The Economist - USA (2021-02-13)

The Economist February 13th 2021 BriefingMaking vaccination work 19

cases of “long covid”, a debilitating form of
the disease in which some effects last for
months, follow original infections that
were not severe enough to require hospital
admission. It is not yet clear whether long
covid is less likely in people who have been
vaccinated.
What is more, this pattern of effects
does not reveal what the vaccines are doing
about transmission. As Natalie Dean, a bio-
statistician at the University of Florida,
points out, there are two ways one can
imagine a vaccine bringing about the pat-
tern of protection the covid-19 vaccines
have been seen to provide (see chart 2 on
next page). In one of them the same num-
ber of infections occurs as would occur
otherwise, but the consequences of these
infections are systematically downgraded.
Thus almost all of the infections which
would lead to severe cases lead to moder-
ate or mild cases, and many of the infec-
tions that would have led to moderate or
mild cases produce no symptoms at all.
The alternative is that the total number
of infections is being reduced, but the ratio
of severe to mild to asymptomatic cases
stays roughly the same. The already low
number of deaths and hospitalisations
shrinks to something hardly there. The
number of mild cases is similarly deflated
(although, since bigger, remains palpable).
And so is the number of asymptomatic
cases. Indeed, the main difference be-
tween the two scenarios is that in one the
asymptomatic cases rise, and in the other
they fall.

The passing game
In the real world there is almost certainly a
bit of both going on: lower infections over-
all and a lessening of the symptoms that
follow, with different vaccines offering dif-
ferent profiles. But considering the two ex-
tremes is still instructive. Vaccines which
do little more than downgrade the symp-
toms will be doing relatively little to stop
the spread of the virus. Honey-I-shrank-
the-infections vaccines, on the other hand,
will be making a big dent in the epidemic’s
now infamous R number—the number of
new infections to which each infection
gives rise. If you imagine reducing what
are known as “non pharmaceutical inter-
ventions”—masks, social distancing, shel-
ter at home orders and the like—that dif-
ference would begin to matter a lot.
Some people will not be vaccinated, ei-
ther because of pre-existing conditions
which make it dangerous for them, be-
cause there isn’t enough vaccine for every-
one, or because they choose not to (see fol-
lowing story). If the vaccines are basically
downgrading symptoms, then these un-
vaccinated people will be at risk. If they are
making the virus less transmissible that
risk will be lessened.
A covid-19 vaccine that is highly effec-

tive in preventing transmission will,

therefore, be particularly useful. Accord-

ing to a model by Imperial College London,

all other things being equal, a vaccine that

blocks 40% of infections and thus pre-

vents 40% of disease would have a similar

impact on the number of covid-19 deaths as

a vaccine that got rid of 80% of disease but

left infection untouched.

Epidemiologists are waiting with bated

breath for results that will tell them how

good existing vaccines are at reducing

asymptomatic infections and infectious-

ness. Data from Israel suggest that the viral

load in swabs from infected individuals is

lower if they have been vaccinated. Clinical

trials of the Oxford/AstraZeneca vaccine

suggest that the jab may halve infections as

detected by pcrtests. Such results suggest

that covid-19 vaccines are likely to reduce

overall transmission of the virus. But un-

derstanding quite how much transmission

is blocked—and the degree to which some

vaccines are better at blocking transmis-

sion than others—will take months.

And then there is the further complica-

tion of the new variants. Vaccines seem to

have no particular problem with b.1.1.7. It

just complicates things by running

through the unimmunised parts of the

population that bit faster. b.1.351, which

has now been found in more than 30 coun-

tries, is of greater concern. At least three

vaccines—those from Oxford/AstraZene-

ca, J&J and Novavax—have been found to

be less effective at stopping it from causing

disease than they are against variants else-

where. There is increasing evidence that

P.1, now also reported in a number of coun-

tries beyond Brazil, also appears to be bet-

ter at avoiding immunity created by prior

infection and by some vaccines.

Countries that have already vaccinated

a lot of people could be brought back to

square one by the spread of such variants.

Britain, where 13m people had been vacci-

nated as of February 10th, and millions

more have been infected and thus have

some immunity (British studies have

found reinfection very rare for at least five

months), is trying hard to keep b.1.351 from

making inroads in the population. Health

authorities are mass-testing neighbour-

hoods where cases of b.1.351 have been

spotted and are doing particularly meticu-

lous contact tracing when a case is found.

Border controls have been tightened.

Eking out an advantage

Not all such new variants can be spotted

and stopped at borders. Mutations can

arise anywhere—sometimes the phone

call is coming from inside the house. But

there may be a limited range of mutations

about which people need to worry. The

new variants all differ from the original vi-

rus and from each other in various ways.

But p.1 and b.1.351 both share a particular

mutational quirk—technically called

e 484 kbut mercifully nicknamed Eric or

Eek—which makes a specific change to the

spike protein on the outside of the virus.

Eek has now been found in some isolates

of b.1.1.7. too. Researchers are beginning to

think that the change Eek represents is

what allows those variants to infect people

even if they have been vaccinated or previ-

ously infected.

It would be great if there were no vac-

cine-resistant strains. But given that there

are, the possibility that they are all using

the same trick offers a bit of comfort. It

suggests that Eek may be the best way for

new variants to avoid immune responses

capable of dealing with the original strain,

or at least the way evolution can most eas-

ily find. If the variants have all converged

on the same trick, tweaking vaccines to

protect against one may protect against

all—and against any later variants to which

natural selection teaches the same ruse. If

the virus had found a whole panoply of

ways by which to avoid existing immune

Sufficiently advanced technology

Israel, covid-19 vaccination and cases, 2020-

Source:“PatternsofCovid-19pandemicdynamicsfollowing

deploymentofa broadnationalimmunisationprogram”,by

Hagai Rossman et al.

1

Shareofpopulationvaccinated,%

Age0-

New positive cases, seven-day moving average

100=start of vaccination

Age 0-

Age60+

Age0-

Startof

lockdown

Age60+

Newhospitalisations,seven-daymovingaverage

100=start of vaccination 300

200

100

Dec Jan Feb

300

200

100

Dec Jan Feb

50

25

0

Dec Jan Feb

100

75

50

25

0

Dec Jan Feb

Age 60+

One dose

Two doses