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COM
C E L E B R AT I N G
YEARS
INSIDE THE
CORONAVIRUS
Everything we know
so far about
the cause of
COVID-19
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THE
The newest coronavirus, SARS-CoV-2, has
created a far deadlier pandemic in part be
cause once it infects a person it can lie unde-
tected for a long time. An individual who had
CORONAVIRUS
the SARS coronavirus did not transmit it until
24 to 36 hours after displaying symptoms such
as fever and dry cough; people feeling ill could
be isolated before they made others sick. But
people with COVID-19 can transmit the virus
INNER WORKINGS
ly because its genome produces proteins that
delay our immune system from sounding an
alarm. Meanwhile lung cells die as the virus
F
might still be able to overcome the intruders.
As virologists learn more, we will update
or all the mysteries that remain these graphics on our Web site (www.
scientificamerican.com). Greater knowledge
about the novel coronavirus and the
can raise the chances for humans to prevail.
COVID-19 disease it causes, scientists
have generated an incredible amount
of fine-grained knowledge in a sur- Gene Machine
prisingly short time. A SARS-CoV-2 virus particle wafting into a person’s nose
or mouth is about 100 nanometers in diameter—visible
Thousands of different coronaviruses may inhabit the plan- only with an electron microscope. It is a near sphere of
et. Four of them are responsible for many of our common colds. protein (cross section shown) inside a fatty membrane that
Two others have already triggered alarming outbreaks of disease: protects a twisting strand of RNA—a molecule that holds
in 2002 a coronavirus caused severe acute respiratory syndrome the virus’s genetic code. Proteins called “S” form spikes
that extend from the surface and grab onto a human cell,
(SARS), which killed more than 770 people worldwide, and in
hundreds of times larger, so the particle, or virion, can slip
2012 a different strain started Middle East respiratory syndrome inside; the crown, or corona, appearance gives the virus its
(MERS), taking more than 800 lives. SARS burned out within name. Structural proteins—N, M and E—move inside the
a year; MERS still lingers. cell, where they help new virions form.
32 Scientific American, July 2020 SOURCE: LORENZO CASALINO, ZIED GAIEB AND ROMMIE AMARO, U.C. SAN DIEGO (s pike model with glycosylations)
RNA
(red)
E protein
(yellow)
M protein
(purple)
Lipid
membrane
S proteins,
spike (orange)
Stem
Protease
Spike enzyme cuts
off top of spike
ACE2
receptor
protein Lung cell
Golgi
2 SLIP INSIDE complex
The virus and lung-cell membranes fuse, allowing the virus’s RNA—a molecule that
encodes the genome (genetic instructions)—to pour into the cell’s body. Additional vesicles
(that come from
Spike decapitation allows the The machinery inserts itself the endoplasmic
fusion machinery to unfold. into the cell membrane ... reticulum and
Golgi complex)
Membranes assemble spike,
M and E proteins
Fusion
machinery
4 BREAK OUT
Vesicles carrying newly formed viruses merge with
the cell membrane, opening a channel that allows
… and pinches the membranes together. the viruses to exit. One cell can release hundreds of
virus copies. It typically dies because its resources
have been used up, or it is killed by the immune
system. Some viruses head off to infect more
Virus particle N protein cells. Others are exhaled into the air.
5 IMMUNE SYSTEM DEFENSE MEASURES ADAPTIVE IMMUNE SYSTEM: Interferon also alerts
When infection begins, the innate immune system tries B cells. They produce “neutralizing antibodies” that
to immediately protect lung cells. The adaptive immune might recognize parts of the spike protein and bind to
system gears up for a greater response. it A , preventing the spike from grabbing onto a lung
cell. Interferon also recruits T cells, which can destroy
INNATE IMMUNE SYSTEM: An infected cell releases interferon proteins viruses and also kill infected cells before viruses inside
that alert neighboring cells to create molecules that try to stop virus them burst out B . Some B and T cells become
Lung cell
particles from entering or reproducing. Interferon also beckons cells such as memory cells that can quickly identify and fight a
macrophages in the bloodstream that can engulf virus particles. future invasion by the virus.
A
Interferon Virus
particle
Antibody
Ribosomes create
polymerase B cell
Interferon
proteins that copy
the virus genome Virus particle Infected cell
Macrophage B
T cell
N proteins link to
RNA to help keep
it stable
Infected cell
Antibody Interferon
SARS-CoV-2
Glycan Lung cell proteins
(sugar chains)
Messenger RNA
Spike Nucleus
36
36 Scientifi
Scientificc American,
American, July
July 2020
2020
PROOFREADING
PROOFREADING
Because
The CoV-2the SARS-CoV-2
virus genome
is about 30,000 is so long,
base-pairs it can
long, nearencode a huge
the limit amount
for an of information,
RNA virus (influenza enabling the novelBecause
is about 14,000). coronavirus
it is sotolarge,
createmutations
many more proteins
couldand
occur perhaps
duringcarry out more
replication, sophisticated
if the replication
viral copying machinestrategies than other
couldn’t correct RNA viruses.
its occasional One of these
errors—and most of
Antibodies advantageous
the proteins
mutations would killisthe
anvirion.
enzyme called
This typeexonuclease (ExoN),orwhich
of quality control, helps the isvirus
proofreading, proofread
common in ourand
owncorrect copies
cells and as they
in DNA are
viruses,
that disable made.
but Only
highly virusesinwith
unusual RNAgenomes
viruses. longer than about 20,000 bases make this enzyme.
virus
Genome5,000
Genome length: length: 5,000 bases10,000 10,000
bases 15,00015,000 20,000
20,000 25,000
25,000 30,000
30,000
Influenza
Rhinovirus
Other virus example tk
HIV
SARS-CoV-2
Zika Question for BG
Influenza Viruses with genomes longer than ~19,000 base pairs (including CoV-1), include RNA from JC: This
B cell instructions for an Exonuclease protein (coded for in the non-structural portion of the genome. ExoN mutation
Ebola chart from your
This protein may help with proofreading. Lorem itpsum text teekay. Lore ipsum.
SARS-CoV-2 lecture is older,
and based on
Killer T cell Mutations occur broader SARS
more
Onceoften when
a SARS-CoV-2 virus has SARS-CoV-2 Polymerase research. Can
theinfected
exonuclease
a lung cell, an enzyme genome and ExoN you provide any
is blocked. Lorem starts to make Genome that is proofread
called polymerase enzymes more recent
ipsum textofteekay
copies its RNA while another CoV-2 specific
lorem ipsumExoN,
enzyme, text finds random references on the
teekay loremand expels these
mutations topic of ExoN and/
genetic mistakes from the copies. Genome that is not proofread or proofreading?
RNA copy Incorrect
gene pieces
Infected ACCESSORY GENES removed ErrorsQuestion for BG
lung cell from JC: Can you
These are an important part of the virus, yet we don’t understand much about them yet.
SOURCE: “THE ARCHITECTURE OF SARS-COV-2 TRANSCRIPTOME,” BY DONGWAN KIM ET AL., IN CELL, VOL 181, MAY 14, 2020 (genome)
please provide
SARS-C0V-2 genome (about 30,000 bases long) the best, most
ACCESSORY GENES RNA instructions for structural and accessory proteins up-to -date
reference for a
Unusual, RNA
shortinstructions
bits of the genome called accessory
for non-structural genes
proteins are clustered
(polymerase, etc)with the structural protein genes. Researchers are not yet genome
sure what they do. Several are thought to encode proteins that help the virus evade the immuneSsystem.protein EM N breakdown, like
this one?
SARS-CoV-2 genome (about 29,900 bases long)
RNA instructions for structural and accessory proteins
Accessory genes
RNA instructions for nonstructural proteins
(including
Include a few polymerase
annotationsand
hereexonuclease)
with leader Include a few annotations S protein E M N
Include a few annotations here
lines to accessory genes, highlighting which here with leader lines to with leader lines to accessory
Antigen-present- are thought to be involved in immune accessory genes, lorem genes, lorem ipsum text teekay
ing cell starts manipulation/escape and/or cell death ipsum text teekay lorem lorem ipsum text teekay
immune response Accessory genes
MORE TO EXPLORE
July
July 2020,
2020, ScientificAmerican.com 37
ScientificAmerican.com 37
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PSYCHOLOGICAL
EXPERIMENT
WHAT CAN
THE PANDEMIC
TEACH US ABOUT
HOW PEOPLE
RESPOND TO
ADVERSITY?
By Lydia Denworth
Photographs by Ethan Hill
disruptions and the sheer numbers develop skills for dealing with stress, and many have
retired and so are less likely to be concerned about work.
involved have experts warning Fancourt began a study in mid-March that grew to