ZIKV infection series in paediaitric brain tumour and NPC cell lines

Zika virus (ZIKV) is a mosquito-borne flavivirus consisting of historical African and epidemic-associated Asian lineages. The latter can access the central nervous system and causes microcephaly in the developing foetus through infection and depletion of neural stem and progenitor cells. The molecular mechanisms involved in this depletion response are grossly unknown for cells arising from CZS-affected children. Since 2017, the concept of employing ZIKV as oncolytic virotherapy against brain tumours has gained momentum. Oncolytic virotherapy exploits viruses that preferentially infect and destroy cancer cells via two distinct routes of therapeutic action. Following infection, intense viral replication induces oncolysis, releasing virions into the tumour microenvironment to infect neighbouring tumour cells. ZIKV induces an oncolytic event in infected pediatric brain tumour cells, but the molecular mechanisms involved in this response are grossly unknown. Here, we sought to investigate the molecular mechanisms underlying both the oncolytic and neuropathogenic responses of ZIKV infection in brain tumour and NPCs, respectively.