Good News (Part 3)


Malaria is a nasty disease, caused by mosquitoes infected with parasites. If you catch malaria, you get feverish and tired. You have headaches, and vomit. If you’re unlucky you may have seizures, fall into a coma and even die.

Almost 200 million people got malaria in 2013. Somewhere between 500,000 and a million died. 90% of these people lived in Africa.

This is good news???

Yes, it is! Since 2000, malaria funding has increased nearly tenfold. From 2000 to 2015, cases of malaria in Africa dropped by 40%. Thanks to this, over 600 million cases of malaria have been avoided!

The main reason? Insecticide-treated nets. If you sleep with one of these over your bed, you’re less likely to get bitten by a mosquito.

And how are people getting these nets? The Global Fund to Fight AIDS, Tuberculosis and Malaria, founded in 2002, has distributed 548 million of them. They provide about half the international funding for malaria control worldwide.

The Bill and Melinda Gates Foundation is helping. They’ve spent almost $2 billion to fight malaria. They’ve also contributed $1.6 billion to the Global Fund.

The war against malaria is far from won. One of the main drugs used to fight it is artemisinin. But a strain that’s resistant to artemisinin is spreading near the border of Thailand and Cambodia.

A vaccine would be great. But there’s no vaccine yet. And it’s not easy: malaria is actually caused by several different organisms. Still, stopping just a few of the main culprits would be great.

New technology can change the game. On November 23rd, something amazing happened.

A team of scientists from the University of California announced that they had gotten mosquitoes to pass on malaria resistance genes to almost all their children—not just half, as you’d normally expect!

With this method, malaria resistance could spread through the mosquito population like wildfire.

This method is called a gene drive, and it was implemented using a system called CRISPR. If you haven’t heard about these things, it’s time to do some reading! I’ll give you some links below.

Being sensible and cautious, the scientists have not tested this method in the wild yet. They could do it in less than a year—but they’re in no rush. Said Anthony James:

It’s not going to go anywhere until the social science advances to the point where we can handle it. We’re not about to do anything foolish.

It may be good to test it on a remote island, where mosquitoes can’t fly to another place.

Gene drives are simultaneously very promising and quite scary. If we used one to spread malaria resistance among mosquitoes we could save half a million lives each year – and let poor countries spend their resources on something better.

We are gaining the power to do many things. We just need some wisdom to go along with this power. In fact, many of us have that wisdom. We just need to get better at making it prevail.

For more

On the CRISPR method for spreading malaria resistance:

• Heidi Ledford and Ewen Callaway, ‘Gene drive’ mosquitoes engineered to fight malaria, Nature News, 23 November 2015.

For more on CRISPR:

• Sarah Zhang, Everything you need to know about CRISPR, the new tool that edits DNA, Gizmodo, 6 May 2015.

For the new discovery:

• Valentino M. Gantza, Nijole Jasinskiene, Olga Tatarenkova, Aniko Fazekas, Vanessa M. Macias, Ethan Bier and Anthony A. James, Highly efficient Cas9-mediated gene drive for population modification of the malaria vector mosquito Anopheles stephensi, Proceedings of the National Academy of Sciences 112 (2015).

3 Responses to Good News (Part 3)

  1. Bruce Smith says:

    The scariest part seems (to me) to be that some mutations in “what is being spread using CRISPR” would be equally well spread, but not helpful (perhaps actively harmful). Without knowing how the spreading works (I didn’t read those links and probably don’t have time to), it’s hard to guess how correctable that would be (e.g. by spreading a corrective or replacement factor the next year).

    A related question is whether whatever is spread keeps spreading indefinitely. (I would guess yes — it just becomes a permanent part of the genome — but I can imagine ways the answer could be no.) If it is, and if (when) it mutates in the future in any individual, can the mutated form sometimes further spread “over the original” (that is, win out over the original form, coming from the other parent)?

  2. Ishi Crew says:

    at least the gates foundation is spending some money on really basic things like mosquito nets—i had seen some discussion of Gates foundation charity which said most anti-malarial reserarch and applications went straight to academics at U Wash seattle—conferences, search for a cure or magic bullet. also, as someone who had to spend almost 2 months in a hospital for pneumonia until i got sepsis –and i had no health insurance and the bill was 3500 dollars/day (my bill was more than i’d made in the last 10 or more years) you get out , get cured, and then what—i’ve lived with many african people (liberians, kenyons, ghanians, and many more off and on—nice and smart and well adjusted–many had or were getting PhDs). but some people end up joining baka harem or whatever those various extremist groups in africa are needs a life cycle analyses—this reminds me of the antiabortion people in the USA—we’ll save the fetus, but then we’ll send them to jail or death row.

    • Mark Myatt says:

      I agree. There has been some “magic bullet” thinking at BMGF.

      I’d counsel against such thinking WRT insecticide treated nets (ITN). The ITN approach relies on the vector (i.e. the mosquito) feeding behaviour and will work well only when the vector feeds indoors and at night. Some vectors feed during the day and / or outside. Another key behaviour is resting behaviour which can be inside or outside. Vector species exist with different combinations of these behaviours and it is important to know which behaviours are dominant locally in order to select an effective intervention.

      If you have a vector that feeds outside and rests outside then source reduction (i.e. destruction of breeding sites) is probably the better option. If the vector rest indoors then residual insecticide spraying is a good option.

      This is not to attack the ITN approach but just to point out that in some settings it will not be the right thing to so. The success we see in Africa is due to the appropriateness of the ITN strategy and may not be replicable elsewhere.

      Since a blood meal is necessary for reproduction we are setting up a selection pressure that may result in population behavioural changes that render the intervention less effective over time (e.g. a shift from night feeding to dusk / dawn feeding). This suggests that broader interventions such as ITNs with source reduction and case-finding with early treatment might be a better longer term option than relying solely on ITNs.

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