Are ancient 'Zombie Viruses' in Human DNA linked to Cancer growth? New study reveals shocking Findings

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In human genomes, some so-called "zombie viruses" — remnants of ancient foreign DNA passed down through generations — have been hiding unnoticed. While it was long thought these viral sequences were inactive, recent research has uncovered that they may actually be causing harm.

Led by bioinformatician Atma Ivancevic from the University of Colorado, a new study has revealed that parts of these ancient viruses can contribute to cancer growth. Edward Chuong, a genome biologist and senior author of the study, explained, "Our research shows that these ancient viral infections can significantly impact modern diseases, something few researchers had previously considered."

These ancient genes, once dismissed as "junk" DNA, are remnants of viruses known as endogenous retroviruses (ERVs). These ERVs played a crucial role in the evolution of mammals, particularly in the development of the placenta. However, not all aspects of ERVs are beneficial to human health.

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Chuong added, "We know that cancer cells often activate genes that should remain off, but it wasn’t clear what was turning them on. It turns out that many of these switches come from ancient viruses."

The researchers discovered how these ancient genes might contribute to cancer by analyzing epigenomic data from 21 types of cancer. They found a specific family of ERVs, known as long terminal repeat 10 (LTR10), that was highly active. This family of ERVs was originally introduced into our primate ancestors about 30 million years ago.

Further studies on colorectal cancer cells revealed that LTR10 influences the expression of genes involved in tumor formation. When the LTR10 genes were deactivated in human colorectal tumor cells and in mice, it resulted in the shutdown of cancer-promoting genes like XRCC4.

This research highlights a surprising link between ancient viral remnants and modern cancer, showing that these long-hidden genes could be influencing disease development.