Pregnancy and hemorrhage have two things in common. First, the human body needs more red blood cells in both cases. Second, a mechanism of viral origin triggers the production of these cells, according to a study recently published in Science.
Viral process. The study uncovered a unique mechanism that the body activates to meet temporary increases in red blood cell demand. Remarkably, dormant viral fragments within our genome help initiate this response.
Hematopoietic stem cells. The key lies in hematopoietic stem cells, which give rise to red blood cells. The team aimed to understand how these cells, typically dormant, spring into action during critical times like pregnancy or bleeding.
The researchers focused on retrotransposons—genetic sequences from ancient viral infections that have become permanently embedded in human DNA. These sequences don’t code for proteins in the usual way but instead use an enzyme, reverse transcriptase, to replicate within our genome.
Genetics in pregnancy. The study began with animal models, comparing stem cells from pregnant and nonpregnant mice. Researchers anticipated that pregnancy would deactivate retrotransposons in these cells, preventing their replication and lowering the risk of mutations during this sensitive period. Instead, they found the opposite.
“It’s the opposite of what we expected. If there’s ever a time to protect the integrity of the genome and avoid mutations, it would be during pregnancy,” said co-author Sean Morrison, a pediatrics professor, in a press release. “There are hundreds of these retrotransposon sequences in our genome. Why not permanently inactivate them, as some species have done? They must have some adaptive value for us.”
The team used reverse transcriptase inhibitors, similar to those used in HIV treatment, and found that these inhibitors blocked red blood cell production, leading the female mice to develop anemia.
From mice to humans. The researchers also conducted blood tests on pregnant women and found that retrotransposons were activated in their cells as well.
Viral inheritance. About 8% of our genome consists of viral inheritance—genetic material “left behind” by ancient infections. Scientists once labeled this genetic pool as “junk DNA,” but research increasingly shows that the term doesn’t capture its significance.
Much remains unknown about the role of this viral inheritance. Some studies suggest that humans may have retained these genes because they help combat new infections.
Another research team has also investigated the potential role of these genes in pregnancy, publishing their findings in Science a few months ago. This study focused on early development, specifically a phase called the “transition to pluripotency,” occurring just hours after fertilization.
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