Endogenous retroviruses in human embryogenesis
Raquel Fueyo, PhD
The early stages of embryogenesis in mammals involve the activation of families of endogenous retroviruses (ERVs), which constitute about 9% of the human genome (Fueyo, Judd et al. 2022). The ERVs repertoire varies significantly across species, hinting at their potential role in shaping species-specific functions. Recently, I discovered how a family of ERVs named HERVK LTR5Hs is essential for human embryogenesis by utilizing CRISPR editing in human blastoids (Fueyo et al. Nature, 2025). This work revealed that the relics of ancient viral infections that we carry in our genomes have been exploited during evolution to evolve novel regulatory functions for our genes, thus shaping species-specific gene expression programs and playing a role in what makes us humans. These findings are just the tip of the iceberg. Our genome contains more than 3000 ERVs that are active in embryogenesis, many of them are specific to humans, and some of them ERVs still produce viral proteins, and even viral particles that co-exist with the human embryo during the early stages of development. Strikingly, the function of most ERVs or the viral products has not been investigated.
In our lab, the doctoral candidate will have the opportunity to work on one of these two topics:
- Analyzing the role of ERVs in the early stages of human development
- Investigating the molecular mechanisms underlying endogenous retroviral regulation in pluripotency and early human development.
The candidate will gain experience in working with stem cells and 3D models of human embryogenesis (blastoids, endometrial organoids, etc.). They will also learn to design and perform CRISPR-related genome editing in human cells. As our lab’s main interest is genome regulation, the candidate will also learn basic molecular biology and genomics techniques (e.g., ChIP-seq, ATAC-seq, RNA-seq, IP-MS…), as well as the computational analysis of the generated datasets.
Do you want to know more? Visit the Fueyo Lab website.
