Galectin-3 is upregulated in activated glia during Junin virus-induced murine encephalitis

CAROLINA JAQUENOD DE GIUSTI, LUCRECIA ALBERDI, JESICA FRIK, MARÍA F. FERRER, EMILIA SCHARRIG, MIRTA SCHATTNER, RICARDO M. GOMEZ.

NEUROSCIENCE LETTERS

ELSEVIER IRELAND LTD

Lugar: Amsterdam; Año: 2011 vol. 501 p. 163 - 166

0304-3940

Argentine haemorrhagic fever (AHF) is a systemic febrile syndrome characterized by several haematological and neurological alterations caused by Junín virus (JUNV), a member of the Arenaviridae family. Newborn mice are highly susceptible to JUNV and the course of infection has been associated with the viral strain used. Galectin-3 (Gal-3) is an animal lectin that has been proposed to play an important role in some central nervous system (CNS) diseases. In this study, we analysed Gal-3 expression at the transcriptional and translational expression levels during JUNV-induced CNS disease. We found that Candid 1 strain induced, with relatively low mortality, a subacute/chronic CNS disease with significant glia activation and upregulation of Gal-3 in microglia cells as well as in reactive astrocytes that correlated with viral levels. Our results suggest an important role for Gal-3 in viral-induced CNS disease.