publisherWiley
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/jnr.23294/abstract
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1002/jnr.23294
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectGFAP
dc.subjectHIV-1
dc.subjectASTROCYTES
dc.subjectTELOMERASE
dc.subjectTELOMERE LENGTH
dc.titleIncreased in vitro glial fibrillary acidic protein expression, telomerase activity, and telomere length after productive human immunodeficiency virus-1 infection in murine astrocytes
dc.typeArtículos de revistas
dc.typeArtículos de revistas
dc.typeArtículos de revistas


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