IIT STARTS WITH a bite near the cow’s ear. Over the next few days, the animal’s lymphocytes multiply. Your lymph nodes swell. He stops feeding and begins to cough as fluid fills his lungs. He develops a fever of up to 41°C. A few weeks after the bite, it dies.
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Such a story is common in African countries where East Coast Fever (ECF) is rampant. ECF, which is caused by protozoan parasites spread by ticks, kills about 1 million head of cattle each year. It also prevents the introduction of higher-yielding, faster-growing European breeds, which are much more susceptible to the disease than their African relatives. Although a vaccine is available and ticks can be attacked with sprayed pesticides (see image), both approaches are expensive. Therefore, most farmers continue to use less productive local varieties, which reduces their income and reduces agricultural production. The difference is stark: a Kenyan cow produces around a tenth of the milk of one in Britain.
New research may offer a solution. Veterinary scientists led by Phil Toye of the International Livestock Research Institute campus in Nairobi and James Prendergast of the Roslin Institute in Edinburgh have found a genetic variant associated with resistance to ECF. This result, published in please Geneticsit opens up the possibility of breeding, or even gene-editing into existence, cattle that can beat it.
The discovery of the variant occurred by chance. As he watched a small ECF vaccination trial in 2013, researchers at the International Livestock Research Institute noted that of the 12 unvaccinated animals involved, all three survivors had been sired by the same bull. Further investigation suggested that the specific genetic element responsible was a version of a gene called FAF1who was called FAF1B. FAF1 it is part of a process of programmed cell suicide called apoptosis, which helps regulate cell number.
The current study examined 20 animals that carried two copies of the variant version. Only one of these succumbed to ECF. In contrast, 44 of 97 cows without the variant succumbed. The results, says Dr. Prendergast, suggest that FAF1B has a “disproportionately large effect” on livestock ECF tolerance. He and his colleagues, while not sure exactly why, believe this variant may prevent cattle lymphocytes from multiplying so quickly.
Their discovery could soon lead to better selective breeding. Once researchers are sure the variant has no adverse side effects, African cattle farmers can test their animals. DNA for him and reproduce from those who bear him, thus producing ECFresistant offspring. In the longer term, gene editing techniques such as CRISPR-Cas9 may allow the protective version to be spliced into productive European breeds, which can then be bred much more successfully in Africa.
Such gene editing programs are becoming more common and gaining official acceptance. In March, regulators in the United States approved the first sales to consumers of meat from gene-edited cattle. (The modification in question gives the animals short, slippery fur, to help them cope with warmer weather.) Meanwhile, the International Livestock Research Institute and Roslin are engineering cattle resistant to other diseases, including trypanosomiasis, a protozoan disease transmitted by the tsetse fly. flies.
By reducing mortality and increasing productivity, gene-edited European cattle could have a useful effect in Africa, although some worry that the benefits may be exaggerated. Dr. Prendergast points out the many other animal diseases that are prevalent on the continent, to which those cattle would still be susceptible. He suggests that farmers might be better off breeding local varieties for resistance (and higher productivity, too). But no matter whether disease resistance is produced through conventional breeding or gene editing, it should lead to healthier livestock and happier farmers. ■
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This article appeared in the Science and Technology section of the print edition under the headline “Cowabunga!”