4 May 2015. Source: National Geographic
With one gene, molecular geneticist Steve Kemp may someday be able to boost the success of small farms across a huge swath of central Africa.
The gene is from a baboon, and it’s important because it produces a protein that kills a diabolical protozoan called Trypanosoma brucei. Trypanosoma brucei causes a deadly wasting disease–trypanomiasis–in both cattle and humans. Now stick with me, here’s where it gets interesting: That protozoan, called a trypanosome, is the reason one-third of the African continent–an area the size of the United States–is almost completely prevented from keeping livestock. That’s because the tse-tse fly, the trypanosome’s preferred method of transportation, lives there. Where flies can infect cattle, cattle usually can’t survive.
The implications of animal-free farming in the developing world are enormous. For starters, there’s malnutrition. A quarter of the 800 million malnourished people on our planet live in sub-Saharan Africa, and lack of protein is a significant contributing factor.
But the larger problem is labor. Kemp, who’s been working on the disease since the 1980’s, says “Western people don’t understand the role of livestock in developing world agriculture. You talk about cows dying or not, and they think of steak and milk. But livestock are fundamental. If someone’s main business is growing maize, but he’s got a bullock that can pull a plow in the field and pull a cart to market, that’s huge. It’s about oiling the wheels of an agricultural system, and you need livestock.” In that cattle-free zone, 90 percent of the land is still worked by hand.
Trypanosomiasis doesn’t just kill livestock. It gets people, too. The human version is called sleeping sickness. The trypanosomes infect the central nervous system and cause confusion, behavior changes, and the sleep disruption that gives the disease its name. Untreated, it’s generally fatal. Livestock are sometimes the source for human infection.
The problem is pressing, and it caught Kemp’s attention when it became apparent that at least one kind of African cattle–the N’Dama breed, native to west Africa–had some natural tolerance of trypanosomes. Kemp, who’s originally from the UK and works at the International Livestock Research Institute (ILRI) in Nairobi, set out to investigate the source of that tolerance, in the hopes of breeding it into other kinds of African cattle.
He ran into two problems. The first was that cattle’s tolerance turned out to be complex. “There are at least ten genes involved,” says Kemp. The more genes involved, the harder it is to breed the trait into an animal. The second was that, because the cattle still played host to the trypanosome, even tolerant animals would be a disease reservoir, threatening humans and other animals.
While Kemp was studying trypanosomiasis in cattle, Jayne Raper, Professor of Biological Sciences at City University of New York’s Hunter College, was studying its absence in baboons. Along with a few other primates, baboons have complete resistance to the disease, and Raper was studying the source of that resistance, looking for clues to fight the human version of trypanosomiasis, which infected 20,000 people in 2012, according to World Health Organization estimates. Raper discovered that a component of baboon cholesterol, a protein with the charismatic name ApoL1, kills the trypanosome by punching holes in its cell walls. (Humans produce a similar protein, which kills some trypanosomes but not T. brucei.)
As Kemp describes it, the two scientists had an a ha moment at a meeting at ILRI in 2006. Raper was working on isolating the baboon gene in the hopes of created trypanosome-resistant transgenic mice to prove her concept. Kemp explained the problem with cattle and, well, a ha! By 2008, Raper had her mice, and Kemp now estimates that they’re about a year away from having a transgenic cow grazing the ILRI pastures…