So maybe when you are asking for immediate blood thinners you ask for heparin. But I'm not medically trained so I know nothing.
So YOU WILL NEED TO ENSURE YOUR DOCTOR DOES THE FOLLOWING:
The autopsy findings caused a stir at many hospitals and influenced some doctors to start giving blood thinners to all covid-19 patients. It is now common practice.
Another takeaway is that the findings underscore the importance of getting people on supplementary oxygen quickly to prevent irreversible brain damage.
Common FDA-approved drug may effectively neutralize virus that causes COVID-19
Newswise: Infectious Diseases|July 15, 2020
A
common drug, already approved by the Food and Drug Administration
(FDA), may also be a powerful tool in fighting COVID-19, according to
research published this week in Antiviral Research.
SARS-CoV-2,
the virus that causes COVID-19, uses a surface spike protein to latch
onto human cells and initiate infection. But heparin, a blood thinner
also available in non-anticoagulant varieties, binds tightly with the
surface spike protein, potentially blocking the infection from
happening. This makes it a decoy, which might be introduced into the
body using a nasal spray or nebulizer and run interference to lower the
odds of infection. Similar decoy strategies have already shown promise
in curbing other viruses, including influenza A, Zika, and dengue.
“This
approach could be used as an early intervention to reduce the infection
among people who have tested positive, but aren’t yet suffering
symptoms. But we also see this as part of a larger antiviral strategy,”
said Robert Linhardt,
lead author and a professor of chemistry and chemical biology at
Rensselaer Polytechnic Institute. “Ultimately, we want a vaccine, but
there are many ways to combat a virus, and as we’ve seen with HIV, with
the right combination of therapies, we can control the disease until a
vaccine is found.”
To
infect a cell, a virus must first latch onto a specific target on the
cell surface, slice through the cell membrane, and insert its own
genetic instructions, hijacking the cellular machinery within to produce
replicas of the virus. But the virus could just as easily be persuaded
to lock onto a decoy molecule, provided that molecule offers the same
fit as the cellular target. Once bound to a decoy, the virus would be
neutralized, unable to infect a cell or free itself, and would
eventually degrade.
In humans, SARS-CoV-2
binds to an ACE2 receptor, and the researchers hypothesized that heparin
would offer an equally attractive target. In a binding assay, the
researchers found that heparin bound to the trimeric SARS-CoV-2 spike
protein at 73 picomoles, a measure of the interaction between the two
molecules.
“That’s exceptional, extremely tight binding,” said Jonathan Dordick,
a chemical and biological engineering professor at Rensselaer who is
collaborating with Linhardt to develop the decoy strategy. “It’s
hundreds of thousands of times tighter than a typical antibody antigen.
Once it binds, it’s not going to come off.”
Internationally recognized for his creation of synthetic heparin,
Linhardt said that, in reviewing sequencing data for SARS-CoV-2, the
team recognized certain motifs on the spike protein and strongly
suspected it would bind to heparin. In addition to the direct binding
assay, the team tested how strongly three heparin variants — including a
non-anticoagulant low molecular weight heparin — bind to SARS-CoV-2,
and used computational modeling to determine the specific sites where
the compounds bind to the virus. All the results confirm heparin as a
promising candidate for the decoy strategy. The researchers have
subsequently initiated work on assessments of antiviral activity and
cytotoxicity in mammalian cells.
“This isn’t
the only virus that we’re going to confront in a pandemic,” Dordick
said. “We don’t really have great antivirals, but this is a pathway
forward. We need to be in a position where we understand how things like
heparin and related compounds can block virus entry.”
In
previous work, a team led by Linhardt and Dordick demonstrated the
decoy strategy on viruses with a mechanism similar to SARS-CoV-2. In
2019, the team created a trap for dengue virus,
attaching specific aptamers — molecules the viral latches will bind to —
precisely to the tips and vertices of a five-pointed star made of
folded DNA. Floating in the bloodstream, the trap lights up when sprung,
creating the world’s most sensitive test for mosquito-borne diseases.
In work prior to that, they created a synthetic polymer configured to
match the sialic acid latch points on influenza virus, reducing influenza A mortality in mice from 100% to 25% over 14 days.
“This
innovative approach to effectively trapping virusus is a prime example
of how biotechnology approaches developed at Rensselaer are being
brought forward to address challenging global health problems,” said
Deepak Vashishth, the director of the Center for Biotechnology and
Interdisciplinary Studies at Rensselaer, of which both Dordick and
Linhardt are a part. “Professors Dordick and Linhardt have worked
collaboratively across disciplines, and their research shows promise
even beyond this current pandemic.”
“Characterization of glycosaminoglycan and novel coronavirus (SARS-CoV-2) spike glycoprotein binding interactions” was published in Antiviral Research.
At Rensselaer, Linhardt and Dordick were joined on the research by
Fuming Zhang, and also by researchers at the University of California
San Diego, Duke University, and the University of George, Athens with
support from the National Institutes of Health.
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