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Head to shopify.com/scishowstarter to learn more and for a 14-day free trial of their new Starter Plan. [♪ INTRO] Our immune system is a pretty amazing adaptation, capable of defending us against all manner of infections. But it’s not perfect and, occasionally, an invader can slip through our defenses and make us sick.

That’s why we’re so fortunate to live in an age of antimicrobial and antiviral medicines. But making those isn’t as simple as snapping our fingers. So today, we’re going to look at a couple of unexpected sources for potential new disease treatments.

A lot of the time, researchers looking to design drugs to fight viruses have to focus on the unique weaknesses of a specific virus. Meaning that while the therapies they develop may be effective, they’re also super specific and won’t work for every infection. But today’s first story might be different.

A broad-spectrum solution. In a new study published this week in the journal PNAS, researchers were interested in something called RNA methylation. It’s a modification to the RNA molecules that our cells use to translate DNA instructions into protein.

In it, a small chemical tag called a methyl group is added to the RNA, which can affect how the cell reads that information. Think of it as kind of like sending a text message, but then adding a smiley emoji after. It’s a tiny change to the message after the fact that can affect how it’s read.

In this study, the team was interested in how RNA methylation affects the immune system. In particular, they wanted to learn more about how viruses might be hijacking RNA methylation as they infect cells. To investigate, the scientists took cells and disabled one of the enzymes used in RNA methylation, and then they infected them with a virus to see what would happen.

They found that doing this suppressed the virus’s ability to replicate itself. Remarkably, though, they found that it wasn’t because the virus needed that enzyme to borrow the cell’s machinery to replicate itself – as viruses do. It actually didn’t seem to affect how much the viral RNA got methyl groups added.

Instead, the effect seemed to be a response by the host cells. The team found that disabling this enzyme seemed to cause a chain reaction in the cells that lead to a rise in the production of interferons, which are proteins found in the immune system that – as their name suggests – interfere with viral infection. It seems that disabling the cell’s ability to chemically tag its own RNA makes the immune system think that RNA may be from a foreign invader.

So it gets put on high alert, making it more likely to bump into the virus. That’s when it really cracks down and churns out the interferons. More experiments with other cell types and live mice showed the same thing, and showed that this could work for a wide range of different viruses, since interferon is one of the body’s go-to general responses.

The scientists said that designing a drug that does this could be a next step. The second story we have is also about a potential drug discovery, but this time it’s about potatoes. In a new paper published in the journal mBio, a new kind of antifungal compound could protect us… and more importantly, our beloved hash browns.

In fact, this story is really more about plants than animals. The story goes that scientists were looking at a bacterium known as Dickeya solani. It was first identified more than 15 years ago and is a pest that caused something called “blackleg disease” in plants.

Scientists studying it years ago made the remarkable discovery that this bacterium could actually produce antimicrobial compounds itself. Specifically, this was a compound called oocydin A that attacked certain species of fungi. Don’t get me wrong, the bacterium wasn’t doing it out of the goodness of its heart… The goodness of its flagella?

Maybe. It was doing this in order to chase away any potential fungal competitors for the potato’s juicy nutrients. It’s actually not unusual for bacteria to try to poison each other with antibiotics.

A single gram of dirt can contain more than a thousand different bacteria species and they are not necessarily all friends with each other. In fact, a lot of our modern antibiotics have come from spying on soil bacteria in particular. Plant ones, not so much, which makes this new development all the more interesting.

Well, recently, scientists looking at this bacteria noticed a strain that seemed to be unable to produce oocydin A. You might think this would leave it defenseless against its fungal competitors, but it seemed like it was still able to fight back. Using DNA sequencing and gene editing, the scientists discovered that lil’ Dickey here had a back-up weapon in its arsenal, a compound the scientists are calling solanimycin.

The scientists weren’t able to figure out exactly how it attacks fungi, but they noted that they could see effects pretty quickly after they exposed fungi to a partially purified version of the compound. This raises the question of why the bacteria doesn’t just spray this out of every pore all the time. But compound seems to be expensive for the bacteria to produce, so it only makes it when it really needs to.

That might explain how solanimycin was able to escape notice for so long. The cool thing is that solanimycin seems to work against a handful of fungi. This includes other plant pathogens – and some human ones as well.

Like Candida albicans, which can cause oral, genital, and other infections in humans. So a drug version of this compound could potentially become a treatment for humans, but also one that helps protect our oh-so-important potatoes. It also shows that it might be worth going back to some other microbes scientists have already examined for antibiotic compounds.

Maybe they, too, have some backup weapons we never noticed before. We’re lucky to live in a time when we know so much about how and why the body gets sick. There’s still a lot of work to do, but it turns out that you can find some really cool answers in surprising places, as these two stories show.

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And thank you for watching! [♪ OUTRO]