GENERATED BY THE GERGELY LAB When the Zika virus enters neural stem cells, a protein known as Musashi-1 (MSI1) latches on to the virus’ s RNA genome, somehow promoting viral replication. Blocking the cells’ capability to produce MSI1 significantly inhibits Zika’ s ability to replicate, according to an in vitro study published today in Science.
The interaction between virus and the human protein appears to make the neural originate cells more vulnerable to cell death. Moreover, by joining to the Zika genome, MSI1 was less likely to content its natural targets within the neural stem cells effectively direct brain development, as evidenced by differences in the particular cells’ gene expression.
The results provide hints as to how Zika causes microcephaly in fetuses in whose mothers were infected while pregnant. Indeed, the group also found that a rare type of inherited microcephaly called autosomal recessive primary microcephaly is associated with mutations in MSI1.
“ We’ ve shown for the first time this particular interaction between Zika and MSI1— with MSI1 obtaining exploited by the virus for its own destructive life routine, turning MSI1 into the enemy within, ” coauthor Fanni Gergely from the University of Cambridge says in a pr release. “ We hope that in the future this discovery could lead to means of generating potential Zika virus vaccines. ”
“ This is the first study to show a clear link in between a specific protein, the Zika virus, and microcephaly, ” adds Mike Turner, head of Infection and Immunobiology at the Wellcome Trust, which partly funded the study. “ This new finding really helps to explain why nerve organs stem cells are so vulnerable to Zika infection and I wish this can be a first step in determining how we could stop this particular interaction and disease. ”