"The Covid-19 pandemic has been a
lesson in speed: the speed at which a novel virus among humans can spread; the
speed at which it can rack up fatalities and cripple economies; the speed at
which vaccines can be designed and produced; the speed at which misinformation
can undermine public health. Amid all that rapidity is a different kind of
speed, which drives the rest, like an engine spinning the cars on a nauseating
carnival ride: the speed of viral evolution.
The coronavirus, like many other
viruses of its ilk (RNA viruses with highly changeable genomes), evolves fast.
It has adapted quickly to us. Now arises the crucial question of whether humans
and human ingenuity can adapt faster.
Unless the answer is yes, we face a long, doleful future of
continued suffering. Some experts reckon the toll of endemic Covid might be somewhere
between 100,000 and 250,000 deaths every year, just in the United States.
Millions of lives depend on whether human science, human governance and human
wisdom can outpace the ingenuity of SARS-CoV-2, a relatively simple but
enterprising agent consisting of four structural proteins plus an RNA genome.
Charles Darwin said the mechanisms
of evolution never move quickly, but Darwin didn’t know about viruses. “That
natural selection will always act with extreme slowness, I fully admit,” he
wrote in “On the Origin of Species,” published in 1859. The first virus
ever discovered, tobacco mosaic virus, didn’t come to scientific attention
until decades later. As evolutionary theory developed from Darwin’s work and
throughout much of the 20th century, it drew mostly on evidence from fields
such as paleontology, biogeography, embryology and comparative anatomy —
visible patterns that can reveal slow changes over long stretches of time.
Those data are generally far less useful for measuring evolution when it
happens fast.
But we have a new form of evidence
for evolution: the sequencing and comparison of genomes. Whiz-bang machines do
the sequencing — reading out the genetic code, letter by letter — and powerful
computers help do the comparing, and it’s all much faster and cheaper than
ever.
Scientists can now track changes,
mutation by mutation, in the DNA or the RNA that encodes each creature’s
genetic instructions, watching and measuring as some of those mutations, the
few that just happen to be useful, spread through a population. They can
assemble a portrait-in-motion of even the fastest-evolving creatures, such as
bacteria and viruses. When the bacteria or viruses happen to be pathogens that
can infect humans, this discipline is called genomic epidemiology.
Among the pioneers of genomic
epidemiology is Sharon Peacock, professor of public health and microbiology at
the University of Cambridge as well as executive director of the Covid-19
Genomics UK Consortium. It’s a group of public health agencies and research
institutions founded in April 2020 to sequence and analyze genomes of the new
coronavirus. At this point, the contribution by labs in Britain accounts for
almost 2.8 million of the globally reported SARS-CoV-2 sequences, about 23
percent of the world’s total.
Dr. Peacock, and those who helped
her establish and fund this effort, recognized early that genomic information
could be crucial to the pandemic response. But just gathering sequences and
making them available to other scientists is not enough. That’s genomics
without epidemiology — the application of population-level knowledge to public
health.
“If you’re talking about speed,” Dr.
Peacock told me recently, “the key thing is to think of the whole pipeline from
start to finish.” What she meant by “pipeline” is a chain of physical steps
(such as sampling a patient), laboratory processes (such as extracting viral
genetic material and sequencing that virus’s genome) and analysis (interpreting
the differences between one genome and another). They yield insights that can
inform both clinical treatment of individuals and protection of the populace.
Hardware tools are important to such
work. Software is also crucial. During the first year of the Covid-19 pandemic,
a young graduate student named Áine O’Toole, along with other members of Andrew
Rambaut’s lab at the University of Edinburgh, developed a tool called PANGOLIN
(Phylogenetic Assignment of Named Global Outbreak Lineages). It became one of
the go-to systems for placing new genomes on the SARS-CoV-2 family tree,
assigning them rational if unmemorable labels (such as B.1.1.7), and
contextualizing new variants of the virus when they emerged.
It was Dr. Rambaut, Dr. O’Toole and
their lab colleagues who helped spot and track the first major variant, now
called Alpha, when it appeared in southeastern England, moving toward London,
in autumn of 2020. One year later, scientists in South Africa and Botswana,
sequencing samples from travelers, detected another rising variant, named
Omicron.
Such quick detection of variants is
enormously valuable, but only if the data are transformed promptly into clear,
actionable guidance. “We still have the important gaps in getting it into the
clinic,” Dr. Peacock said. These gaps include making it easy for public health
and medical personnel not trained in sequencing to use the data and the
willingness of health care providers like hospitals to finance such work. “At the
moment, the majority of sequencing beyond Covid-19 is funded by public health
agencies and research funding,” Dr. Peacock said.
That hasn’t changed since 2014, when
Pardis Sabeti, a computational geneticist at Harvard University, led a team of
genomic scientists responding to the horrific Ebola virus outbreak in West
Africa. They sequenced 99 genomes of the virus, sampled from patients at a
hospital in Sierra Leone. Comparing sequences revealed that all those cases
most likely resulted from human-to-human transmission, rather than from
spillovers from a wildlife host.
The West Africa outbreak ended after
more than 28,000 Ebola cases and 11,000 deaths, by which point genomic
epidemiology had proved its value by revealing how the virus was spreading.
With Covid-19, there have been 589 million known cases and
more than six million deaths so far.
The new discipline is scarcely able
to keep up, let alone get ahead of the virus. Sarah Cobey, an evolutionary
biologist at the University of Chicago who works at the juncture of immunology,
viral evolution and epidemiology, sees “gaping holes” in the genetic
surveillance of Covid-19.
“Even though we do have lots and
lots of sequences, they are disproportionally from a few locations,” Dr. Cobey
told me. During the first year of the pandemic, Britain, New Zealand, Australia
and Iceland were among the countries that sequenced a high share of
cases. The Netherlands and the Democratic Republic of Congo were also notable
for prompt sequencing. As the pandemic progressed, scientists in South Africa
mounted an important sequencing effort (as reflected in the detection first of
the Beta variant, then of the Omicron), and coverage improved also in Canada
and Scandinavia. Other parts of the world remain “blind spots,” Dr. Cobey said.
The sad but not surprising fact is
that high-income countries sequenced 16 times more coronavirus genomes as a
proportion of cases than low- and middle-income countries. Money is a limiting
factor, but not just money. “I think the fundamental problem is really lack of
scientific leadership to coordinate this kind of data gathering,” Dr. Cobey
said. Few countries have had their Sharon Peacock, or political leadership to
heed and support the scientific leaders.
The world needs that leadership,
broadening and paying for sequencing surveillance of this coronavirus and its
changes, everywhere the virus goes. But we need much more, as Dr. Cobey and Dr.
Peacock and other scientists warn.
We need ambitious seroprevalence
studies (screening of blood samples for evidence of past infection) that will
help scientists learn how many undetected infections have occurred.
What’s the real case total in each country and around the world? We need
farsighted and well-funded research on vaccine platforms that can be quickly
adapted for use against whole classes of newly emerged pathogens, not just
hurried efforts to create a booster for the latest variant.
We need a universal coronavirus vaccine and a universal
influenza vaccine, although neither — given the formidable capacity of those
viruses to evolve — may be achievable.
More simply, we need
temperature-stable and needle-free vaccines that can reduce the problems of
vaccine refusal in high-income countries and vaccine unavailability in
low-income countries that are hot. We need better antiviral drugs, even for
rare but dangerous viruses (such as Nipah virus), entailing development efforts
that may never be profitable for pharmaceutical companies.
Even more simply, as Dr. Cobey noted, we need investments
toward much better ventilation and air filtration in our public buildings,
reducing the spread of the coronavirus and other airborne pathogens. That’s not
scientifically exciting, she conceded; it’s just important and cost-effective.
The evolutionary journey of this
coronavirus has been grim and awesome. Arguably, the measured transformations
of SARS-CoV-2 over the past 31 months, from the original strain to the
subvariants of Omicron, provide one of most precise pictures of swift evolution
at a global scale in the wild. In the wild: that is, not in beakers and
flasks, not in laboratories, but in us. Evolution deniers, take note.
All of us should take note. We have
12 million snapshots of this thing in motion — which is enough, at the standard
cinema projection rate of 24 frames per second, to make a movie of SARS-CoV-2
evolution 138 hours long.
But because evolutionary biology is a descriptive science,
not a predictive one, we still don’t know how the story might end. Probably it
doesn’t end at all. And the genomic epidemiologists, as smart as they are,
can’t save us from what’s still coming. We have to save ourselves.
David Quammen is a science writer.
His forthcoming book, “Breathless: The Scientific Race to Defeat a Deadly
Virus,” will be published in October.”
1 percent of sick are dying from Covid in the world.
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