The Economist - UK (2022-04-30)

The Economist April 30th 2022 Science & technology 73

ma”. This renders the margin for error

slim.Were thestagetotip slightly,and

touchthisplasmaknife,hesays,itwould

becutthroughalmostasif it werebutter.

FrictionfrompassingthroughtheWall

willslowthestage,butnotenoughforit to

deploy itsmain parachute immediately.

Instead,atan altitude ofabout13km, a

pneumaticmortarwillshootouta smaller

droguechute.Onlywhenthedescending

stagehasreachedanaltitudeof6kmwill

thebigparachutebereleased.Eventhen,a

circular “reefing” cord will restrict its

openingtoa quarterofitsmaximumsur­

facearea.Roughlya minutelater,thatcord

willbesevered,topermittheparachuteto

inflatefully.Thiswillslowthestage’sde­

scenttojusttenmetresa second.Asthe

earliertrialshaveshown,atthatspeedthe

helicopter’spilotisabletosnagthespent

stagewithneither greatdifficultynor a

dangerousdownwardyankontheaircraft.

Rocket Labis notthe only company

whichhopestoemulateSpaceX’sfeatofre­

cycling.QuiltyAnalytics,a firmthatadvis­

esthespaceindustry,isawareofatleast

five others—though none is as far ad­

vanced as Rocket Lab.Asto how much

moneythefirmmightsaveif allthisproves

successful,MrBeckremainscoy.However,

Chris Quilty, Quilty Analytics’ founder,

reckonstheElectron’sfirststagemaywell

accountformorethantwo­thirdsofthe

launcher’scost,soreusingitwillcheapen

thingsconsiderably.Itisa fairbet,then,

thatRocketLab’scompetitorswillbeal­

mostaskeenasthefirmitselftoseejust

howwelltheoperationsucceeds. n

EastCoastFever

Cowabunga!

I

t beginswitha bitenearthecow’sear.
In  the  next  few  days,  the  animal’s  lym­
phocytes multiply. Its lymph nodes swell.
It stops feeding and starts coughing as flu­
id fills its lungs. It develops a fever as high
as 41°C. A few weeks after the bite, it dies.
Such  a  story  is  common  in  African
countries  where  East  Coast  Fever  (ecf)  is
rampant.  ecf,  which  is  caused  by  proto­
zoan parasites spread by ticks, kills around
1m cattle a year. It also prevents the intro­
duction of faster­growing, higher­yielding
European  breeds,  which  are  much  more
susceptible to the illness than their African

kin.Thougha vaccine is available, and the

ticks  can  be  attacked  with  sprayed  pesti­

cides (see picture), both of these approach­

es  are  costly.  Most  farmers  thus  continue

to use less­productive local varieties—cur­

tailing their incomes and reducing agricul­

tural output. The difference is stark: a Ken­

yan cow produces around a tenth as much

milk as one in Britain.

New research may offer a solution. Vet­

erinary scientists led by Phil Toye of the In­

ternational  Livestock  Research  Institute’s

campus in Nairobi and James Prendergast

of the Roslin Institute, in Edinburgh, have

found a gene variant associated with resis­

tance to ecf. This result, published in plos

Genetics, opens up the possibility of breed­

ing—or even gene­editing into existence—

cattle that can beat it.

The variant’s discovery came about ser­

endipitously. While observing a small ecf

vaccination trial in 2013, researchers at the

International Livestock Research Institute

noticed that of the 12 unvaccinated animals

involved, all three survivors had been sired

by  the  same  bull.  Further  investigation

suggested the specific genetic element re­

sponsible  was  a  version  of  a  gene  called

faf1, which they dubbed faf1b. faf1is part

of  a  process  of  programmed  cellular  sui­

cide called apoptosis, which helps regulate

cell numbers. 

The current study examined 20 animals

carrying two copies of the variant version.

Just one of these succumbed to ecf. In con­

trast,  44  of  97  cows  without  the  variant

succumbed.  The  results,  says  Dr  Prender­

gast,  suggest  that  faf1bhas  a  “dispropor­

tionately large effect” on cattle’s ecftoler­

ance.  He  and  his  colleagues,  though  not

sure exactly why that might be, think this

variant may stop cattle lymphocytes from

multiplying as quickly.

Their discovery could soon lead to bet­

ter  selective  breeding.  Once  researchers

are sure the variant does not have adverse

side­effects,  African  cattle  breeders  can

test  their  animals’  dnafor  it  and  breed

from those carrying it, thus producing ecf­

resistant  offspring.  In  the  longer  term,

gene­editing  techniques  such  as  crispr­

Cas9 may permit the protective version to

be  spliced  into  productive  European

breeds, which can then be raised far more

successfully in Africa. 

Such  gene­editing  programmes  are

increasingly  common,  and  are  achieving

official acceptance. In March, regulators in

America  approved  the  first  sales  to  con­

sumers  of  meat  from  gene­edited  cattle.

(The modification in question gives the an­

imals  short,  slick  hair,  to  help  them  cope

with a warming climate.) The Internation­

al Livestock Research Institute and Roslin,

meanwhile,  are  designing  livestock  resis­

tant  to  other  diseases,  including  trypano­

somiasis,  a  protozoan  illness  spread  by

tsetse flies.

By  reducing  mortality  and  increasing

productivity,  gene­edited  European  live­

stock could have a useful effect in Africa—

though  some  worry  the  benefits  are  over­

stated.  Dr  Prendergast  points  to  the  many

other  animal  diseases  prevalent  on  the

continent, to which such cattle would still

be susceptible. He suggests farmers might

be better off breeding local varieties for re­

sistance (and also higher productivity). But

no  matter  whether  disease  resistance  is

brought about by conventionalbreeding or

gene  editing,  it  should  lead tohealthier

cattle—and happier farmers.n

A genetic discovery could help Africa’s cattle farmers

Ticked off about cattle fever