Exploring miRNAs as the key to understand symptoms induced by ZIKA virus infection through a collaborative database.

Zika virus (ZIKV) is an emerging mosquito-borne flavivirus, first isolated in 1947 from the serum of a pyrexial rhesus monkey caged in the Zika Forest (Uganda/Africa)1. In 2007 ZIKV was reported to of been responsible for an outbreak of relatively mild disease, characterized by rash, arthralgia, and conjunctivitis on Yap Island, in the western Pacific Ocean2. In the past year, ZIKV has been circulating in the Americas, probably introduced through Easter Island (Chile), by French Polynesians3. In early 2015, a new outbreak was recognized in northeast Brazil4, where concerns over its possible links with infant microcephaly have been discussed5,6. Providing a definitive link between ZIKV infection and birth defects is still a big challenge7. MicroRNAs (miRNAs), are small noncoding RNAs that regulating post-transcriptional gene expression by translational repression, and play important roles in viral pathogenesis8 and brain development9. It is estimated that more than 60% of human protein-coding genes contain at least one conserved miRNA-binding site10. The potential for flavivirus-mediated miRNA signaling dysfunction in brain-tissue develop provides a compelling mechanism underlying perceived linked between ZIKV and microcephaly. Here, we provide strong evidences toward to understand the mechanism in which miRNAs can be linked to the \"congenital Zika syndrome\" symptoms. Moreover, following World Health Organization (WHO) recommendations11, we have assembled a database that could help target mechanistic investigations of this possible relationship between ZIKV symptoms and miRNA mediated human gene expression, helping to foster potential targets for therapy.