Practice question

Zika virus neuropathogenesis involves manipulation of host noncoding RNA regulation beyond protein targeting. In neural progenitors infection dysregulates microRNA biogenesis, altering levels of brain-enriched miRNAs such as miR-9, miR-124, let-7 family and miR-132 that control cell cycle, differentiation timing and apoptosis. Subgenomic flavivirus RNAs sequester Dicer and Ago proteins impairing processing. Changes in microRNA profiles lead to premature cell cycle exit, increased caspase activation and reduced proliferation of cortical progenitors. DNA methylation or phosphorylation alterations less central. Consequently brain growth reduction after Zika reflects altered microRNA levels governing neurogenesis and cortical expansion.