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A study has shed light on a potential link between ancient viruses and cancer development. Researchers discovered that a specific lineage of viruses, embedded in human DNA, might be reactivated with age, contributing to various cancers.
When ancient viruses that infiltrated and eventually embedded themselves into human DNA are reactivated, they are likely to contribute to a variety of cancers, including lung and colon cancers, according to the study published in journal Science Advances.
These viruses, known as endogenous retroviruses, infected our primate ancestors 30 million years ago. Over time, they became integrated into our genetic makeup and now constitute roughly 8 per cent of the human genome.
As people get older, these viruses are more likely to resurface, the paper suggested. Though they no longer trick our cellular machinery into producing functional viruses for their propagation, they appear to activate cancer-promoting genes.
Edward Chuong, an assistant professor at Colorado University in the United States and one of the study’s authors, explains that previous research has shown that ancient viruses can be domesticated and activate genes that contribute to beneficial functions such as immunity and development.
Chung and his colleagues suspected that these viruses could deal damage as well. In diseases like cancer, scientists have recorded dysregulation of parts of the gene that contribute to cancer.
“This motivated us to look for endogenous retroviruses that show this activity specifically in cancer cells,” he told Down To Earth.
Scientists have identified over 98,000 human endogenous retrovirus remnants present in the human genome. The team focused on one: LTR10, which, Chuong says, was relatively understudied compared to others.
The researchers analysed genomic data from 21 human cancer types from publicly available datasets to explore the link between the virus and cancer. They found surprisingly high levels of activity in several types of cancer, including lung and colon cancer.
The LTR10 elements, they found, were more accessible than what would be expected for a random piece of genomic DNA. Accessible regions are generally understood to be active or turned on, Chuong explained.
Further analysis of tumours from dozens of colorectal cancer patients revealed that LTR10 was active in about a third of them.
They were especially active in epithelial tumours, which can develop in epithelial tissues that forms the covering on all internal and external surfaces of the body and lines body cavities and hollow organs.
The LTR10 sequence contains sites that are recognised by AP-1, a protein involved in cancer promotion in the lung, breast, gastrointestinal tract, brain, skin, ovaries and bone. Furthermore, researchers believe that LTR 10 contains sites for other proteins unique to epithelial lineages.
When the team used gene-editing tools to remove or inactivate LTR-10, they discovered that critical genes known to promote cancer development and growth were also rendered inactive. Treatments to shrink tumours in mice performed better after the ancient virus was deactivated.
The new findings explain that ancient viruses may be turning on many genes that promote cancer. The team will now investigate how endogenous retroviruses influence other cancers, including ovarian cancer.
