Researchers at Kobe University in Japan have shown that fragments left by ancient viruses may shape how the human genome works and could influence the risk of developing certain forms of autism. The discovery, published in a psychiatric research journal, marks a meaningful advance in the effort to understand how these viral remnants interact with human biology over the course of evolution.
The human genome contains pieces of retroviruses that disappeared long ago. These fragments make up about 8 percent of our DNA. Most of them lie dormant, with little obvious effect on health. Yet scientists recognize that these genetic relics can take part in a range of biological processes, and their precise roles remain an active area of study.
In their study, Kobe University scientists used mouse models that display idiopathic autism, a form without a clearly identified genetic or environmental cause. Brain imaging of two related mouse strains, BTBR/J and BTBR/R, revealed notable structural differences across 33 brain regions. The most striking disparities were found in the corpus callosum, the thick nerve bundle that links the brain’s two hemispheres and supports cross-hemispheric communication.
The researchers observed that BTBR/R mice carried more active viral insertions within their DNA than their non-autistic counterparts. They propose that during fetal development, a mechanism normally responsible for keeping these viral elements inactive can fail, raising the risk for autism-related changes in brain structure and function.
Although the findings illuminate possible biological pathways, the team stresses that further work is needed to clarify exactly how activation of these genomic regions can influence autism risk. The results pave a path toward refining how different autism subtypes are classified and may eventually guide new strategies for intervention and treatment. This line of inquiry highlights the link between ancient viral remnants and modern brain development, inviting continued study in both animal models and human populations. [1] [2] [3]