Even though Zika virus was first identified in 1947, the infectious disease remained obscure until a 2015 outbreak in Central and South America. That’s when doctors noted a dramatic rise in infants with underdeveloped heads and brains (a condition known as microcephaly) born to women who were infected with the virus when pregnant. Now, researchers have found that mutation of a single amino acid in one of the Zika virus’s structural proteins, known as prM, may be responsible for causing microcephaly by enabling the virus to kill developing brain cells (Science 2017, DOI: 10.1126/science.aam7120). A team led by Cheng-Feng Qin of the Beijing Institute of Microbiology & Epidemiology and Zhiheng Xu of the Chinese Academy of Sciences compared three recent strains of Zika virus with one from 2010 and found the more recent versions to be deleterious or deadly to neonatal and fetal mice, whereas the 2010 virus was not. Biochemical sleuthing led them to discover that a serine residue in prM of the 2010 virus had mutated to an asparagine in the more recent strains. When the researchers made this single mutation to a virus that was otherwise identical to the 2010 strain, it was dramatically more deadly to neonatal mice than the unmutated version. When the researchers modified this asparagine to a serine in a 2016 version of the virus, it proved to be less deadly.