From xxxxxx <[email protected]>
Subject Genes May Leave Some People More Vulnerable to Severe Covid-19
Date June 8, 2020 6:50 AM
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[Geneticists have turned up intriguing links between DNA and the
disease. Patients with Type A blood, for example, seem to be at
greater risk.] [[link removed]]

GENES MAY LEAVE SOME PEOPLE MORE VULNERABLE TO SEVERE COVID-19  
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Carl Zimmer
June 3, 2020
New York Times
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_ Geneticists have turned up intriguing links between DNA and the
disease. Patients with Type A blood, for example, seem to be at
greater risk. _

A transmission electron microscope image of a U.S. case of
coronavirus., CDC, via Science Source

 

Why do some people infected with the coronavirus suffer only mild
symptoms, while others become deathly ill?

Geneticists have been scouring our DNA for clues. Now, a study by
European scientists is the first to document a strong statistical link
between genetic variations and Covid-19
[[link removed]], the
illness caused by the coronavirus.

Variations at two spots in the human genome are associated with an
increased risk of respiratory failure in patients with Covid-19, the
researchers found. One of these spots includes the gene that
determines blood types.

Having Type A blood was linked to a 50 percent increase in the
likelihood that a patient would need to get oxygen or to go on a
ventilator, according to the new study.

The study was equally striking for the genes that failed to turn up.
The coronavirus attaches to a protein called ACE2 on the surface of
human cells in order to enter them, for example. But genetic variants
in ACE2 did not appear to make a difference in the risk of severe
Covid-19.

The findings suggest that relatively unexplored factors may be playing
a large role who develops life-threatening Covid-19. “There are new
kids on the block now,” said Andre Franke, a molecular geneticist at
the University of Kiel in Germany and a co-author of the new study,
which is currently going through peer review.

Scientists have already determined that factors like age and
underlying disease put people at extra risk of developing a severe
case of Covid-19. But geneticists are hoping that a DNA test might
help identify patients who will need aggressive treatment.

Figuring out the reason that certain genes may raise the odds of
severe disease could also lead to new targets for drug designers.

As the pandemic gained momentum in February, Dr. Franke and his
colleagues set up a collaboration with doctors in Spain and Italy who
were struggling with a rising wave of Covid-19.

The doctors took blood samples from 1,610 patients who needed an
oxygen supply or had to go on a ventilator. Dr. Franke and his
colleagues extracted DNA from the samples and scanned it using a rapid
technique called genotyping.

The researchers did not sequence all three billion genetic letters in
the genome of each patient. Instead, they looked at nine million
letters. Then the researchers carried out the same genetic survey on
2,205 blood donors with no evidence of Covid-19.

The scientists were looking for spots in the genome, called loci,
where an unusually high number of the severely ill patients shared the
same variants, compared with those who were not ill.

Two loci turned up. In one of these sites is the gene that determines
our blood type. That gene directs production of a protein that places
molecules on the surface of blood cells.

It’s not the first time Type A blood has turned up as a possible
risk. Chinese scientists who examined patient blood types also found
that those with Type A were more likely to develop a serious case of
Covid-19.

No one knows why. While Dr. Franke was comforted by the support from
the Chinese study, he could only speculate how blood types might
affect the disease. “That is haunting me, quite honestly,” he
said.

He also noted that the locus where the blood-type gene is situated
also contains a stretch of DNA that acts as an on-off switch for a
gene producing a protein that triggers strong immune responses.

The coronavirus triggers an overreaction of the immune system in some
people, leading to massive inflammation and lung damage — the
so-called cytokine storm. It is theoretically possible that genetic
variations influence that response.

A second locus, on Chromosome 3, shows an even stronger link to
Covid-19, Dr. Franke and his colleagues found. But that spot is home
to six genes, and it is not yet possible to say which of them
influences the course of Covid-19.

One of those gene candidates encodes a protein known to interact with
ACE2, the cellular receptor needed by the coronavirus to enter host
cells. But another gene nearby encodes a potent immune-signaling
molecule. It is possible that this immune gene also triggers an
overreaction that leads to respiratory failure.

Dr. Franke and his colleagues are part of an international effort
called the Covid-19 Host Genetics Initiative
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A thousand researchers in 46 countries are collecting DNA samples from
people with the disease. They are now beginning to post data on the
initiative’s website.

Andrea Ganna, a genetic epidemiologist at the University of Helsinki,
said that initiative’s collected data were beginning to point to a
single spot on Chromosome 3 as a potentially important player.

It’s not common for genetic variants to emerge out of studies of so
few people, said Jonathan Sebat, a geneticist at the University of
California, San Diego, who was not involved in the new study.

“We were all hoping optimistically this was one of those
situations,” Dr. Sebat said.

Previous attempts to find any genetic loci that varied significantly
between sick people and healthy ones have failed. Dr. Sebat speculated
that the new study succeeded because the researchers focused only on
people who had respiratory failure and were clearly vulnerable to
serious forms of Covid-19.

“They had the ideal cohort,” he said.

New studies, such as the one Dr. Sebat is running in California, will
allow scientists to see if the two loci really do matter as much as
they seem to now.

The geneticists may be able to zero in on exactly which gene in each
locus affects the disease, he said. And researchers will most likely
find many other genes with subtler influences on the course of
Covid-19.

Carl Zimmer reports from the frontiers of biology, where scientists
are expanding our understanding of life.

He began writing about science for the _New York Times_ in 2004,
where he now writes his weekly column “Matter.” 
[[link removed]] Zimmer
has won many awards for his work, including the Stephen Jay Gould
Prize
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awarded by the Society for the Study of Evolution to recognize
individuals whose sustained efforts have advanced public understanding
of evolutionary science.

Zimmer is the author of thirteen books about science. His latest
is _She Has Her Mother’s Laugh: The Power, Perversions, and
Potential of Heredity_
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Zimmer started his journalism career at _Discover,_ where he went on
to serve for five years as a senior editor. In addition to his work
for the _New York Times_, he has written for magazines
including _National Geographic, Wired,_ and _The Atlantic._ In
2003, Zimmer also launched “The Loom,” an award-winning blog which
has been hosted by _Discover_ and _National Geographic_. In 2015,
Zimmer became a contributing national correspondent for STAT
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health and medicine, where he hosted “Science Happens,”
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video series that was a finalist for a National Magazine Award. In
2019, Zimmer created “What Is Life?” 
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eight-episode series of live conversations with leading thinkers about
why life exists, how it began, and other big questions about
existence. He is now working on a book on the subject, to be published
in 2021.

Zimmer is also the author of two widely praised textbooks. _The
Tangled Bank: An Introduction to Evolution_ 
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the first textbook about evolution ever published intended for
non-majors. _Choice _named it an academic title of the year. Zimmer
also co-authored _Evolution: Making Sense of Life_
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textbook for biology majors, with University Montana biologist Doug
Emlen. The third edition of the book was published in 2019.

He is, to his knowledge, the only writer after whom a species of
tapeworm has been named.
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