Name: Why You Wouldn't Exist Without Viruses
Uploaded: 2024-11-25T08:22:38.000Z
Duration: 11 min 4 s
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Relative clauses (Restrictive vs. nonrestrictive)

This episode of Real Science is brought to you by Skillshare, home to thousands of classes that can teach you a new life skill.

In a year when a single virus has killed millions, it's hard to think of viruses as anything other than bad.

Our understanding of them is largely based around the death and destruction they cause.

HIV has caused the deaths of over 33 million people since the start of that epidemic in the 80s.

The Ebola virus kills up to 90% of people who get infected with it in a gruesome and awful way.

Zika, dengue, yellow fever still ravage the tropics.

So from where we're standing, it very much seems that viruses are not our friend.

There are an estimated quadrillion quadrillion individual viruses, 10 to the 31st power, that exist on this earth with than all the stars in the universe.

Only a small few have the ability to cause us harm, and the vast majority don't affect us at all.

But over time, some have become beneficial to us, in fact, a part of us.

Viruses have been infecting us and our ancestors for as long as we've been around.

And around a hundred million years ago, our mammalian ancestor was from that point on.

The traces of this infection, and many others, exist as viral fossils within our genome.

Around 8% of our DNA is not human at all, but viral.

And in recent years, scientists have started to see that these viral gene sequences are not simply leftover genetic baggage, strange and purposeless, but are sequences that code for essential proteins in human development.

How did these viral segments of DNA become a part of us?

And what do they do for us that's so important?

No one knows for sure where viruses came from, whether they existed before any cells did, assembling themselves from molecules in the environment, or whether they are derived from cellular life, leaking out of or being reduced from a viruses are perfect parasites.

They are tiny particles of genetic material enclosed in a protein coating, and their existence depends on invading cells to hijack the cellular machinery to replicate themselves.

To invade a cell, a virus recognizes and binds to the cell via a receptor molecule on the cell surface, and then breaks in.

Once inside, the viral genes are expressed, viral proteins are created, and new virus particles are assembled and are ready to be released.

In some cases, the exiting viruses leave the host cell intact so it can continue cranking out more virus particles.

But sometimes, the viruses cause the host cell to burst, killing it.

The viruses then float within the extracellular space, poised to infect more cells.

This is likely the story of viral infection that you've heard.

It's the primary mechanism of spread for most viruses.

But some viruses, like HIV, measles, and the herpes simplex virus, can also spread directly between two cells that are in contact with each other, in a process called cell-to-cell transmission.

This is particularly insidious, as it enables viruses to evade the body's immune response.

Viruses that can spread in this way have a few mechanisms to achieve it.

Perhaps most notably, genes that code for proteins, that force host cells to fuse together, allowing the viruses to jump from cell to cell.

And these genes, that seem absolutely harmful to humankind by allowing some viruses to wreak havoc on our bodies, have also enabled us to exist at all.

When these particular genes got inserted into our ancestors' genomes a hundred million years ago, the course of human evolution was changed forever.

The human genome contains around 100,000 fragments of viral DNA, and the story of how it got there begins with retroviruses.

Retroviruses are viruses that have an RNA genome and work backwards from how other viruses work.

Instead of using DNA to make RNA, which is then used to make transcriptase, this DNA then makes its way to the nucleus and inserts itself into the host cell's DNA, thus changing the genome of the host cell.

HIV, for example, is a retrovirus that incorporates itself into the genome of a cell, where it lives as a template for creating more HIV viruses.

The HIV virus infects immune cells, but some viruses infect the cells that will be passed through the generations.

And this is where our history with viral genes begins.

If retroviruses infect reproductive cells, the cells that produce eggs or sperm, the virus inserts its DNA into the heritable genome of the host.

Once a retrovirus has embedded itself in this way, it's known as an endogenous retrovirus.

At first, endogenous retroviruses forced cells to make more retroviruses that can infect other cells.

But over the generations, the viral DNA mutates, and endogenous retroviruses eventually lose the ability to infect new cells.

Much of the viral DNA within our genomes is therefore thought to be dormant, evidence of our ancestors' past infections, but nothing that affects us now.

But for some endogenous retroviruses, the story is more complicated.

Scientists have realized that even after being disabled and no longer being able to fully replicate itself, some retrovirus sequences can still make some of their proteins.

And over time, two of these viral proteins became essential in human development, evolution co-opting viral genes for human needs.

In human pregnancy, there are many biological marvels, and the placenta is at the front of that list.

It's an organ that develops in the uterus during pregnancy and provides oxygen and nutrients to the growing baby and removes waste products from the baby's blood.

The placenta attaches to the wall of the uterus and is where the baby's umbilical cord arises from, and it may have never developed without the help of viral proteins since SIDIN-1 and since SIDIN-2.

Around five days after fertilization, the two distinct cell types, the inner cell mass, which will develop into the fetus and eventually become the baby, and trophoblasts, which will develop into the placenta and external membranes.

Around the seventh day, the blastocyst starts to implant onto the uterine wall, where it will remain attached until birth.

At this point, the syncytiotrophoblast starts to form around the developing placenta.

It's a structure that determines which substances cross the placenta, such as nutrients and oxygen, and which substances do not, such as certain maternal hormones and toxins.

It's both life-giving and protective, and is the structure that results from the once viral syncytin proteins.

In viruses, the syncytin proteins allow them to fuse host cells together, so they can spread from one cell to another in the cell-to-cell viral transmission I syncytin proteins allow placental cells to fuse together to form this vital layer next to the uterus.

Without syncytin, the placenta does not form correctly, and if it had never been introduced into the human gene pool, the placenta would not have evolved as it is today.

Without it, internal pregnancy would have developed very differently, or perhaps not at all.

Viral sequences that live in our genome act as raw material for new adaptations.

Lines of code that should be useless to us, turned into something valuable in what feels like a miraculous turn of events.

It reminds us that evolution has no plan.

There is no single track on which it operates.

It's a machine of randomness and variability, and in all likelihood, our history of past retroviral infections, and even current ones, will continue to shape our Behind the scenes at Real Science and Real Engineering, we are constantly trying to improve our creativity and workflow to bring you all better and better videos.

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