Genetic Engineering and Diseases – Gene Drive & Malaria
What if you could use genetic engineering to stop humanity's most dangerous predator, the deadliest animal on the planet responsible for the death of billions, the mighty mosquito? Along with other diseases, it plays host to malaria, one of the cruelest parasites on Earth, possibly the single biggest killer of humans in history. In 2015 alone, hundreds of millions were infected and almost half a million people died. A new technology could help us eradicate malaria forever, but to do so, we need to engineer a whole animal population. This is not a hypothetical problem; the modified mosquitoes already exist in a lab. Should we use the technology, and is malaria bad enough to risk it?
Malaria is caused by a group of microorganisms: Plasmodia, very weird microorganisms that consist of just a single cell. They're parasites that completely rely on mosquitoes. Malaria always starts with an insect bite. In its salivary glands, thousands of sporozoites wait until the insect penetrates your skin. Immediately after invading you, they head for the liver, where they quietly enter big cells and hide from the immune system. For up to a month, they stay here in stealth mode, consuming the cells alive and changing into their next form: small drop-like merozoites. They multiply, generating thousands of themselves, and then burst out of the cells.
So thousands of parasites head into the bloodstream to look for their next victims, red blood cells. To stay unnoticed, they wrap themselves in the membranes of the cells they killed. Imagine that! Killing someone from the inside and then taking their skin as camouflage—brutal! They now violently attack red blood cells, multiplying inside them until they burst, then finding more red blood cells, and this cycle repeats over and over. Pieces of dead cells spread lots of toxic waste material, which activates a powerful immune response causing flu-like symptoms. Among the symptoms are high fever, sweats and chills, convulsions, headaches, and sometimes vomiting and diarrhea. If malaria breaches the blood-brain barrier, it can cause coma, neurological damage, or death.
The parasites are ready for evacuation now. When another mosquito bites the infected human, they get a ride, and the cycle can start over. In 2015, the Zika virus, which causes horrible birth defects if it infects pregnant women, spread rapidly into new areas around the globe. It too is carried by a mosquito. The mosquito is the perfect carrier for human diseases; they've been around for at least 200 million years. There are trillions of them, and a single one can lay up to 300 eggs at a time. They are practically impossible to eradicate and the perfect parasite taxi.
But today, we have a new revolutionary technology that could enable us to finally win the war against them: CRISPR. For the first time in human history, we have the tools to make fast, large-scale changes to entire species, changing their genetic information as we please. So instead of attacking isolated groups of insects, why not just change the types that transmit diseases? Using genetic engineering, scientists successfully created a strain of mosquitoes that are immune to the malaria parasite by adding a new antibody gene that specifically targets Plasmodium. These mosquitoes will never spread malaria.
But just changing genetic information is not enough. The edits would only be inherited by half the offspring because most genes have two versions inside the genome as a fail-safe. So, after just two generations, at most, only half of the offspring would carry the engineered gene. In a population of billions of mosquitoes, they would hardly make a difference. A genetic engineering method called the gene drive solves this problem. It forces the new gene to become dominant in the following generations, overpowering the old gene almost completely.
Thanks to this twist, 99.5% of all the engineered mosquito offspring will carry the anti-malaria edit. If we were to release enough engineered mosquitoes into the wild to mate with normal mosquitoes, the malaria-blocking gene would spread extremely quickly. As the new gene becomes a permanent feature of the mosquito population, Plasmodium would lose its home base. Scientists hope that the change would be so fast that they could not adapt to it quickly enough. Malaria could virtually disappear. If you take into account that maybe half a million children are killed by it every year, about five have died since this video started.
Some scientists argue that we should use the technology sooner rather than later. The mosquitoes themselves would probably only profit from this; they don't have anything to gain from carrying parasites, and this might only be the first step. Malaria might just be the beginning. Different mosquitoes also carry dengue fever and Zika; ticks transmit Lyme disease; flies transmit sleeping sickness; fleas transmit the plague. We could save millions of lives and prevent suffering on an unbelievable scale.
So, why haven't we done this yet? For one, CRISPR editing is barely four years old, so until very recently, we just couldn't do it as fast and easily. And there are valid concerns. Never before have humans consciously changed the genetic code of a free-living organism on this scale. Once we do it, there is no going back. So, it has to be done right, because there could be unwanted consequences if we set out to edit nature.
In this specific case of malaria, though, the risk might be acceptable since the genetic modification doesn't make a big change in the overall genome. It only changes a very specific part. The worst-case scenario here is probably that it might not work, or that the parasite adapts in a negative way. There is still much debate. Technology as powerful as gene drive needs to be handled with a lot of care, but at some point, we have to ask ourselves: Is it unethical to not use this technology when every day 1,000 children die? Humanity has to decide how to act on this in the next few years. The public discussion is way behind the technology in this case.
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