Our genomes are riddled with the detritus of ancient viruses. They infected our hominid ancestors tens of millions of years ago, inserting their genes into the DNA of their hosts. Today, we carry about 100,000 genetic remnants of this invasion. So-called endogenous retroviruses make up 8 per cent of the human genome.
Mostly, these genetic fragments are generally nothing more than molecular fossils. Over thousands of generations, they have mutated so much that they cannot replicate in our cells. And our cells keep the viral DNA muzzled to minimise the harm it might cause.
But scientists are finding that some endogenous retroviruses do wake up, and at the strangest time.
A new study published in the journal Nature on Monday suggests that endogenous retroviruses spring to life in the earliest stages of the development of human embryos. The viruses may even assist in human development by helping guide embryonic development and by defending young cells from infections by other viruses. “The fact that viruses may be playing a vaccine role in the cell is pretty amazing,” said Guillaume Bourque, a genomicist at McGill University, who was not involved in the study.
When an ordinary retrovirus, like HIV, infects a cell, it inserts its genes into the cell’s DNA. The cell then makes new retroviruses by making a copy of the virus genes as RNA molecules. The cell uses some of those RNA molecules to make proteins for the virus. Those proteins form a shell around the other RNA molecules, which become the new virus genes.
‘Part of the programme’
In recent years, scientists have discovered that embryonic cells produce RNA molecules from certain endogenous retroviruses lurking in the genome. But scientists have struggled to understand why.
Do retroviruses come out of hiding to take advantage of their young hosts when their defences are weak? Or, are these just biochemical accidents embryonic cells mistakenly turning viral genes into RNA, then destroying their molecular mistakes?
Joanna Wysocka, a developmental biologist at Stanford University, and her colleagues recently discovered evidence that embryonic cells are not turning to their viral genes by accident. It’s an elaborate process that happens at a specific time in the development of an embryo. “It’s part of the program,” she said.
Wysocka and her colleagues did not set out to study viruses when they started their research. Instead, they were investigating how a single fertilised egg turns into the hundreds of different types of cells in the human body.
In the early stages of development, an embryo is largely made up of cells that can potentially become any sort of tissue. Over the course of many divisions, the cells continue to hold on to this potential. A crucial reason is a protein called Oct4. It’s not entirely clear how Oct4 keeps embryonic cells in their flexible state, but scientists know it works by latching on to DNA in order to turn genes on and off.
Not clinching evidence
Jonathan Stoye, a virologist at the Francis Crick Institute in London, considered the study thought-worthy, but cautioned that Wysocka and her colleagues had not proved that the retroviral genes are providing clear benefits to human embryos. “Endogenous retroviruses might behave merely as very successful parasites,” he said.
— New York Times News Service
