Many viruses are like bad party guests—they show up uninvited and wreak havoc. But some viruses are more cooperative guests. A virus may have even made us mammals!
What do you imagine when you think of a bad party guest? It's probably someone who shows up uninvited, annoys everyone, selfishly eats and drinks his fill, and then leaves you exhausted with a mess to clean up. Viruses are a lot like that. They enter our bodies when we don't want them to, take over our cells so they can replicate themselves, and use us as hosts, usually with detrimental effects.
But what if the goals of the virus aren’t necessarily at odds with our own?
A stealthier virus will learn to live more symbiotically with its host. It needs that host, after all, to survive. Think of it as someone who has to couch surf with you for a while, but makes an effort to be a cooperative guest rather than a destructive one. Some viruses have integrated so successfully that they've even played a role in our evolution. In fact, a virus is credited with making us mammals.
How retroviruses affect our DNA
Retroviruses, a subclass of viruses, get their name for the methods they use to replicate within a cell. Once a retrovirus attaches to its would-be host cell it fuses with the cell’s outer membrane so it can slip inside. Retroviruses then use an enzyme called reverse transcriptase to convert their own RNA into DNA. This stealthy tactic makes them more compatible so they can insert themselves into a host cell’s DNA and become part of the host cell’s genome. And once that integration happens, the retrovirus can then use the host cell’s own processes to create new viral components. Those new viral agents can then go on to infect other cells.
Some scientists estimate that as much as eight percent of our genome may be made up of DNA donated to us by retroviruses.
In the case of the retrovirus known as the human immunodeficiency virus (or HIV), the virus infects CD4 T cells, which means it can have a significant impact on our immune system. And when a host cell dies, this merged viral-and-host genome dies also.
But what happens when a virus infects a sperm or egg cell? That part-host/part-virus genome can get passed on to the host’s descendants. We call these viruses endogenous retroviruses—in other words, viruses that come from within. Some scientists estimate that as much as eight percent of our genome may be made up of DNA donated to us by retroviruses.
Did a virus make us mammals?
Not all of this viral DNA does anything meaningful for us—it just hitches an evolutionary ride. But sometimes it can have significant consequences.
In mammals, the placenta is an entirely new organ that a pregnant body forms in order to serve as a barrier between the growing fetus and its host. It helps supply the fetus with oxygen and other nutrients, removes waste like carbon dioxide, prevents infection, and keeps the blood of the host separate from the blood of the fetus.
An ancient virus inserted itself into our genome—and the genome of other mammals—and gave us the ability to form a placenta that fuses with the womb of its host.
In 2000, a team led by molecular biologists John McCoy and Sha Mi discovered a protein called syncytin. It's produced by the cells in the placenta that are in direct contact with the uterus. They further noticed that syncytin closely resembled a viral protein called env, a known mechanism that viruses use in order to fuse with their host cells. The placenta attaches to the womb by using the same genetic tool viruses use to attach to the cells they plan to infect.
So, an ancient virus inserted itself into our genome—and the genome of other mammals—and gave us the ability to form a placenta that fuses with the womb of its host, a key tool for a fetus’s survival. But the full story is a complicated one that researchers are still trying to piece together.
For instance, humans and other primates have two forms of syncytin—cleverly called syncytin 1 and syncytin 2—that both appear to be a necessary component for fetal survival. Syncytin 2 is a key player in lowering a mother’s immune system so the pregnant body doesn’t attack the fetus as the growing invader it is.
Researchers have also found forms of syncytin in other mammals, including mice, rabbits, dogs, and cats. But not all of these viral-like proteins are identical. So there may have been not one virus but many that merged with the DNA of our mammalian ancestors to give the placenta an evolutionary advantage.
There are also incidents of species that are close relatives, like the rabbit and the pika, or carnivorans like the hyena and the pangolin, that don't have the same forms of syncytin being produced in the placenta.
Why would different species develop different tools to do the same job? This isn’t easily explained within the picture of predators or environmental conditions driving evolutionary changes. But if that tool is derived from a virus, the differences could be explained by different viral origins. These differences further provide a timeline for the viral origin—the branches of the evolutionary tree that separate rabbits from pikas happened somewhere around 30-million years ago. So the merging of viral and host mammal DNA must have happened after this split.
A wider look will allow us to see the bigger picture of how we adapt as a species, particularly in the face of a viral pandemics.
Research into viruses and the viral proteins they contribute to their hosts has typically focused on individual proteins—in particular, those that affect our immune system since they have the potential to wreak the most havoc. But as both our understanding of these viral proteins and our computing power increases, biologists are also looking to studies that follow a wider range of viruses. This wider look will allow us to see the bigger picture of how we adapt as a species, particularly in the face of a viral pandemics.
And the evolution of the placenta is just the tip of the viral iceberg. Although there are still more questions than answers in these other areas of study, some suggest the very nuclei of our cells may have originated from a virus that infected a bacterium, an idea known as viral eukaryogenesis.
As the coronavirus pandemic plays out around us, we can already see the outward adaptations we must make to survive it, from social distancing to mask-wearing to addressing the systemic inequalities that lead to its spread. But these adaptations are also occurring on a microscopic scale within us and we will be studying their impacts for decades to come.