tetano
Editor, Senior Moderator
Brief Report
[h=1][/h] [h=1]Expression Analysis Highlights AXL as a Candidate Zika Virus Entry Receptor in Neural Stem Cells[/h] Tomasz J. Nowakowski[SUP]3[/SUP]
, Alex A. Pollen[SUP]3[/SUP]
, Elizabeth Di Lullo
, Carmen Sandoval-Espinosa
, Marina Bershteyn
, Arnold R. Kriegstein
[SUP]3[/SUP]Co-first author
Publication stage: In Press Corrected Proof
DOI: http://dx.doi.org/10.1016/j.stem.2016.03.012
[h=2]Main Text[/h] In February 2016, the World Health Organization declared the 2015 outbreak of the Zika virus (ZIKV) in Central and South America a global health emergency (Heymann et al., 2016) following a strong correlation between cases of ZIKV infection and a dramatic increase in microcephaly cases in Brazil (Oliveira Melo et al., 2016, Schuler-Faccini et al., 2016). Subsequent reports have now established the ability of ZIKV to cross the human fetal-placental barrier to infect the developing central nervous system (Calvet et al., 2016, Martines et al., 2016, Mlakar et al., 2016). The neurotropism and neurovirulence of ZIKV has been appreciated in model systems since the earliest description of the virus (Bell et al., 1971, Dick, 1952, Dick et al., 1952), but it has only recently been described in human neural stem and progenitor cells using in vitro systems (Tang et al., 2016; P.P. Garc?z, E.C. Loiola, R.M. da Costa, L.M. Higa, P. Trindade, R. Delvecchio, J.M. Nascimento, R. Brindeiro, A. Tanuri, and S.K. Rehen, 2016, PeerJ, preprint). Although pathology data is currently limited, the first imaging studies and cases with confirmed ZIKV infection in the prenatal brain showed devastating consequences, including severe microcephaly, lissencephaly, hydrocephaly, necrosis, periventricular and cortical calcification, diffuse astrogliosis, and activated microglia (Mlakar et al., 2016, Schuler-Faccini et al., 2016). The findings of massive cell death and necrosis reflect a far more destructive process than occurs in many genetic forms of microcephaly.
full text
http://www.cell.com/cell-stem-cell/fulltext/S1934-5909(16)00118-1
[h=1][/h] [h=1]Expression Analysis Highlights AXL as a Candidate Zika Virus Entry Receptor in Neural Stem Cells[/h] Tomasz J. Nowakowski[SUP]3[/SUP]
, Alex A. Pollen[SUP]3[/SUP]
, Elizabeth Di Lullo
, Carmen Sandoval-Espinosa
, Marina Bershteyn
, Arnold R. Kriegstein
[SUP]3[/SUP]Co-first author
Publication stage: In Press Corrected Proof
DOI: http://dx.doi.org/10.1016/j.stem.2016.03.012
[h=2]Main Text[/h] In February 2016, the World Health Organization declared the 2015 outbreak of the Zika virus (ZIKV) in Central and South America a global health emergency (Heymann et al., 2016) following a strong correlation between cases of ZIKV infection and a dramatic increase in microcephaly cases in Brazil (Oliveira Melo et al., 2016, Schuler-Faccini et al., 2016). Subsequent reports have now established the ability of ZIKV to cross the human fetal-placental barrier to infect the developing central nervous system (Calvet et al., 2016, Martines et al., 2016, Mlakar et al., 2016). The neurotropism and neurovirulence of ZIKV has been appreciated in model systems since the earliest description of the virus (Bell et al., 1971, Dick, 1952, Dick et al., 1952), but it has only recently been described in human neural stem and progenitor cells using in vitro systems (Tang et al., 2016; P.P. Garc?z, E.C. Loiola, R.M. da Costa, L.M. Higa, P. Trindade, R. Delvecchio, J.M. Nascimento, R. Brindeiro, A. Tanuri, and S.K. Rehen, 2016, PeerJ, preprint). Although pathology data is currently limited, the first imaging studies and cases with confirmed ZIKV infection in the prenatal brain showed devastating consequences, including severe microcephaly, lissencephaly, hydrocephaly, necrosis, periventricular and cortical calcification, diffuse astrogliosis, and activated microglia (Mlakar et al., 2016, Schuler-Faccini et al., 2016). The findings of massive cell death and necrosis reflect a far more destructive process than occurs in many genetic forms of microcephaly.
full text
http://www.cell.com/cell-stem-cell/fulltext/S1934-5909(16)00118-1