The following is an excerpt from the article “How Viruses Shaped Our World,” published in the February issue of National Geographic:
Imagine what Earth would be like without viruses.
The results are not as straightforward as you might think.
In fact, we live in a world of viruses, and there are countless kinds of viruses.
In addition to its huge numbers, the virus has a significant impact.
Far from being harmless, many viruses offer an evolutionary advantage to life on Earth, including humans.
We can’t survive without a virus;
Without a virus, we can’t get out of the original morass.
For example, two segments of DNA derived from viruses are now ensnared in the genomes of primates such as humans.
Surprisingly, without these two pieces of DNA, there would be no pregnancy.
Even more surprising, another type of viral DNA helps to package and store memories.
There are other genes from viruses that promote embryonic development, regulate the immune system or ward off cancer, whose significance is only now becoming clear.
Viruses, it turns out, have also played a key role in triggering significant evolution.
If all viruses were removed, the biodiversity of the planet would collapse, as if all the nails had suddenly been removed from a beautiful wooden house.
“What is a virus” hard to define
To understand the ever-changing nature of viruses, one must first address the basic question of what a virus is and what it is not.
It’s relatively easy to figure out what viruses aren’t, they’re not living cells.
Cells contain multiple sophisticated mechanisms, including the synthesis of proteins and the performance of specific functions depending on the cell type.
Bacteria are also cells, with similar characteristics, but with a much simpler structure.
Viruses are different from any of them.
Viruses are easier to describe than to define.
Each virion contains a piece of genetic instruction written by either DNA or another information-carrying molecule called RNA, encased in a protein shell called a capsid.
Some viruses have a capsule around their capsid that protects the virus and helps it attach to cells.
Once inside a cell, the virus commandeers the cell’s “stereophotographic” machinery, which turns genetic information into proteins, so that it can replicate itself.
If the host cell is unlucky, many new virions are produced.
New viruses spew out, and cells are reduced to debris.
Novel coronavirus caused such damage to human respiratory epithelial cells, and partly explains how viruses become pathogens.
But if the host cell is lucky, the virus may simply stay in its safe home, either going dormant or reverse-coding its tiny genome into the host’s, and biding its time.
The latter could have multiple implications for genomic mixing, evolution, and even our sense of identity as humans.
Cells and viruses love to kill each other
Viruses bring innovation, but cells respond with innovations in their own defenses, so it’s an arms race that’s getting more complex.
Many scientists have postulated that viruses evolve significantly by “viral pickpocketing,” that is, scooping up a piece of DNA here and there from the organisms they infect, and then applying the stolen genetic pieces to their own genome.
But Patrick Fortel, of the Pasteur Institute in Paris, suggests that perhaps more common is reverse theft, in which cells acquire genes from viruses.
Scientists like Fortel also take a more radical view: that viruses are the pacesetters for genetic diversity.
Over the past few billion years, the argument goes, viruses have enriched cellular organisms’ evolutionary options by inserting new genetic material into their genomes.
This peculiar process is something called horizontal gene transfer.
Horizontal gene transfer refers to the lateral flow of genes between different gene sequences, while vertical gene transfer is the more common way of passing genes from parent to offspring.
Fortel et al. suggest that viral genes have been flowing “overwhelmingly” into cell genomes, which could help explain some of the most important parts of evolution, such as the origin of DNA, the origin of the nucleus in complex organisms, the origin of cell walls, and perhaps even the differentiation of the tree of life.
Among viruses is a retrovirus whose RNA genome works in the opposite way.
The conventional way is to use DNA to make RNA, which then acts as a messenger and instructs the “stereo printer” to make proteins.
But retroviruses make DNA from their own RNA, which they then incorporate into the genome of an infected cell.
Some retroviruses infect germ cells, thus embedding their DNA into the host’s heritable genome-and thus leading to significant evolution.
These embedded gene segments are called “endogenous” retroviruses, and when they bind to the human genome, they become “human endogenous retroviruses” (HERVs).
Eight percent of human genes come from viruses
Eight percent of the human genome is made up of this virus’s DNA, which retroviruses inserted into our genetic code during evolution.
Each of us carries about one in 12 HERVs, and one of the more far-reaching genes is syncytosin-2.
A gene that initially helps a virus fuse with a host cell has since found its way into the genomes of ancient animals.
The gene is then transformed to produce a similar protein that helps cells fuse to form a special structure that eventually evolves into the placenta, opening up a new possibility for some animals: pregnancy in vivo.
It was an evolutionary innovation that allowed females to carry their young wherever they went, rather than leaving their developing offspring vulnerable and helpless, as insects and birds do when they leave their eggs in their nests.
The gene was originally derived from endogenous retroviruses and eventually replaced by other similar genes better suited for this role.
Over time, the placenta evolves as new reproductive patterns evolve.
One such gene obtained from the virus is syncytosin-2.
Two types of syncytin help human cells fuse to form the placental layer near the uterus.
This unique structure is responsible for connecting the mother and fetus, absorbing nutrients and oxygen, removing waste and carbon dioxide, and possibly protecting the fetus from the mother’s immune system.
Evolution’s ability to insert viral elements into humans is a near miracle of effective design.
Other studies have found evidence that a viral fragment produced by another endogenous human retrovirus, HERV-K, is present in the earliest human embryos and plays a positive role in protecting embryos from viral infection, helping control fetal development, or both.
If 8 per cent of your genome and mine is retroviral DNA, then the notion of human uniqueness, let alone supremacy, may not be as clear-cut as we think.
Are viruses a blessing or a curse
There is, of course, a downside to this evolutionary flexibility: a virus can sometimes switch hosts, jumping from one organism to another and becoming a pathogen of an unfamiliar new host, a process called spillover.
The transmission of viruses from animal hosts to humans is the source of most human infections.
In their original hosts, the virus would have waited for thousands of years, with limited numbers and impact.
Viruses may have reached an evolutionary compromise with their natural hosts, staying out of trouble in return for their own safety.
But in a new host, such as a human, the virus does not necessarily follow the old protocol.
An outbreak occurs if the virus can not only replicate, but also spread from person to person, in groups of dozens of people;
If it sweeps across a community or country, it’s an epidemic.
If it ravages the world, it will lead to a pandemic.
Novel Coronavirus does.
So viruses take and they give.
Viruses have trouble relocating on the tree of life, perhaps because their life histories are not entirely tree-shaped.
The tree is just the traditional way we interpret evolution, because Darwin was the golden rule.
But even as great as Darwin, he knew nothing about horizontal gene transfer.
In fact, he knew nothing about genes, nothing about viruses.
Now we realize that everything in the world is pretty complicated.
Even a virus that seems so simple at first glance is so complex.
If seeing the complexity of viruses makes us more aware of the intricacies of nature, and if the thought of viral genes in our bodies partly dispels our sense of aloofness, then I invite you to judge whether viruses are a blessing or a curse.
