CD38 is a key mediator of NAD⁺ depletion in the brain of ZIKV-infected mice.

ABSTRACT: Zika virus (ZIKV) infection is a major health concern, particularly during pregnancy, as it can lead to neurodevelopmental delays and congenital brain abnormalities, including microcephaly. Here, we investigated the mechanisms of NAD⁺ depletion in the brains of ZIKV-infected neonatal mice, a model that developmentally corresponds to third-trimester infection in humans. We observed a progressive decline in NAD⁺ levels, which became significant at later stages of infection (18-30 dpi). This decrease did not correlate with viral replication and early Parp10 or Parp12 induction, which increased alongside Nampt expression, possibly as a compensatory response to NAD⁺ consumption. Instead, NAD⁺ depletion coincided with increased CD3

SUBMITTER: Saraiva GN 

PROVIDER: S-EPMC12682054 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature