The Economist December 18th 2021 47
InternationalThespreadoftheOmicronvariantSeeing the need for speed
E
xponential growth is a dizzying
thing. In the week to December 8th Brit
ain saw 536 new cases of covid19 ascribed
to the Omicron variant, less than 0.5% of
the number caused by the dominant Delta
variant. But the week before there had been
only 32 cases of Omicron—and by Decem
ber 14th the case number was over 10,000.
Omicron looks set to become the country’s
dominant strain in terms of cases before
advent calendars run out of windows.
Cases lag behind infections. On Decem
ber 13th Britain’s health minister, Sajid Ja
vid, said that there were estimated to have
been 200,000 infections in the country
that day, most of them Omicron. Three
more doublings and the total number of
infections a day will be more than 1m.
It is not just in Britain that Omicron is
outstripping Delta. It has already displaced
it in South Africa, where it first came under
scrutiny and where its growth, though pos
sibly now slowing a little, has been spec
tacular. Studies in various European coun
tries show similar growth, though with a
later start. The same is true in America. The
variant has now been detected in almost allcountries, including China. The numbers
involved are often small. But with expo
nential growth small is not much comfort:
it doesn’t last.
Omicron seems to have two attributes
that enable such rapid spread. Some subset
of its many mutations seems to make it
more transmissible. Contacttracing stud
ies in Britain have found that the risk of a
given Omicron infection spreading is two
to three times that for a Delta infection.
And because it is better at infecting peo
ple who have previously been vaccinated,
or infected, it has a larger pool of people to
infect. On December 14th Discovery
Health, South Africa’s largest health insur
er, produced the initial results of work on
Omicron undertaken with the South Afri
can Medical Research Council. They found
that, whereas two doses of the PfizerBioN
Tech mrnavaccine offered 80% protec
tion against infection before the Omicron
wave, against Omicron the protection
dropped to 33%. Its effectiveness in reduc
ing the risk of severe disease is also lower:
two doses of the Pfizer vaccine reduced the
risk by 70% (down from 93% for Delta). That still makes being vaccinated a very
good thing. Most of the people who have
been hospitalised with Omicron in South
Africa, and 84% of those in intensive care,
are unvaccinated. And it does not look as if
the sort of vaccine someone was given
matters all that much. The other vaccine in
use in South Africa, made by J&J, an Amer
ican company, relies on a modified adeno
virus, rather than mrna, to get its message
into the body, as does the more widely used
AstraZeneca vaccine. It, too, seems to pro
tect against severe disease.
These realworld findings support the
hope that two doses of all the existing vac
cines will continue to offer significant pro
tection against severe disease, even if they
are not so good at blocking infection. That
makes sense. Evolution has shaped the im
mune system to reduce the risk of death.
Stopping a virus which the body has seen
before from infecting it again is a helpful
step in that direction, and one of the prim
ary purposes of the antibody response. But
it is not the only step; the defence is deep
and layered. Incoming Omicron may be
good at evading the antibodies produced
by vaccines and previous infections—it is
38 times more likely to infect someone
who has previously been infected than
other variants. But further foes await it.
After infection has started, cellbased
immunity joins in the fight, seeking out
and destroying the cells which the virus
has suborned. This response is greatly
strengthened by prior vaccination. And it
is less easily fooled by a few changes to theThe new variant advances at an incredible rate. That means action is urgent