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Symptomatic dengue virus (DENV) infections range from mild fever to severe haemorrhagic
disease and death. Host‐viral interactions play a significant role in deciding the fate of the
infection. The unfolded protein response (UPR) is a prosurvival cellular reaction induced in
response to DENV‐mediated endoplasmic reticulum stress. The UPR has complex interactions
with the cellular autophagy machinery, apoptosis, and innate immunity. DENV has evolved to
manipulate the UPR to facilitate its replication and to evade host immunity. Our knowledge of
this intertwined network of events is continuously developing. A better understanding of the
UPR mediated antiviral and proviral effects will shed light on dengue disease pathogenesis and
may help development of anti‐DENV therapeutics. This review summarizes the role of the UPR
in viral replication, autophagy, and DENV‐induced inflammation to describe how a host response
contributes to DENV pathogenesis.
