The Economist - USA (2019-08-17)

(Antfer) #1

62 Science & technology The EconomistAugust 17th 2019


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eopardsealsresembletheirterres-
trialnamesakesintwoways.They
havepolka-dotpelts.Andtheyarepow-
erful,generallysolitarycarnivoresthat
arequitecapableofkillinga human
beingif theysochoose—ashasindeed
happenedonce,in2003,whena British
marinebiologistwasthevictim.
Curiously,though,therehavealso
beenreportsofleopardsealsbehavingin
a friendlymannertowardspeople—
apparentlytryingtopresentgifts,inthe
formofprey,todivers.Untilnow,there
hasbeennoexplanationforthisphilan-
thropy.ButworkjustpublishedinPolar
BiologybyJamesRobbinsofPlymouth
University,inBritain,suggeststhatwhat
thesealsareactuallylookingforisa
diningpartner.
MrRobbinsandhisteamwerestudy-
ingleopardsealsinthewatersaround
SouthGeorgia,anislandintheSouthern
Ocean1,500kmfromthetipoftheAnt-
arcticpeninsula.Insteadofdiving,or
watchingfromships,theyuseddronesto
carryouttheirobservations.These
dronesrecordedhithertounobserved
behaviouronthepartoftheanimals.

First,belyingtheirsolitaryreputa-
tion,thesealscametogetheringroupsto
attackkingpenguins(twicethesizeof
thegentoopenguininthephotograph)
thatwereenteringtheseafroma rookery
ontheisland.Second,whena sealdid
catcha penguininthesecircumstancesit
wouldsometimesoffertoshareit witha
neighbourina wayreminiscentofdiv-
ers’talesofgiftgiving.Whatlookedlike
anaberrationmightthusbea normal
wayofbehaving.Butwhy?
MrRobbins’ssuggestionisthatshar-
inga penguinwitha neighbourmakesit
easiertoeat.A closelookatfootagethe
dronesrecordedshowsthatsealsinsuch
partnershipstakeit inturnstofeed.One
holdsthebirdtightinitsjawswhilethe
otherripsoffa chunkoffleshandswal-
lowsit.Thentheyswaproles.Bycon-
trast,fora lonesealtoreducea penguin
tobite-sizedchunksmeanswhipping
thepreyaroundinitsjawswithasmuch
forceasit canmuster,inordertotear
lumpsoffleshfreefromthecarcass.This
commonlyhappens,butisthoughttobe
extremelytiring.Better,therefore,tofind
a buddyandenjoya mealtogether.

P-P-Pickupa penguin


Animalbehaviour

Antarcticpredatorssharetheirsupper

N


ews aboutEbola, a viral disease that
kills up to 90% of those it infects, is
usually grim. The latest Ebola outbreak, in
the Democratic Republic of Congo, has
thus far killed nearly 1,900 people and
rages on. But on August 12th the grimness
lifted somewhat with the announcement
that two anti-Ebola treatments being test-
ed in the country have proved effective. If
administered when the first signs of infec-
tion appear, they boost survival rates to
about 90%.
The treatments in question employ
antibodies. These are special protein mole-
cules made by the immune system in re-
sponse to infection. They work by locking
onto specific parts of invading pathogens,
or of body cells infected by those patho-
gens—either gumming the target up and
disabling it or marking it for destruction by
other parts of the immune system. It is pos-
sible, however, to give the immune system
a helping hand by identifying suitable anti-
bodies in advance, manufacturing them in
bulk, and then injecting them into those
infected by the pathogenic target.
One of the successful treatments, code-
named regn-eb3, is a cocktail of three such
antibodies, mixed by Regeneron, an Amer-
ican biotechnology firm. The other,
mab114, is a single antibody developed by
America’s National Institute for Allergies
and Infectious Diseases. regn-eb3 and
mab114 were among four experimental
treatments tested in a randomised trial at
clinics in Congo. Based on preliminary re-
sults from 500 patients, an oversight com-
mittee led by the World Health Organisa-
tion concluded that the trial should be
stopped immediately, in order that the two
successful treatments could be made avail-
able to everyone.
Prompt use after infection is vital. Over-
all, 29% of those receiving regn-eb3 died.
But of people treated when their viral loads
were still low, only 6% succumbed. For
mab114 the numbers were 34% and 11% re-
spectively—superficially less good, but ac-
tually indistinguishable statistically from
the results for regn-eb3. Two other candi-
date treatments had significantly worse
figures than these, and were therefore re-
jected by the overseers.
Both regn-eb3 and mab114 have histor-
ies. Regeneron developed the former in
2016, in response to an Ebola epidemic in
west Africa in which 11,000 people died.
But that outbreak came to an end before the

treatment could make its way into clinics,
and until this year there had been no op-
portunity to test it. The story of mab114
goes back even further. Its pertinent anti-
body was isolated from a survivor of an epi-
demic of Ebola in Congo in 1995.
Both treatments will now be deployed
in the field—but, given the smallish size of
the trial that approved them, doctors will
be looking closely at their relative effica-
cies to determine whether, in light of more
data, one is actually better than the other.

Regardless of that, effective treatment will
surely help break the epidemic directly, by
stopping those cured from passing on the
virus. It may help indirectly, too. At the mo-
ment, those who have become infected,
seeing others go into clinics alive only to
leave in coffins, are understandably reluc-
tant to follow suit. That means they remain
in their homes and spread the illness to
others. The prospect of going to a clinic for
a cure will change this, and thus also help
to break the chain of transmission. 7

Two treatments for Ebola emerge from
a clinical trial in Africa

Ebola

Hope

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