COVID | Sileri: “Virus all’angolo, abbiamo quasi vinto la guerra”
“Ma non
si può indicare una data di fine. Noi arriveremo ad una buona
percentuale di popolazione vaccinata entro ottobre, ma poi dovremo fare i
richiami e verosimilmente nel 2022 si passerà dalla fase di pandemia a
quella di endemia”
COVID | Sileri: “Virus all’angolo, abbiamo quasi vinto la guerra”
Pierpaolo Sileri, sottosegretario alla Salute, è intervenuto su Radio
Cusano Campus e sulle prospettive legate alla pandemia ha detto: “La
mia visione deriva dalla lettura del panorama che sono davanti a noi con
la vaccinazione. Siamo con il virus messo all’angolo e abbiamo quasi
vinto completamente la guerra. Ovviamente come tutte le guerre non ci
può essere una data di fine certa. Difficilmente avremo l’esperienza di
mille morti al giorno come abbiamo avuto diversi mesi fa, avremo un
virus che continuerà a circolare e si trasformerà da pandemia a endemia.
Sarà un virus che continuerà a circolare tra noi senza creare grossi
danni a coloro che sono vaccinati. Potrebbe fare dei danni anche a
coloro che sono vaccinati se nel frattempo si sono presi un’altra
malattia e sono soggetti particolarmente fragili. Purtroppo avremo un
numero di persone che si infetteranno sempre, a meno che il virus non si
trasformi in un comune raffreddore. Ovviamente se sei vaccinato te la
caverai con poco, se non sei vaccinato, così come il virus influenzale,
può portarti a morte”.
“La mortalità del covid è di gran lunga superiore a quella
dell’influenza ma con la vaccinazione l’abbassi. Le vaccinazioni stanno
andando molto bene nei Paesi occidentali, ma non è lo stesso in Africa e
in Paesi molto popolosi come l’India. Il problema che può cambiare le
carte in tavola è la diffusione di un’ulteriore variante più contagiosa.
Noi arriveremo ad una buona percentuale di popolazione vaccinata entro
ottobre, ma poi dovremo fare i richiami e verosimilmente nel 2022 si
passerà dalla fase di pandemia a quella di endemia, ma questo deve
accadere anche nelle altre aree del mondo. Nelle zone del mondo più
indietro nella vaccinazione rimarrà la coda della pandemia e ci dovremo
sforzare per aiutare questi Paesi. Il giro di boa in Italia e in Europa è
stato fatto, vivremo il 2022 con degli aggiustamenti, magari con
richiami di vaccini più moderni aggiornati alle varianti che girano. Non
diciamo baggianate affermando che lotteremo ancora 5-10 anni contro il
covid”.
Sulla durata del vaccino. “La cosa che il vaccino dura 6-8 mesi non è
certa. Il vaccino lo conosciamo da 10 mesi e per ora gli anticorpi ci
sono ancora, verosimilmente dureranno 12-18 mesi, forse anche due anni,
lo scopriremo più avanti. Una quota della popolazione può avere una
riduzione degli anticorpi dopo 6 mesi, significa che in quelle persone
bisognerà fare un richiamo. E’ possibile che ogni anno si debba fare un
richiamo come per l’influenza”.
Sul vaccino ai giovani. “Il vaccino non è obbligatorio, ma il virus
circolerà con maggiore frequenza nei soggetti più giovani che potranno
ammalarsi anche gravemente, sebbene in casi rari, inoltre se in alcune
fasce di popolazione il virus circola liberamente si possono generare
delle varianti”.
Sui vaccinati con vaccini non autorizzati in Europa. “Credo che
debbano essere riconosciuti per il Green pass. Chi vive a San Marino e
ha fatto lo Sputnik non può non essere riconosciuto dal SSN. Mi sto
battendo per questo così come per la terza dose. Va organizzata la terza
dose per i pazienti immunodepressi e malati oncologici, così come
bisogna trovare una soluzione per i medici e infermieri che hanno fatto
per primi i vaccini e che a settembre vedranno scadere il proprio Green
pass”.
The Capital as Power working paper series showcases cutting edge
research on the political economy of capitalist power. The series is
open to a wide-range of issues: theoretical, empirical, historical or
contemporary. The aim is to stimulate debate and discussion on the
capital as power framework. If you are interested in submitting a
working paper, please email us and put “Working Papers” in the subject
line.
ABSTRACT We write this essay for both lay readers and scientists,
though mainstream economists are welcome to enjoy it too. Our subject is
the basic toolbox of mainstream economics. The most important tools in
this box are demand, supply and equilibrium. All mainstream economists –
as well as many heterodox ones – use these tools, … Read more
ABSTRACT Humanity’s most pressing need is to learn how to live within
our planet’s boundaries — something that likely means doing without
economic growth. How, then, can we create a non-growth society that is
both just and equitable? I attempt to address this question by looking
at an aspect of sustainability (and equity) that is … Read more
ABSTRACT FROM THE ARTICLE: According to the capital as power
framework, pecuniary earnings, or profits, are a symbolic representation
of the struggle for power between different capitalist groups. In this
struggle, capitalists measure their own power differentially – that is,
relative to other capitalist entities. The focus on differential power,
expressed in differential earnings, leads … Read more
ABSTRACT Until the late 2000s, our work focused primarily on why
capitalism should be understood as a mode of power. We argued that
capital itself is a form of organized power and researched how
capitalists sustain, defend and augment their capitalized power. We
called our approach ‘capital as power’ – or CasP, for short. But … Read more
ABSTRACT Neoclassical economists fundamentally misunderstand the role
of natural resources in the economy. I discuss here the source of this
misunderstanding, and the ways we can better understand the role of
energy to human societies. Download PDF | bnarchives
ABSTRACT A recent New Political Economy article by Baines and Hager
(2020) critiqued Shimshon Bichler and Jonathan Nitzan’s capital-as-power
(CasP) model of the stock market (Bichler & Nitzan, 2016). Bichler
and Nitzan’s model of the stock market seeks to explain how financial
crises are tied to the (upper) limits of redistributing income through
power. Bichler … Read more
ABSTRACT The French Revolution changed the world. In the new order,
the masters no longer need Monsieur Fouche and the thought police. They
don’t need guillotines to clip brains and scissors to censor pamphlets.
They don’t need strategic-studies institutes to manage oppression and
navigate conflict. Instead, they prefer to subsidize ‘cultural
pluralism’ and ‘critical studies’, … Read more
ABSTRACT This interview was commissioned in October 2019 for a
special issue on ‘Accumulation and Politics: Approaches and Concepts’ to
be published by the Revue de la régulation. We submitted the text in
March 2020, only to learn two months later that it won’t be published.
The problem, we were informed, wasn’t the content, which … Read more
Originally
published at dtcochrane.com DT Cochrane In Part 2, I looked at the
shifts in U.S. household consumption that occurred during WWII. While
aggregate consumption increased alongside massive government
intervention, …
Originally
published at dtcochrane.com DT Cochrane In Part 1, I explained the
motivation for this series. I want to use the analogy of WWII, as
invoked by economists JW Mason …
Originally
published at dtcochrane.com DT Cochrane Economist JW Mason recently
tweeted the following: Bloomberg writer Peter Coy was motived to perform
this research by an NYT op-ed from Mason and …
Breaking Out of Stagflation: Some Regional Comparisons
Nakhjavani, Mehran and Nitzan, Jonathan. (1995). Vol. 3. No. 9. January. pp. 7-8. (Article - Magazine; English).
Pharmaceuticals: Beating the Hell Out of the Average
Bichler, Shimshon and Nitzan, Jonathan. (2021). Research Note. June. pp. 1-5. (Article - Working Paper; English).
ABSTRACT
Today, human capital theory dominates the study of personal income. But
this has not always been so. In this essay, I chart the rise of human
capital theory, and …
ABSTRACT
The theory of capital as power (CasP) is radically different from
conventional political economy. In the conventional view, mainstream as
well as heterodox, capital is seen a ‘real’ economic …
ABSTRACT
This two-part paper details the arguments and evidence that have been
marshalled by both climate scientists and social scientists to critique
the current procedures and methodologies deployed by the …
Some
breakdown of U.S. drug cost, based on: Sood, Jeeraj, Tiffany Shih,
Karen Van Nuys, and Dana Goldman. 2017. The Flow of Money Through the
Pharmaceutical Distribution System. Los Angeles, …
Fascinating,
Jonathan. It still blows my mind that we allow chemical compounds to be
put under intellectual property. Imagine if Marie Curie had patented
the formula for Radium. Or worse …
According
to Kinch et. al., ownership of new molecular entities (NMEs) has grown
highly concentrated – in 2013, the top 10 pharmaceutical firms owned
more than 2/3rds of all NMEs, …
Ever
wondered what profit is good for? Lazonick et. al. show that, in
2006-2015, the 18 U.S. pharmaceutical firms in the S&P500 used 99%
of their net income to buy …
ABSTRACT
We write this essay for both lay readers and scientists, though
mainstream economists are welcome to enjoy it too. Our subject is the
basic toolbox of mainstream economics. The …
ABSTRACT
Humanity’s most pressing need is to learn how to live within our
planet’s boundaries — something that likely means doing without economic
growth. How, then, can we create a …
ABSTRACT
FROM THE ARTICLE: According to the capital as power framework,
pecuniary earnings, or profits, are a symbolic representation of the
struggle for power between different capitalist groups. In this …
From
Commodities to Assets Capital as Power and the Ontology of Finance
JESÚS SUASTE CHERIZOLA May 2021 Abstract Assets are a crucial concept of
the practice and mindset of the …
Mladen
Ostojić Abstract This paper maps an empirical history of corporate
profit and taxation in the United States, with a special focus on the
differential profit and taxation of banks …
Growing
Through Sabotage Energizing Hierarchical Power SHIMSHON BICHLER and
JONATHAN NITZAN June 2020 Abstract According to the theory of capital as
power, capitalism, like any other mode of power, is …
'A Power Theory of Personal Income Distribution', Public Lecture by Blair Fix
October 17, 2017
Due in no small part to the work of Thomas Piketty, the empirical
study of income inequality has flourished in the last decade. But this
plethora of new data has not led to a corresponding theoretical
revolution. Why? The problem, I believe, is an unwillingness to question
and test the basic assumptions on which current theory rests. Most
theories of personal income distribution are deeply wedded to the
assumption that income is proportional to productivity. However, this
approach has a simple, but little discussed problem: income is
distributed far more unequally than documented differentials in human
labor productivity. But if not productivity, then what explains income? I
propose that income is explained most strongly by social power, as
manifested by one’s rank in an institutional hierarchy. Using a novel
array of evidence, I show (for the first time) that there is a strong
quantitative relation between income and hierarchical power. Moreover, I
show that hierarchical power affects income more strongly than any
other factor. I conclude that this is evidence for a power theory of
personal income distribution.
Refreshment will be served and everyone is welcome.
WHERE: Verney Room, South 674 Ross Building, Keele Campus, York University
WHEN: 2:30 – 5:30 pm, Tuesday, 17 October 2017
More details can found here.
Illustrations by Laura Edelbacher; Animation by Patryk Senwicki
For
thousands of years, a parasite with no name lived happily among
horseshoe bats in southern China. The bats had evolved to the point that
they did not notice; they went about their nightly flights unbothered.
One day, the parasite—an ancestor of the coronavirus, SARS-CoV-2—had
an opportunity to expand its realm. Perhaps it was a pangolin, the
scaly anteater, an endangered species that is a victim of incessant
wildlife trafficking and sold, often secretly, in live-animal markets
throughout Southeast Asia and China. Or not. The genetic pathway remains
unclear. But to survive in a new species, whatever it was, the virus
had to mutate dramatically. It might even have taken a segment of a
different coronavirus strain that already inhabited its new host, and
morphed into a hybrid—a better, stronger version of itself, a pathogenic
Everyman capable of thriving in diverse species. More recently, the
coronavirus found a new species: ours. Perhaps a weary traveller rubbed
his eyes, or scratched his nose, or was anxiously, unconsciously, biting
his fingernails. One tiny, invisible blob of virus. One human face. And
here we are, battling a global pandemic.
The world’s confirmed cases (those with a positive lab test for COVID-19, the disease caused by SARS-CoV-2) doubled
in seven days, from nearly two hundred and thirteen thousand, on March
19th, to four hundred and sixty-seven thousand, on March 26th. Nearly
twenty-one thousand people have died. The United States now has more
confirmed cases than any country on earth, with more than eighty
thousand on March 26th. These numbers are a fraction of the real,
unknown total in this country and around the world, and the numbers will
keep going up. Scientists behind a new study, published earlier this month in the journal Science,
have found that for every confirmed case there are likely five to ten
more people in the community with an undetected infection. This will
likely remain the case. “The testing is not near adequate,” one of the
study’s authors, Jeffrey Shaman, an environmental-health sciences
professor at Columbia University, said. Comments from emergency-room
doctors have been circulating on social media like S.O.S. flares. One,
from Daniele Macchini, a doctor in Bergamo, north of Milan, described
the situation as a “tsunami that has overwhelmed us.”
Scientists
first discovered that coronaviruses originate among bats following the
outbreak of Severe Acute Respiratory Syndrome (SARS)
in 2003. Jonathan Epstein, an epidemiologist at the EcoHealth Alliance
in New York who studies zoonotic viruses—those that can jump from
animals to people—was part of a research team that went hunting for the
source in China’s Guangdong Province, where simultaneous SARS
outbreaks had occurred, suggesting multiple spillovers from animals to
people. At first, health officials believed palm civets, a mongoose-like
species commonly eaten in parts of China, were responsible, as they
were widely sold at markets connected to the SARS
outbreak, and tested positive for the virus. But civets bred elsewhere
in Guangdong had no antibodies for the virus, indicating that the market
animals were only an intermediary, highly infectious host. Epstein and
others suspected that bats, which are ubiquitous in the area’s rural,
agricultural hills, and were, at the time, also sold from cages at
Guangdong’s wet markets, might be the coronavirus’s natural reservoir.
The
researchers travelled through the countryside, setting up field labs
inside limestone caverns and taking swabs from dozens of bats through
the night. After months of investigation, Epstein’s team discovered four
species of horseshoe bats that carried coronaviruses similar to SARS,
one of which carried a coronavirus that was, genetically, a more than
ninety per cent match. “They were found in all of the locations where SARS clusters were happening,” he said.
After years of further bat surveillance, researchers eventually found the direct coronavirus antecedent to SARS,
as well as hundreds of other coronaviruses circulating among some of
the fourteen hundred bats species that live on six continents.
Coronaviruses, and other virus families, it turns out, have been
co-evolving with bats for the entire span of human civilization, and possibly much longer.
As the coronavirus family grows, different strains simultaneously
co-infect individual bats, turning their little bodies into virus
blenders, creating new strains of every sort, some more powerful than
others. This process happens without making bats sick—a phenomenon that
scientists have linked to bats’ singular ability, among mammals, to fly.
The feat takes a severe toll, such that their immune systems have
evolved a better way to repair cell damage and to fight off viruses
without provoking further inflammation. But when these viruses leap into
a new species—whether a pangolin or a civet or a human—the result can
be severe, sometimes deadly, sickness.
In
2013, Epstein’s main collaborator in China, Shi Zheng-Li, sequenced a
coronavirus found in bats, which, in January, she discovered shares
ninety-six per cent of its genome with SARS-CoV-2.
The two viruses have a common ancestor that dates back thirty to fifty
years, but the absence of a perfect match suggests that further mutation
took place in other bat colonies, and then in an intermediate host.
When forty-one severe cases of pneumonia were first announced in Wuhan,
in December, many of them were connected to a wet market with a
notorious wildlife section. Animals are stacked in cages—rabbits on top
of civets on top of ferret-badgers. “That’s just a gravitational
exchange of fecal matter and viruses,” Epstein said. Chinese authorities
reported that they tested animals at the market—all of which came back
negative—but they have not specified which animals they tested,
information that is crucial for Epstein’s detective work. Authorities
later found the virus in samples taken from the market’s tables and
gutters. But, because not all of the first patients were tied to the
market, nor were they connected to one another, Epstein said, “it raised
the question of, well, perhaps those forty-one weren’t the first
cases.”
Analyses of the SARS-CoV-2
genome indicate a single spillover event, meaning the virus jumped only
once from an animal to a person, which makes it likely that the virus
was circulating among people before December. Unless more information
about the animals at the Wuhan market is released, the transmission
chain may never be clear. There are, however, numerous possibilities. A
bat hunter or a wildlife trafficker might have brought the virus to the
market. Pangolins happen to carry a coronavirus, which they might have
picked up from bats years ago, and which is, in one crucial part of its
genome, virtually identical to SARS-CoV-2. But no
one has yet found evidence that pangolins were at the Wuhan market, or
even that venders there trafficked pangolins. “We’ve created
circumstances in our world somehow that allows for these viruses, which
would otherwise not be known to cause any problems, to get into human
populations,” Mark Denison, the director of pediatric infectious
diseases at Vanderbilt University Medical Center’s Institute for
Infection, Immunology, and Inflammation, told me. “And this one happened
to say, ‘I really like it here.’ ”
According
to researchers at Rocky Mountain Laboratories, some viral particles
remain viable up to four hours on copper, twenty-four hours on
cardboard, and seventy-two hours on plastic and stainless steel, though
the number of viable particles begins to decrease within minutes.
The
new coronavirus is an elusive killer. Since people have never seen this
strain before, there is much about it that remains a mystery. But, in
just the past few weeks, genetic sleuthing, atomic-level imaging,
computer modelling, and prior research on other types of coronaviruses,
including SARS and MERS
(Middle East Respiratory Syndrome), have helped researchers to quickly
learn an extraordinary amount—particularly what might treat or eradicate
it, through social-distancing measures, antiviral drugs, and,
eventually, a vaccine. Since January, nearly eight hundred papers about the virus have been posted
on BIORxiv, a preprint server for studies that have not yet been
peer-reviewed. More than a thousand coronavirus genome sequences, from
different cases around the world, have been shared in public databases.
“It’s insane,” Kristian Andersen, a professor in the Department of
Immunology and Microbiology at Scripps Research, told me. “Almost the
entire scientific field is focussed on this virus now. We’re talking
about a warlike situation.”
There are endless
viruses in our midst, made either of RNA or DNA. DNA viruses, which
exist in much greater abundance around the planet, are capable of
causing systemic diseases that are endemic, latent, and persistent—like
the herpes viruses (which includes chicken pox), hepatitis B, and the
papilloma viruses that cause cancer. “DNA viruses are the ones that live
with us and stay with us,” Denison said. “They’re lifelong.”
Retroviruses, like H.I.V., have RNA in their genomes but behave like DNA
viruses in the host. RNA viruses, on the other hand, have simpler
structures and mutate rapidly. “Viruses mutate quickly, and they can
retain advantageous traits,” Epstein told me. “A virus that’s more
promiscuous, more generalist, that can inhabit and propagate in lots of
other hosts ultimately has a better chance of surviving.” They also tend
to cause epidemics—such as measles, Ebola, Zika, and a raft of
respiratory infections, including influenza and coronaviruses. Paul
Turner, a Rachel Carson professor of ecology and evolutionary biology at
Yale University, told me, “They’re the ones that surprise us the most
and do the most damage.”
Scientists discovered the
coronavirus family in the nineteen-fifties, while peering through early
electron microscopes at samples taken from chickens suffering from
infectious bronchitis. The coronavirus’s RNA, its genetic code, is
swathed in three different kinds of proteins, one of which decorates the
virus’s surface with mushroom-like spikes, giving the virus the
eponymous appearance of a crown. Scientists found other coronaviruses
that caused disease in pigs and cows, and then, in the
mid-nineteen-sixties, two more that caused a common cold in people.
(Later, widespread screening identified two more human coronaviruses,
responsible for colds.) These four common-cold viruses might have come,
long ago, from animals, but they are now entirely human viruses,
responsible for fifteen to thirty per cent of the seasonal colds in a
given year. We are their natural reservoir, just as bats are the natural
reservoir for hundreds of other coronaviruses. But, since they did not
seem to cause severe disease, they were mostly ignored. In 2003, a
conference for nidovirales (the taxonomic order under which
coronaviruses fall) was nearly cancelled, due to lack of interest. Then SARS emerged, leaping from bats to civets to people. The conference sold out.
SARS
is closely related to the new virus we currently face. Whereas
common-cold coronaviruses tend to infect only the upper respiratory
tract (mainly the nose and throat), making them highly contagious, SARS
primarily infects the lower respiratory system (the lungs), and
therefore causes a much more lethal disease, with a fatality rate of
approximately ten per cent. (MERS, which emerged
in Saudi Arabia, in 2012, and was transmitted from bats to camels to
people, also caused severe disease in the lower respiratory system, with
a thirty-seven per cent fatality rate.) SARS-CoV-2
behaves like a monstrous mutant hybrid of all the human coronaviruses
that came before it. It can infect and replicate throughout our airways.
“That’s why it is so bad,” Stanley Perlman, a professor of microbiology
and immunology who has been studying coronaviruses for more than three
decades, told me. “It has the lower-respiratory severity of SARS and MERS coronaviruses, and the transmissibility of cold coronaviruses.”
One reason that SARS-CoV-2
may be so versatile, and therefore so successful, has to do with its
particular talent for binding and fusing with lung cells. All
coronaviruses use their spike proteins to gain entry to human cells,
through a complex, multistep process. First, if one imagines the spike’s
mushroom shape, the cap acts like a molecular key, fitting into our
cells’ locks. Scientists call these locks receptors. In SARS-CoV-2,
the cap binds perfectly to a receptor called the ACE-2, which can be
found in various parts of the human body, including the lungs and kidney
cells. Coronaviruses attack the respiratory system because their ACE-2
receptors are so accessible to the outside world. “The virus just hops
in,” Perlman told me, “whereas it’s not easy to get to the kidney.”
While the first SARS virus attached to the ACE-2 receptor, as well, SARS-CoV-2
binds to it ten times more efficiently, Kizzmekia Corbett, the
scientific lead of the coronavirus program at the National Institutes of
Health Vaccine Research Center, told me. “The binding is tighter, which
could potentially mean that the beginning of the infection process is
just more efficient.” SARS-CoV-2 also seems to have a unique ability, which SARS and MERS
did not have, to use enzymes from our human tissue—including one,
widely available in our bodies, named furin—to sever the spike protein’s
cap from its stem. Only then can the stem fuse the virus membrane and
the human-cell membrane together, allowing the virus to spit its RNA
into the cell. According to Lisa Gralinski, an assistant professor in
the Department of Epidemiology at the University of North Carolina at
Chapel Hill, this supercharged ability to bind to the ACE-2 receptor,
and to use human enzymes to activate fusion, “could aid a lot in the
transmissibility of this new virus and in seeding infections at a higher
level.”
Once a coronavirus enters a
person—lodging itself in the upper respiratory system and hijacking the
cell’s hardware—it rapidly replicates. When most RNA viruses replicate
themselves in a host, the process is quick and dirty, as they have no
proofreading mechanism. This can lead to frequent and random mutations.
“But the vast majority of those mutations just kill the virus
immediately,” Andersen told me. Unlike other RNA viruses, however,
coronaviruses do have some capacity to check for errors when
they replicate. “They have an enzyme that actually corrects mistakes,”
Denison told me.
It was Denison’s lab at
Vanderbilt that first confirmed, in experiments on live viruses, the
existence of this enzyme, which makes coronaviruses, in a sense, cunning
mutators. The viruses can remain stable in a host when there is no
selective pressure to change, but rapidly evolve when necessary. Each
time they leap into a new species, for example, they are able to hastily
transform in order to survive in the new environment, with its new
physiology and a new immune system to battle. Once the virus is
spreading easily within a species, though, its attitude is, “I’m happy,
I’m good, no need to change,” Denison said. That seems to be playing out
now in humans; as SARS-CoV-2 circles the globe,
there are slight variations among its strains, but none of them seem to
affect the virus’s behavior. “This is not a virus that is rapidly
adapting. It’s like the best car in the Indy 500. It’s out in front and
there is no obstacle in its path. So there is no benefit to changing
that car.”
The
coronavirus binds to host cells and fuses with the cell’s membrane,
releasing its viral genome and hijacking the cell’s machinery to
duplicate its RNA and create new viral proteins. The RNA and proteins
are packaged into new virus particles, which are excreted from the cell
to infect more cells.
A
virus replicates in order to shed from its host—through mucus, snot,
phlegm, and even our breath—as soon as possible, in great quantities, so
that it can keep spreading. The coronavirus happens to be a brilliant
shedder. A preprint study
by German researchers, published earlier this month, and one of the
first outside China to examine data from patients diagnosed with COVID-19,
found clear evidence that infected people shed the coronavirus at
significant rates before they develop symptoms. In effect—possibly due
to that supercharged ability to bind and fuse to our cells—the virus
wears an invisibility cloak. Scientists recently estimated that undocumented cases of COVID-19, or infected people with mild symptoms, are fifty-five per cent as contagious as severe cases. Another study found
that in more severe cases (requiring hospitalization), patients shed
the virus from their respiratory tracts for as long as thirty-seven
days.
Outside a host, in parasitical purgatory, a
virus is inert, not quite alive, but not dead, either. A hundred million
coronavirus particles could fit on the head of a pin—typically,
thousands or tens of thousands are necessary
to infect an animal or a person—and they might remain viable for long
stretches. Researchers at the Virus Ecology Unit of Rocky Mountain
Laboratories, in Montana, a facility connected to the National Institute
of Allergy and Infectious Diseases, have found that the virus can
linger on copper for four hours, on a piece of cardboard for twenty-four
hours, and on plastic or stainless steel for as long as three days.
They also found that the virus can survive, for three hours, floating
through the air, transmitted by the tiny respiratory droplets an
infected person exhales, sneezes, or coughs out. (Other research suggests the virus might be able to exist as an aerosol, but only in very limited conditions.) Most virus particles, though, seem to lose their virulency fairly quickly. The infection window is highest in the first ten minutes. Still, the risk of infection has turned many of us, understandably, into germophobes.
The
coronavirus enters the body through the mouth, eyes, and nose, then
makes its way to the lungs, where particles replicate. It is primarily
transmitted to others through coughing and sneezing.
All
a virus wants is an endless chain of hosts. Contagion is the
evolutionary end goal. Based on experiments so far, researchers estimate
that COVID-19 is slightly more communicable than
the common flu and less communicable than the most highly infectious
viruses, like measles, with which a single sick person can infect around
twelve other people. There are likely coronavirus
super-spreaders—people who, for whatever reason, are almost entirely
asymptomatic but transmit the disease to many other people. But pinning
down an exact infection rate, at this point, is an impossible task. “We
tend to focus on these absolute numbers as telling us how worried we
should be,” Denison said. “Look, it’s like flooding. You know, is it up
to my knees or is it up to my chin? It doesn’t matter. I need to do
something to try to make sure I’m not gonna drive my car into the
flood.”
In
many places, we already have driven into the flood. As hundreds of
people die each day, hospitals are running out of supplies, beds, and
ventilators. In these severe COVID-19 cases,
according to scientists’ current understanding, the disease may have
more to do with a haywire immune response to the virus than anything
else. Because the virus can gain a foothold in our lower respiratory
system while still wearing that invisibility cloak, it “basically beats
the immune system to the punch and starts replicating too rapidly,”
Perlman said. When the immune system finally does register its presence,
it might go into overdrive, and send everything in its arsenal to
attack, since it has no specific antibodies to fight these strange new
invaders. “It’s like pouring gas on the fire,” Denison told me. The lung
tissue swells and fills with fluid. Breathing is restricted, as is the
exchange of oxygen. “The host immune response just gets triggered to
such an extreme level, and then builds on itself and builds on itself
until ultimately the body kind of goes into shock,” Gralinski said. It
is almost like an autoimmune disease; the immune system is attacking
parts of the body that it should not.
This type of response might be why the elderly are, on the whole, more vulnerable to COVID-19, just as they were to the SARS
outbreak in 2003. (In that outbreak, there were almost no deaths among
children under the age of thirteen, and, when kids did get sick, the
disease was, on average, milder than what affected adults.) When
studying SARS in mice models, Denison told me
that he has observed a phenomenon known as “immune senescence,” in which
older mice no longer had the capacity to respond in a balanced way to a
new virus; their immune systems’ overreaction then caused even more
severe disease. This occurred in some of the worst cases during the
first SARS outbreak, too, Denison said, and
explains why antiviral drugs may be significantly more helpful at the
onset of illness, before the immune system has had a chance to wreak
havoc.
In
the last decade, Denison’s lab and collaborators at the University of
North Carolina have been researching antiviral treatments to try to find
something that worked not just against SARS and MERS
but for a new coronavirus which, they knew, would inevitably arrive.
Together, they did much of the early research into the drug now known as
Remdesivir, which is currently in development by Gilead and in studies
on infected patients, and another antiviral drug compound, known as NHC.
Both drugs, in animal models, were able to bypass, avoid, or block the
coronavirus’s proofreading function, which helped stop the virus from
replicating successfully in the body. “They worked very effectively
against all the coronaviruses that we’ve tested,” Denison told me.
Coronaviruses
likely have that proofreading enzyme because they are huge—one of the
largest RNA viruses in existence—and they need a mechanism that
maintains such a long genome’s structure. From our perspective, the
benefit of such a big genome, Andersen told me, “is that the more genes
and protein products a virus has, the more opportunities we have to
design specific treatments against them.” For instance, the virus’s
unique ability to use the human enzyme furin offers promise for
antiviral drugs that act as furin inhibitors.
COVID-19,
while still new to us hosts, will continue to be responsible for
widespread infection and death. But, Epstein said, “Over time, as
viruses evolve with their natural habitats, they tend to cause less
severe disease. And that is good for both the host and the virus.” The
more virulent strains might burn out (which, however, means many more
awful deaths), while the remaining hosts might build up some immunity.
More immediately, and urgently, the virus’s stability—how much it is
thriving among us right now, and mutating only minimally—bodes well for
the performance of antiviral drugs and, eventually, a vaccine. If the
growing number of mitigation measures—this unprecedented national and
international shutdown—are held in place for enough time, the speed at
which the virus is spreading should slow, giving hospitals and health
workers some relief. “The virus is our teacher,” Denison told me. It has
spent thousands of years evolving to get where it is. We’re now just
rushing to catch up.
A Guide to the Coronavirus
How to practice social distancing, from responding to a sick housemate to the pros and cons of ordering food.
