1995
DOI: 10.1016/0304-3940(95)12105-d
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Glial fibrillary acidic protein (GFAP) immunochemical profile after Junin virus infection of rat cultured astrocytes

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Cited by 8 publications
(4 citation statements)
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“…Lassa virus, Junin virus, and other hemorrhagic arenaviruses enter the brain and cause neurological symptoms that can include encephalitis, hearing loss, and tremors [41,42]. Similar to our observations in CCHFV brain infection of SGM3 humanized mice, Junin virus also infects astrocytes, and neurodegenerative reactive astrogliosis may play a role in the pathogenesis of acute and late neurological symptoms in Junin virus infection [43][44][45][46]. Furthermore, many closely related bunyaviruses, including those of the California serogroup (genus Orthobunyavirus) and Rift Valley fever virus (genus Phlebovirus) are well characterized as causing neurological symptoms in human disease, supporting the potential for more frequent neurological involvement in CCHF than currently recognized.…”
Section: Discussionsupporting
confidence: 82%
“…Lassa virus, Junin virus, and other hemorrhagic arenaviruses enter the brain and cause neurological symptoms that can include encephalitis, hearing loss, and tremors [41,42]. Similar to our observations in CCHFV brain infection of SGM3 humanized mice, Junin virus also infects astrocytes, and neurodegenerative reactive astrogliosis may play a role in the pathogenesis of acute and late neurological symptoms in Junin virus infection [43][44][45][46]. Furthermore, many closely related bunyaviruses, including those of the California serogroup (genus Orthobunyavirus) and Rift Valley fever virus (genus Phlebovirus) are well characterized as causing neurological symptoms in human disease, supporting the potential for more frequent neurological involvement in CCHF than currently recognized.…”
Section: Discussionsupporting
confidence: 82%
“…In our experimental model, we confirmed the presence of widespread astrocyte reaction in infected animals. In this connection, JV induction of astrocyte activation has also been described in rat brain cell cultures [Berría and Lascano, 1985] and such increased cell maturation proved concomitant with transient enhancement of both phagocytic activity [Iacono et al, 1991] and GFAP immunochemical profile [Iacono et al, 1995]. Bearing in mind that greater mortality was observed in AG-treated mice displaying lower astrocyte reactivity, as appreciated by cursory inspection, though viral infectivity titers were similar regardless of treatment, intense astrocyte activation seemed as mainly beneficial, likely by exerting supportive functions or even by restoring damaged tissues.…”
Section: Discussionmentioning
confidence: 90%
“…In contrast, the marked increase in GFAP was delayed compared with iNOS expression, and there was no co-localization of viral and GFAP antigens on days 3-7 PI. In addition, the concomitant enhanced expression of GFAP mRNA rules out that this result is due to the previously described transient soluble detection fraction of GFAP following JV infection [13]. Moreover, GFAP expression was observed in the monolayer as foci that were increased both in number and intensity over time, suggesting a paracrine mechanism as the cause of such astrocyte activation.…”
mentioning
confidence: 71%