20 SUNDAY, NOVEMBER 15, 2020for decades? Along with the prognostica-
tions we’re also getting postgnostications
(it’s not my neologism), efforts to under-
stand the past by predicting what hap-
pened: Where did this virus come from? A
wild animal? Which animal? How did it
manage to be so nefariously well adapted
for human infection? How did it get into us
at the start? Has it evolved since? Scien-
tists are at work on those questions, trap-
ping wildlife in China, taking fecal samples
and blood, culturing viruses, sequencing
genomes from bats, pangolins and hu-
mans, and comparing them, as the clock
ticks.
“Apollo’s Arrow,” by Nicholas Christakis,
is a useful contribution to this initial wave of
Covid books, sensible and comprehensive,
intelligent and well sourced, albeit a little
programmatic and dull. (Touching on past
pandemics and epidemics, as well as our cur-
rent crisis, the book takes its title from those
terrible arrows, representing plague, that
Apollo rained down on the Greeks in Book 1
of the “Iliad.”) It’s a broad survey, not a deep
dive, and sweeps across most of the signal
topics: the inept early responses to the out-
break, first in China and then in the United
States; the back story of modern pandemics
and pandemic threats, notably the 1918 influ-
enza and SARS in 2003; the social shut-
downs, the mask issue and the tension be-
tween civil liberties and public health; the
grief, fear and lies that make a pandemic
emotionally as well as medically punishing;
the social and economic changes, forced by
this virus, that may become permanent; the
general question of how plagues end and the
specific, more speculative question of how
this one might.
Given that Christakis is a physician and
sociologist, the co-author of an earlier book
about social networks and how they shape
lives, the co-author also of an influential
paper on “social contagion theory” and the
co-director of the Institute for Network Sci-
ence at Yale, one naturally expects that
“network science” might afford him spe-
cial insight into Covid-19. This book deliv-
ers on that expectation moderately, with a
short section on the superspreader phe-
nomenon and such disease-math variables
as the basic reproduction number (the av-
erage number of persons infected by each
infected person in a naïve population), the
case fatality rate, the threshold for herd
immunity and a few others that have be-
come familiar in recent months.
There’s also dispersion, less familiar,
which is the variation in actual (not aver-
age) reproduction number from one in-
fected person to another. If some people
cause few secondary infections and some
cause many, the dispersion is high. (The
dispersion of Covid-19 is high.) Why? Al-
though part of the answer may be that
some individuals simply shed more virus,
or wash their hands less, or refuse to wear
masks or cough more, another contributor
to superspreading, Christakis explains, is
that certain people have many more social
contacts than the average. He calls those
“popular people,” and notes that they “are
more likely to become infected themselves
as well as more likely to infect numerous
others.”He illustrates this with some dots-and-
lines network figures, showing who might
have contact with whom. (These figures
are weirdly resonant, resembling a similar
graphic in an epidemiology paper from
1984 that depicted sexual connectivity
among 40 early AIDS patients, which led to
one man at the center, labeled “Patient O”
by the researchers, to be demonized in a
popular book as “Patient Zero.”) Although
superspreader events — in a choir, at a fu-
neral, during a White House reception —
seem alarming, the existence of high varia-
tion in reproduction number for Covid-
may actually have an ameliorating effect.
According to Christakis, it may reduce thethreshold for herd immunity. How so? Be-
cause “popular people” are more likely to
get infected early in the pandemic, and
most of them will survive, presumably
with some immunity. “And if all the popular
people became immune early, relatively
more paths for the virus to spread through
society would be cut off.”
That’s the good news. But because of its
capacity to spread from asymptomatic
cases and its relatively low case fatality
rate, Christakis estimates, Covid-19 maystill infect 40 percent of the global human
population, and possibly as much as 60
percent, unless a vaccine becomes avail-
able soon. And what about when it does?
Do we vaccinate the “popular people”
first?
Another fascinating and controversial
idea that Christakis examines is that the
virus may become less virulent. He notes
that “one way a pandemic... can come to
an end is that the virus mutates over a peri-
od of years to get much milder.” But to say
that this virus might mutate is a mislead-
ing truism; viruses continually mutate as
they replicate, introducing small random
errors into their genomes; and coronavi-ruses mutate more abundantly than many
others. The mutations are raw material on
which Darwinian natural selection may
act, or not, to produce new adaptations.
This is Evolution 101. If an increase in
transmissibility or a decrease in virulence
was adaptive for the virus, it would proba-
bly change in that way. Viruses do some-
times — not always — evolve toward lesser
virulence within their hosts, if it allows
them to spread more widely. But so far
there’s very little evidence that either a re-
duction in virulence or an increase in
transmissibility has occurred. Maybe this
virus doesn’t need to evolve much because
it’s already so damn successful.
Christakis describes an intriguing prece-
dent, though, with some circumstantial evi-
dence to support it. The virus called OC43 is
a human coronavirus that causes nothing
more severe than the common cold. In fact,
along with one other coronavirus, it ac-
counts for as much as 30 percent of all colds.
Christakis cites research suggesting that
OC43 spilled into people, from cattle, around
1890, which happened to coincide with the
beginning of a severe pandemic that was
known as the “Russian flu,” because its first
major outbreak occurred in St. Petersburg,
in December 1889. This “flu” swept out of
Russia, across Europe, to the United States
and much of the rest of the world, as fast as
trains and ships could carry it, killing about a
million people. Was it truly influenza? No
one knows, because the concept “virus” had-
n’t yet been defined, because viruses could-
n’t be seen through a light microscope and
because no modern scientific team has yet
found a frozen victim of that 1890 pandemic,
awakened a virus and identified it by ge-
nome sequencing.
There are hints. The lethality of the 1890
bug was low among children and especially
high among people over 70. In addition to
causing respiratory illness, it sometimes at-
tacked the gastrointestinal tract or produced
blazing headaches and body aches, symp-
toms that Christakis calls less typical of in-
fluenza. He suggests that the 1890 event was
a pandemic of OC43, a coronavirus passed to
humans from some Russian cow. “After be-
ing among us for a century, this virus would
have further evolved to be a mild pathogen
that just causes the common cold today.”
Routine exposure to OC43 during childhood,
he posits, would give a person some ac-
quired immunity.
“It is still too early to know,” Christakis
writes, how the Covid-19 virus might mu-
tate. It is indeed early, and many more
books will offer to help us understand the
pandemic. But “Apollo’s Arrow” is a good
start. Another volume, a useful addition to
the same shelf, was published in 1859: “On
the Origin of Species.” Infectious disease is
all about evolution. If you don’t believe in
that, you may as well not hold your breath
for rescue by modern medicine. And there
will always be another virus going
around. 0Our Pandemic Future
CONTINUED FROM PAGE 1
DAVID QUAMMENis the author, most recently, of
“The Tangled Tree: A Radical New History of
Life.”
EDDIE GUY3-6-1-6-6-7-5-1-