A genetic breakthrough could help fight a disease in African cattle

IT 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 eating and starts coughing as fluid fills his lungs. Develops a fever as high as 41°C. A few weeks after the bite, he 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 cattle each year. It also prevents the introduction of faster-growing, higher-yielding European breeds, which are much more susceptible to the disease than their African relatives. While a vaccine is available and ticks can be attacked with sprayed pesticides (see image), both approaches are expensive. Most farmers, therefore, continue to use less productive local varieties – reducing their yields and reducing agricultural production. The difference is stark: a Kenyan cow produces about a tenth of the milk that a cow in Britain.

New research may offer a solution. Veterinary scientists led by Phil Toye from the International Livestock Research Institute campus in Nairobi and James Prendergast from the Roslin Institute in Edinburgh have found a genetic variant associated with resistance to ECF. This result, published in PLOS geneticsopens up the possibility of creating – or even editing genes – cattle that can beat you.

The discovery of the variant happened by chance. By observing a small ECF In the 2013 vaccination trial, researchers at the International Livestock Research Institute noted that of the 12 unvaccinated animals involved, all three survivors were sired by the same bull. Further investigation suggested that the specific genetic element responsible was a version of a gene called FAF1that they nicknamed FAF1B. FAF1 it is part of a programmed cell suicide process called apoptosis, which helps regulate cell numbers.

The current study examined 20 animals carrying two copies of the variant version. Only one of them succumbed 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, although they don’t know exactly why this happens, think that this variant might stop the cattle’s 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 livestock farmers can test their animals. DNA for it and reproduce from those who carry it, thus producing ECF– resistant offspring. In the long term, gene editing techniques such as CRISPR-Cas9 may allow the protective version to be patched into productive European breeds, which can then be bred much more successfully in Africa.

These gene editing programs are increasingly common and are gaining official acceptance. In March, regulators in the United States approved the first consumer sales of gene-edited beef. (The modification in question gives the animals short, smooth fur to help them cope in a hot climate.) Meanwhile, the International Institute for Livestock Research and Roslin are designing animals resistant to other diseases, including trypanosomiasis, a protozoan disease. transmitted by the tsetse. flies.

By reducing mortality and increasing productivity, gene-edited European cattle could have a useful effect in Africa – although some worry that the benefits are exaggerated. The Doctor. Prendergast points to many other animal diseases prevalent on the continent to which these cattle would still be susceptible. He suggests that farmers may be better off growing local varieties for resistance (and also higher yields). But whether disease resistance is brought about by 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 title “Cowabunga!”

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