Contributions of Immune Response to Individual Differences in Zika Virus Infection

Zika virus has emerged as a public health crisis and is associated with a number of neurological deficits; however, only subsets of individuals who contract a Zika virus infection develop severe symptoms. The mechanism underlying Zika virus-induced neuropathogenesis is still poorly understood. Recent studies have implicated the host immune response as a key regulator in Zika virus neuropathology. Specifically, immune responses generated from previous flavi virus infection may contribute to antibody-dependent enhancement of Zika virus infection. Innate immunity may also play an important role for the broad array of individual symptomatic differences. Therefore, host immunity may serve as a therapeutic target to reduce Zika-associated neuropathogenesis.