Because inflammation inhibits PARP1-dependent DNA repair69 and PARP1 modulates chromatin modification and gene expression, potentially regulating myelination66, CaMKII-dependent neurogenic program70, and long-term memory formation65, future studies are required to determine if these functions of PARP1 are affected in AD brains and contribute to cis-and trans-RSV-mediated neuronal effects shown here. Here, CAMK2G is linked to Alzheimer disease.