Abstract
Zika virus (ZIKV), circulating in more than 70 countries since 2014, is causing severe developmental abnormality to compare to pre-epidemic infection. ZIKV related flaviviruses as the ability to produce subgenomic flaviviral RNAs (sfRNAs) which are associated with pathogenicity in foetal mice. This study, delineate the increased virulence of ZIKV through sfRNA mediated host protein interaction. Phylogenetically ZIKV sfRNA formed three distinct clades of African, Asian and American strains. Compare with pre-epidemic, the epidemic ZIKV sfRNA has genetic, RNA secondary structure and host protein interacting profile diversity. Interestingly this study found that ZIKV sfRNA interacting proteins involved in neuronal development, differentiation, proliferation, and apoptosis along with spermatogenesis, host immunity, and viral pathogenesis. The difference in the interaction profile and interaction strength between pre-epidemic and epidemic virus could be the reason for the increased virulence of the recent epidemic viruses. Targeting this protein will be the potent choice for antiviral drug designing.
