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

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

NEUROSCIENCE LETTERS

ELSEVIER IRELAND LTD

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.