How Are Novel Viruses Created?
Every now and then (as of today, it’s now) a virus sneaks up on us as a species and kind of… Explodes. Technically speaking it makes a pandemic. Sometimes it becomes endemic too, like the flu; starting out as a pandemic but now something we just deal with on a yearly cycle and have to vaccinate against. Between SARS, MERS, swine flu, and whatnot, COVID-19 isn’t our first pandemic rodeo. Though as an aside, a lot of unprecedented things are going on in the world as a result of COVID-19. But regardless, pandemics are like the tide–they rise and fall. So how do these new viruses come about? What makes a new virus?
Further Reading: What Is SARS?
What Is a Virus Anyway?
Quick recap, viruses are little balls of DNA or RNA that invade our cells and replicate within them. They basically hijack other cells to become virus factories. Then those cells explode and viruses come out to repeat the process.
Fun fact, COVID-19 is inside a ball of fat–which is why washing your hands is a really good idea to deal with it. Soap is really good at getting rid of fats–you’ll know this if you cook a lot.
You can read more about viruses in the post below.
Further Reading: Are Viruses Alive?
So a valuable investigation may be to look at where the first viruses came from. There’s the progressive and regressive hypothesis–both assuming cells existed before the very first virus.
The progressive hypothesis essentially argues that retroviruses made of a single strand of RNA originated as a kind of “defect” within a parent cell. Then it kinda became its own thing once it exited the cell. On the other hand, the regressive hypothesis holds that viruses didn’t become more complicated from the simple RNA strand. Alternatively, they could have developed from far more complex organisms. Hence the name “regressive.” Essentially, the first viruses were intracellular parasites that got simpler as their design became more efficient.
A virus-first hypothesis argues that viruses came before their larger cell victims. Since it’s agreed upon that RNA was likely among the first self-replicating molecules–opposed to its DNA counterpart.
Regardless, the truth likely lies somewhere in the middle.
We’re going to assume, for the rest of this post, that we’re not dealing with man-made viruses or bio-weapons.
We know that viruses can evolve pretty quickly. Evolution is change over time, where short life cycles typically lead to more change. Viruses replicate a lot, so random mutations are pretty common. Good ones will stick around. You can see this fairly quick turnaround in real time–there’s a reason we have to get a flu vaccination every year.
Related post: Why Is the Flu Seasonal?
So when it comes to new pathogens coming to people, it’s not uncommon to see a “spillover infection.” Essentially, a virus that once affected a different organism (like a pigeon or whatever) develops a random mutation that allows it to infect some other organism (like a cat). Then bang, new virus.
Oftentimes, the mutation that allows a virus to jump to other organisms makes it far less effective at infecting its original host. Since it’s also new to its new host, it might not be great at infecting them either (and that’s assuming it even got the chance to encounter its new host). Thus, a spillover infection can often just resolve itself.
But viruses mutate quickly, and as such random chance still allows for spillover infections to explode and become problematic. Like the bird flu, and even HIV.
Viral recombination is kind of like an exchange between two different viruses. This is where things can get kind of scary if you really think about it.
Two viruses, when put together, can by chance squish traits together to create a new virus. What emerges is going to be whatever has the most reproductive viability–which means it’s probably going to have the best of both worlds. Here’s a paper about viral recombination if you want to get into some nitty gritty biology.
When you apply this concept to spillovers, you can get some pretty effective viral scenarios. A virus that lives in animal A may have a hard time infecting new hosts–but it’s really good at killing the host cells. Another inside animal B may be super good at infecting new hosts, but has a problem taking them down. Perchance both those specimens end up inside animal A or B by a spillover.
If recombination goes right (or wrong, if you’re unfortunate enough to be animal A or B), you could end up with a virus that’s both really good at reproducing inside your cells and really good at jumping to new hosts. Then that virus spills over and so on.
Such quick-jump nightmare scenarios are uncommon, though that’s exactly what happened with the swine flu. It was a strain in pigs that had become recombinant with viruses found in birds and humans. Thus, a bad time for humans.
Sometimes we think viruses are actually bacteria and vice versa. Split them here.