Basic insights into Zika virus infection of neuroglial and brain endothelial cells

• DOI: 10.1099/jgv.0.001416
• Publication Date: 2020-05-07T07:37:49Z
• Authors: Margit Mutso; James A. St John; Zheng Lung Ling; Felicity J. Burt; Yee Suan Poo; Xiang Liu; Eva Žusinaite; Georges E. Grau; Linda Hueston; Andres Merits; Nicholas J.C. King; Jenny A.K. Ekberg; Suresh Mahalingam
• Keywords: Vero cell; Zika Virus; Pathogenesis

Zika virus (ZIKV) has recently emerged as an important human pathogen due to the strong evidence that it causes disease of central nervous system, particularly microcephaly and Guillain-Barré syndrome. The pathogenesis disease, including mechanisms neuroinvasion, may include both invasion via blood-brain barrier peripheral (including cranial) nerves. Cellular responses infection are also poorly understood. This study characterizes in vitro laboratory-adapted ZIKV African MR766 two Asian strains (1) brain endothelial cells (hCMEC/D3 cell line) (2) olfactory ensheathing (OECs) (the neuroglia populating cranial nerve I bulb; mouse OEC lines) comparison kidney epithelial (Vero cells, which is well characterized). Readouts included kinetics, intracellular localization, viral persistence cytokine responses. Although not high Vero titres exceeded 104 plaque-forming units (p.f.u.) ml-1 endothelial/neuroglial types, except hOECs. Despite these substantial titres, a relatively small proportion neuroglial were primarily infected. Immunolabelling infected revealed localization envelope NS3 proteins cytoplasm; staining overlapped with dsRNA replication intermediate endoplasmic reticulum (ER). Infected OECs produced levels pro-inflammatory chemokines. Nevertheless, was able establish persistent hOEC hCMEC/D3 cells. Taken together, results provide basic insights into will form basis for further mechanisms.