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Uploaded:2018-11-05
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Medicine has made leaps and bounds in treating illnesses in the last century, but are they ever going to get around to curing the common cold? We might be closer than you think.

Hosted by: Hank Green

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Sources:

https://www.frontiersin.org/articles/10.3389/fmicb.2015.00517/full
https://www.theguardian.com/news/2017/oct/06/why-cant-we-cure-the-common-cold
https://www.researchgate.net/profile/Ronald_Eccles/publication/7512788_Understanding_the_symptoms_of_the_common_cold_and_inf/links/5a57a788a6fdccf0ad199299/Understanding-the-symptoms-of-the-common-cold-and-inf.pdf?origin=publication_detail
https://www.researchgate.net/profile/Asuncion_Mejias/publication/317790178_Rhinovirus_-_not_just_the_common_cold/links/59ada7aca6fdcce55a416971/Rhinovirus-not-just-the-common-cold.pdf?origin=publication_detail
https://www.scientificamerican.com/article/how-do-antibiotics-kill-b/
http://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0022572&type=printable
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https://www.healthline.com/health-news/are-we-closer-to-curing-the-common-cold#1
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http://jvi.asm.org/content/88/10/5217.full
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[ intro ].

Medicine has made some pretty big leaps forward in the last century. But one disease still outwits even the best medical minds: the common cold.

Part of the problem is that it’s caused by a suite of pathogens, not just one. And those pathogens happen to be viruses that mutate fast and hide inside their hosts’ cells. That said, we might be closer to getting rid of it than you think—and knocking out a slew of other viral diseases at the same time.

One of the reasons the common cold is so difficult to attack is that it’s not a single target. The main culprits behind the common cold are rhinovirus, but there are hundreds of variants of them and they aren’t the only viruses to blame. All that diversity has kept us from making any kind of ‘cold vaccine’ or targeted drug.

It’s also why our best chance to defeat the common cold once and for all is to develop a broad spectrum antiviral: a medication that can wipe out many different viruses at once. Since we’ve already done this with antibiotics, you might think it would be easy to apply the same strategy to viruses. But there’s a pretty big catch.

Most broad spectrum antibiotics work by inhibiting key proteins the bacteria need to reproduce or make their protective cell walls. These are usually things that are structurally unique to bacteria as opposed to multi-celled organisms like us, so for the most part, the drugs don’t harm human cells. Viruses hijack their host’s cells to reproduce, using our cell’s machinery for their own ends.

So fighting these viral invaders while leaving our cells intact is a lot trickier. Not that we haven’t tried. The first attempts at a universal antiviral tried boosting our body’s natural immune system.

When our cells detect a virus, they start making interferons: chemical messengers that signal the viruses’ presence to the rest of the body. So some of the first antivirals either were interferons themselves, or boosted their effectiveness. And these drugs can work pretty well if taken before the virus gets out of control.

One kind of interferon, interferon a, is still routinely used to treat hepatitis B and C, for example. But these drugs tend to come with the mess of side effects that happen when you somewhat indiscriminately ramp up your immune system. And what most antiviral researchers really want to find is something that targets viruses more directly … kind of like the antivirals used against HIV.

These medications take advantage of the way HIV inserts its genes into a person’s DNA by targeting the viral proteins which allow it to do that. But the meds are designed to inhibit things specific to HIV, so they don’t work against other viruses. And finding a single achilles heel common to many different viruses has proven difficult.

Still, back in 2011, a team from M. I. T. may have found one.

They developed a protein that detects double stranded RNA, a type of genetic code that is made by a lot of the most common viruses while they’re replicating. These molecules aren’t completely unique to viruses, but the ones made by viruses are much longer than the ones that happen naturally in human cells. In fact, their presence is one of the ways your own immune system figures out that you’re infected.

So the researchers took a protein that can detect these molecules, and they attached it to another protein which triggers cell suicide when more than one of the drug molecules binds to the same chunk of double-stranded RNA. And in a 2011 PLoS ONE study, they showed that this combined construct works against more than a dozen different viruses without harming several types of human cells. Killing infected cells might sound extreme, but the viruses kill your cells anyway when they’ve made enough copies, so the drug simply speeds things up and limits the number of viruses made.

Unfortunately, the project has been in a constant battle for funding, so they haven’t gotten far enough along in the research for human trials. Luckily, there are other promising antivirals in the works. A team of researchers in San Francisco is developing drugs that stop viruses from making the protein shells or capsids they need to move about within and between hosts.

Traditional studies have looked at capsid formation as a thing that just sort of happens on its own, but these developers tested the idea that the host cell unwittingly helps the virus with construction. And they found what appear to be traitorous proteins scientists had no clue were aiding the viruses— any of which could be a target for a broad-spectrum antiviral. Using this framework, the team has found inhibitors that work in animals against rabies, influenza, and Ebola viruses.

But, they still have a lot of testing to do before anything would be ready for human trials. And there’s another potential broad-spectrum antiviral hoping to beat them to those. This one takes advantage of natural hiccups in viral replication—because, just like us, viruses aren’t perfect.

Sometimes during the gene-copying process they end up deleting big chunks of their genes. These defective viruses are unable to make some really important proteins, so they can’t infect healthy cells, but they can still create copies of themselves. And those copies, though harmless to your cells, get in the way of other viruses— so scientists have taken to calling them defective interfering viruses.

Researchers are hoping to capitalize on these helpful defects by creating clones or synthetic versions. And so far, they’ve successfully treated multiple strains of influenza in mice with this approach. Of course, mice aren’t people, so like the other universal antivirals in development, there’s a lot more work to be done.

Still, the fact that there are so many potential broad-spectrum antivirals already in development is a good sign. While scientists have yet to come up with the silver bullet, we live in exciting times. And it might not be too long before we actually get to say “I remember catching the cold.” Thanks for watching this episode of SciShow!

If you liked learning about the latest cold-fighting advances, you might like our episode on how cold medicines actually treat those awful symptoms. [ outro ].