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Felisa Maria Herrero, Dr. sc. nat.

Written by:

Felisa Herrero, M.Sc.

Ph.D. Student

University of Zurich

My journey into psychosis research began during my doctoral studies at the University of Zurich, Switzerland. Driven by a deep curiosity about the brain, I had the opportunity to work with Prof. Dr. Urs Meyer, whose research on the impact of maternal immune activation during pregnancy, and its implications for neuropsychiatric disorders, fascinated me. Through my work, I discovered the intriguing potential of endogenous retroviruses to explain patterns seen in psychiatric conditions.

Endogenous retroviruses (ERVs) are genetic elements in our DNA that come from viral infections that occurred throughout evolution. These viral remnants have shaped our biology, but growing evidence suggests they may also contribute to neuropsychiatric disorders. Specifically, I’m studying a family of these retroviruses called HERV-W, which may play a role in conditions like psychosis and other developmental disorders. For my research, I use a mouse model that expresses a human version of the HERV-W gene, particularly one that produces a viral protein involved in the infection process.

Our findings suggest that just expressing this gene causes significant changes in behavior and cognition in the mice, such as difficulties with memory, social interactions, and repetitive behaviors. These findings point to a potential link between this endogenous retrovirus and psychiatric conditions like schizophrenia.

We also observed that the expression of this viral gene altered the activity of many brain genes. Particularly, it affected genes related to cognition and brain development. For example, we found that genes linked to schizophrenia, such as Setd1a and Shank3, were turned down, along with genes that are crucial for the brain's synaptic development. This suggests that HERV-W may influence brain function in ways that contribute to these disorders.

One of the most interesting aspects of our findings was how the gene expression changes also affected the brain’s "epigenetic" profile. Epigenetics refers to the way environmental factors can turn genes on or off without changing the underlying DNA sequence of our genomes. We saw that in these mice, the altered expression of certain genes affected the way their brain cells were able to "read" other genes, which partially explain the cognitive and behavioral issues.

Nevertheless, we found promising results by using a drug that targeted the epigenetic changes in these mice, we were able to reverse some of the cognitive and behavioral deficits caused by the viral gene expression. This drug is currently being tested as a potential treatment for psychiatric disorders.

At the SIRS 2024 conference, I had the chance to share these findings and receive valuable feedback, which has inspired new directions for my research.
Although much remains to be discovered, I hope the field of endogenous retroviruses gains more attention. Understanding the role of these genes could improve our knowledge of psychosis development and individual differences. This research may pave the way for more personalized medical approaches, recognizing what we all already know: one-size-fits-all treatments are not effective for everyone.

As I move forward in my postdoctoral research, I am eager to deepen our understanding of how endogenous retroviruses contribute to schizophrenia. I hope to uncover new insights that not only enhance our scientific knowledge but also bring us closer to developing personalized treatments. By continuing to collaborate with fellow researchers and engaging with the wider scientific community, I am optimistic that we can make meaningful strides in improving the lives of individuals affected by psychosis.

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