Zika virus: Critical crosstalk between pathogenesis, cytopathic effects, and macroautophagy

Abstract

Zika virus (ZIKV) is a re‐emerging positive‐sense RNA arbovirus. Its genome encodes a polyprotein that is cleaved by proteases into three structural proteins (Envelope, pre‐Membrane, and Capsid) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5). These proteins have essential functions in viral replication cycle, cytopathic effects, and host cellular response. When infected by ZIKV, host cells promote macroautophagy, which is believed to favor virus entry. Although several authors have attempted to understand this link between macroautophagy and viral infection, little is known. Herein, we performed a narrative review of the molecular connection between macroautophagy and ZIKV infection while focusing on the roles of the structural and nonstructural proteins. We concluded that ZIKV proteins are major virulence factors that modulate host‐cell machinery to its advantage by disrupting and/or blocking specific cellular systems and organelles' function, such as endoplasmic reticulum stress and mitochondrial dysfunction.

Antiviral Activity of Flavonoids from Bauhinia holophylla Leaves against Zika virus

“…There is limited understanding regarding the mechanisms through which ZIKV causes these conditions or which viral proteins are responsible for the associated ZIKV-induced cytopathic effects, including cell hypertrophy, growth restriction, cell-cycle dysregulation, and cell death [64]. According to Bernardo-Menezes et al [65], ZIKV proteins are major virulence factors that modulate the host cell machinery by disrupting and/or blocking specific cellular systems and organelle functions, such as endoplasmic reticulum stress and mitochondrial dysfunction.…”