Longevity & AgingCD38 Drives Brain NAD+ Collapse During Zika Virus Infection
Researchers at UFRJ investigated why NAD+ levels fall in the brains of Zika-infected neonatal mice — a model mimicking third-trimester human infection. Using a detailed time-course analysis, they found that NAD+ depletion is a late-stage event, emerging one week after peak viral replication. Early induction of antiviral PARPs (PARP10, PARP12) tracked viral load but not NAD+ decline. Instead, NAD+ loss coincided precisely with rising CD38 expression and enzymatic activity, driven by infiltration of CD38-positive immune cells — particularly lymphocytes — into the brain. Blocking CD38 pharmacologically prevented NAD+ loss, identifying CD38 as the primary NAD+-depleting enzyme in this context and a potential therapeutic target for Congenital Zika Syndrome.
