# Role of Mertk in pathological neurodevelopment in mice with congenital Zika virus infection

> **NIH NS K08** · WASHINGTON UNIVERSITY · 2026 · $234,303

## Abstract

Project Summary/ Abstract
Congenital and perinatal infections are a leading cause of fetal and infant morbidity and mortality. There is
increasing evidence that brain injury in babies with congenital and perinatal infections is caused not only by direct
injury from the pathogen itself, but also may be due to the inflammatory or immune response to the pathogen.
Targeted immunotherapies that allow pathogen control and removal but minimize bystander brain injury are
largely unexplored. This proposal investigates the role of the receptor tyrosine kinase, Mertk, in cognitive and
behavioral dysfunction in mice after congenital Zika virus (ZIKV) infection. Recent global epidemics link
congenital ZIKV infection to neurodevelopmental abnormalities including microcephaly, intracranial
calcifications, ventriculomegaly, and cognitive and behavioral impairment. Recent data indicate that ZIKV-
exposed children without major structural brain abnormalities at birth may still have cognitive and behavioral
deficits. Mertk, a receptor tyrosine kinase expressed by astrocytes and microglia, has been implicated in
autoimmune, infectious and oncologic processes. It is not expressed by neurons, so immune-specific pathways
can be probed without disturbing neuronal biology.
Mertk facilitates microglial- and astrocyte- mediated synaptic
pruning during early brain development and also mediates phagocytosis of cells and cellular debris in the brain.
The hypotheses to be tested are: (1) Increased prenatal and early postnatal Mertk signaling during congenital
ZIKV infection mediates immune-mediated neuronal injury; (2) increased postnatal Mertk signaling in microglia
and astrocytes during congenital ZIKV leads to increased phagocytosis of mature neurons and synaptic pruning;
and (3) increased Mertk signaling due to congenital ZIKV infection mediates abnormalities in functional
connectivity, cognition, and behavioral deficits following congenital ZIKV infection. Understanding mechanisms
of brain i

## Key facts

- **NIH application ID:** 11259567
- **Project number:** 5K08NS136766-02
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** Shannon Christine Agner
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NS
- **Fiscal year:** 2026
- **Award amount:** $234,303
- **Award type:** 5
- **Project period:** 2025-01-15T00:00:00 → 2029-12-31T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11259567

## Citation

> US National Institutes of Health, RePORTER application 11259567, Role of Mertk in pathological neurodevelopment in mice with congenital Zika virus infection (5K08NS136766-02). Retrieved via AI Analytics 2026-06-25 from https://api.ai-analytics.org/grant/nih/11259567. Licensed CC0.

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