Unleashing “tethered DNA” at the most critical moments for health reveals surprising effects from ancient viruses.
Scientists from the Center for Pediatric Research (CRI) at the University of Texas Southwestern have discovered that the DNA of ancient viruses within the human genome operates in unexpected ways during pregnancy and significant blood loss.
Originating from epidemics endured by our ancestors, remnants of ancient viruses are often referred to as “junk DNA” because they do not encode proteins that contribute to cell function.
These remnants utilize a type of enzyme known as reverse transcriptase, similar to the enzyme found in the human immunodeficiency virus (HIV), to replicate themselves.
However, the recent findings presented in the journal Science indicate that they are not entirely “junk.”
Ancient virus DNA provides unexpected value to humans – (Illustration AI: ANH THƯ).
These viral remnants are closely linked to how hematopoietic stem cells—which typically divide infrequently—are activated during pregnancy and after significant blood loss.
By comparing the active genes in stem cells from pregnant mice with those from non-pregnant mice, researchers found that the retrotransposons—the DNA of ancient viruses—were activated in the stem cells of pregnant mice.
Humans have developed mechanisms to suppress retrotransposons for most of their lives, as these elements can damage DNA when they replicate and insert themselves back into different parts of the genome.
The sudden “unleashing” of these foreign DNAs during pregnancy is completely unexpected, as this is the crucial time to protect the integrity of the genome and avoid mutations.
“There are hundreds of these retrotransposon sequences in our DNA. Why not permanently disable them, like some species have done? They must provide some adaptive value to us,” the authors argue.
They used reverse transcriptase inhibitors, commonly used to prevent HIV replication in patients, to suppress retrotransposon replication in mice.
The results were astonishing: these drugs did not alter blood cell production in normal mice but did prevent the increase of hematopoietic stem cells and red blood cell production during pregnancy, leading to anemia.
These “junk DNAs” also trigger certain immune sensor factors, enhancing the production of interferon, a group of crucial proteins in the immune system that help reduce inflammation, combat invading viruses and bacteria, and also indirectly affect hematopoiesis.
Tests on several volunteers later confirmed the surprising value of DNA from ancient viruses.
Moreover, scientists discovered a similar mechanism occurring in cases of severe blood loss, suggesting that what has been labeled as “junk” may play more significant roles in human health than previously thought.
