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You might get the impression that all viruses are terrible, awful, no-good things that just wreak havoc on humanity. But, surprise: The truth is way more interesting!

Hosted by: Hank Green

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Image Sources:
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https://commons.wikimedia.org/wiki/File:Gray26.png
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{♫Intro♫}.

When somebody’s talking about viruses in biology, they’re usually talking about things that make you sick — stuff like the flu virus. And based on that, you might get the impression that all viruses are terrible, awful, no-good things that just wreak havoc on humanity.

But, surprise: That’s not actually true! And the truth is way more interesting! In reality, not only have some viruses helped us: A specific clade of them has given us some great adaptations and influenced our evolution for the better.

Much of this research focuses on the human genome. Your genome is the complete collection of your genetic material, including all of your. DNA and the genes that comprise it.

It contains everything you need to know to make a human. A lot of this material has been passed down from species to species for thousands or millions of years, which is why generally, our genomes are pretty similar to those of other animals. But!

There are also places in the human genome that are totally unique — maybe because some sequences got rearranged, or because some were inserted or deleted. Those kinds of changes translate to things like the proteins our bodies make or the ways we develop. They're part of what makes us human.

So it’s not surprising that researchers have spent a lot of time trying to figure out where these changes came from. Over the years, they’ve learned that genomes can change thanks to a series of random DNA mutations — which might sound familiar from biology class. But what most bio classes don’t talk about is how viruses also have a huge role to play here.

Especially a group called retroviruses. Retroviruses are kind of freeloaders. Like other viruses, they don’t have much complex machinery, so they can’t reproduce themselves.

Instead, they depend on living things to do that for them. Retroviruses take their genetic material, insert it into a host cell’s genome, and then rely on the host to replicate that material. Over time, the host helps crank out more and more copies of the virus, and the virus goes on to infect other cells and repeat this process all over again.

Normally, when we talk about these things, we tend to focus on the viruses themselves, since those end products can cause illness. But there’s a whole different piece of the puzzle here. Because you have to remember: Those retroviruses don’t just show up, replicate, and leave.

They embed instructions for making new viral products in our DNA. Sometimes, that’s not a big deal, because those instructions can get eliminated by our immune systems. Or if the virus only infected something like a skin cell, its genetic code won’t get passed on to the host’s offspring.

But at multiple points in our past, our ancestors picked up viruses that happened to infect germ cells, like egg or sperm cells. That means those viruses’ DNA was passed to their host’s offspring — and their offspring, and their offspring, for thousands or millions of years. Until virtually all modern humans had instructions for making certain types of viruses.

These instructions — ones that have been passed down through germ cells for generations — are called human endogenous retroviruses, or HERVs. They make up almost eight percent of our entire genetic code — eight percent! — and they’ve had a significant influence on how our bodies work. That influence starts early, too.

Like, take one family of retrovirus called HERV-H. It’s a family that only primates have, and it started influencing your genetic code just a few days after you were conceived. For a short amount of time, your embryonic cells were pluripotent, meaning they could become any type of cell, from branching neurons to dense muscles.

Of course, your body needed specific cells in specific places, so that your brain and heart and muscles would end up in the best spots. So eventually, instructions in your genome told the cells what kind of tissue to permanently become. But before then, HERV-H stepped in.

This retrovirus marked your cells as pluripotent and kept them in that state — preventing them from turning into muscle or skin cells for just a little bit longer than they would otherwise. This likely benefits the virus, since the longer cells stay pluripotent, the more time a virus has to be replicated and infect every cell. But this process might also affect human development.

In 2015, researchers were comparing the genomes of humans and macaque monkeys, and they found a few identical genes in both species. But they also noticed that those genes were only expressed in humans while the embryo was pluripotent. In other words, the body was only reading those genes and following their instructions during that stage.

It’s not exactly clear what the implications are there, but if HERV-H is keeping cells pluripotent for longer, it means those genes are expressed for longer, too. The fact that a random virus could hold an embryo like this is kind of a big deal. That’s not a small impact!

And HERV-H might have other consequences, too. Like, it might play a role in disease. It’s still preliminary work, but in 2018, one paper found evidence that this retrovirus could have a role in shaping heart cell development — maybe even a role in heart disease.

So one way or another, your body might not be quite the same if it weren’t for HERV-H. Now, even once your cells were on their way to specialization, they still had months of growing to do, which carried some risk. Like, an infection could have easily come along and wiped out your little clump of cells.

But it didn’t — maybe thanks to another endogenous retrovirus, called HERV-K. Among other things, HERV-K helps embryos develop a built-in immune system that keeps them safe even before they develop antibodies to pathogens in the outside world. It codes for a small protein called Rec.

And Rec helps HERV-K make viral copies and proteins so it can infect other cells. That might sound like bad news for us, because it seems like the last thing an embryo probably needs is a bunch of virus particles. But in reality, this is actually really useful for embryos.

These particles trigger embryonic cells to start making antiviral proteins, and that builds one of its first defenses against other viruses. This kind of thing is far from a complete immune system, but for an embryo, it might make the difference between getting an infection or not. And who knows?

Maybe this even made a big difference for you, once upon a time. So, endogenous retroviruses affected your pluripotency, and they helped with your immunity as an embryo. But they also played a major role in helping you develop into a fully-grown fetus.

At about a week after fertilization, a human embryo is a hollow ball of cells that starts attaching to the uterus. At this time in development, humans, just like all other mammals, will develop a placenta, a temporary organ that forms during pregnancy. This structure is crucial for human pregnancy — it provides nutrition to the developing fetus and helps it get rid of waste.

But for it to work, it needs to be connected to the fetus. I know, that sounds obvious. But like, somehow, a mechanism had to evolve to do that job.

And as it turns out, an endogenous retrovirus might have played a big role there. Researchers have found that the placenta secretes a protein that binds it to the embryo, keeping the two attached for the next few months of development. And the DNA that makes up that protein is nearly identical to a region of a retrovirus that allows the virus to attach to the host cell.

I’m definitely not saying that fetuses are basically like viruses attached to a host…. But this does suggest that without this retrovirus, placentas might not work — or at least, might not work the same way. So!

HERVs shape how your body develops and how it stays protected and cared for during development. But these things don’t stop being important as soon as you’re born; they have a real impact on your adult body, too. For example, endogenous retroviruses didn’t just help your embryonic immune systems; they help defend your adult body from pathogens as well.

In fact, some research suggests that all of our existing immune system pathways depend on enzymes created by retroviruses and things like them. If you think about it, that’s kind of amazing. The remnants of ancient viruses are protecting our bodies against… microbes and other viruses.

HERVs have a role beyond the immune system, though. They’re also responsible for small, but significant changes in how the human body works in general. Take this enzyme called amylase.

All mammals have it in their pancreas, and it’s used to break complex sugars into simple sugars. But a few mammals — including humans — have it in their saliva. This could be thanks to a retrovirus called HERV-E, which may have converted one of the genes that codes for amylase in our pancreas into a salivary gland version.

This isn’t just a weird quirk, either. Although it’s not confirmed, one hypothesis suggests this salivary amylase might help us taste sugary foods better and identify good sources of nutrition. So it could play a big role in your everyday life.

Scientists are always interested in learning more about endogenous retroviruses, because they can tell us a lot about why humans look and act like humans. But these days, they’re also interested in how we can use HERVs to understand specific diseases. For example, some evidence suggests that HERV-W might be involved in multiple sclerosis, and.

HERV-K might contribute to the pathway that leads to ALS. These things are just now being investigated, but scientists hope that understanding these viruses will eventually lead to cures for both of these neurological diseases. And that’s just the tip of the iceberg.

At the end of the day, human genetics are complicated, and there are a lot of variables that shaped our species and our adaptations. But the next time you taste a sugary food, recover from a cold, or hear that a friend delivered a healthy baby — well, you might have some ancient viruses to thank. If you want to learn more about how you went from a clump of cells to a fully-grown baby, you might want to check out the pregnancy episode of our podcast, SciShow Tangents.

Tangents is a weekly, lightly competitive podcast hosted by some of the people who have brought you SciShow over the years: Stefan Chin, Sam Schultz, Ceri Riley, and myself. In every episode, we show off our best science facts, try and stump our co-hosts with lies, and always end up talking a little bit about butts. I’m not kidding, there’s a butt segment.

It’s a great time, and I always learn a lot from it. If you want to join us, you can listen to SciShow Tangents by searching for it anywhere you get your podcasts. {♫Outro♫}.