Infection with cytomegalovirus (CMV) during pregnancy is the most common non-genetic cause of congenital birth defects. The aim of this project is to develop a CMV mouse model that replicates congenital CMV (cCMV) infection to better understand the mechanisms at play, and eventually develop new therapeutic strategies.
2026 Tullie and Rickey Families Spark Awards finalist
Remi Marrocco, Ph.D.
What if an experimental model held the key to stopping CMV-caused birth defects?
Congenital CMV infections affect 1% of global births, and up to 15% of infected infants develop symptoms. The most common symptoms of cCMV are hearing loss, microcephaly, and heightened risk of spontaneous abortion.
As of today, we don’t have working therapies, nor routine screening of pregnant women. Therefore, infections are usually only detected late during pregnancy or after birth, missing critical intervention windows and creating a $1-4 billion annual economic burden in the US alone.
The biggest challenge for the development of cCMV therapies has been the lack of available mouse models that replicate cCMV infection. With the support of SPARK, we aim to develop the first mouse model that transmits the virus to the developing fetus during gestation, by targeting the type I interferon (IFN-I) pathway. Interrupting this crucial antiviral immunity pathway enabled Zika congenital infection in mice, and we hypothesize that a similar disruption will allow cCMV infection.
By infecting IFN-deficient pregnant mice at various gestation times and analyzing placental/fetal transmission through PCR and microscopy, this groundbreaking model could revolutionize antiviral drug and vaccine development.
“My SPARK project represents an opportunity to develop a tool that could be used all over the world by scientists who wish to study congenital CMV. It could represent the beginning of a new era in the study of congenital CMV, thus drastically increasing the odds of finding a new treatment.”
