Griffithsin
vs Coronaviruses
On the 18th of March 2021, there are 120,915,219
confirmed cases of SARS-CoV-2 with 2,674,078
confirmed deaths reported (WHO)
UPDATE: As of the 22nd of November 2021, there are now 258,172,735 confirmed cases of SARS-CoV-2 and 5,158,642 confirmed deaths recorded (Johns Hopkins Coronavirus Resource Center)
Please note that SARS is an acronym for severe acute
respiratory syndrome.
The SARS-CoV-2 viral infection may cause extreme damage
to the respiratory system but also affects other organs of the body.
Coronaviruses are single stranded RNA viruses. They are enveloped viruses. The RNA is enclosed inside a protective
spherical coat of protein. These relatively
large virions (virus particles) and have around 74 mushroom shaped protrusions,
the spikes. This gives the virion a look
that some say resembles a crown, which is the origin of the name coronavirus. Some
of the glycoproteins are structural, such as the famous spike protein, and others
are glycosylated non-structural proteins.
These envelope and spike glycoproteins play a role in the infection of
cells by attaching to a host cell and acting as a doorway for endocytosis or
the taking in of the now naked RNA by the receptors of the cell (the envelope
does not enter the cell). Once inside the host cell, in the cytoplasm, the RNA can
instruct the ribosomes to replicate more of the virus.
Remembering that GRFT is a lectin, with the ability to
bind carbohydrates, we can now start to see how the antiviral action of GRFT is
to attach to the glycoproteins, such as the spike protein and block the viral
entry into the host cell.
3 deadly coronaviruses,
SARS, MERS, and Covid-19
SARS coronavirus first appeared in humans in 2002 with 8096
reported cases.
MERS (Middle East respiratory syndrome) had an outbreak
in 2012 with 2260 reported cases.
Covid-19 first appeared in 2019
SARS and MERS show a higher percentage of fatalities
than Covid-19 with MERS being the most deadly.
Covid-19 is more easily transmissible than SARS or
MERS.
SARS, MERS and Covid-19 were infecting animals,
probably bats, at first and then zoonotic transmission occurred, the jump from
animal to human. Besides bats, with
MERS, camels were a reservoir of the virus and humans were infected from camels
(Please don’t touch a sick camel, or at least wash your hands after).
Once a coronavirus made the jump, human to human
transmission spread it quickly.
Is it
probable that GRFT can prevent infection by coronaviruses?
We had been doing research related to Griffithsin for a
few years and in March 2020 when the covid-19 pandemic was sweeping across the
world, we searched through our library of papers and found one, published in
the March 2010 issue of Journal of Virology:
Broad-Spectrum In
Vitro Activity and In Vivo Efficacy of the Antiviral Protein Griffithsin against
Emerging Viruses of the Family Coronaviridae. (O'Keefe BR,
Giomarelli B, Barnard DL, Shenoy SR, Chan PK, McMahon JB, Palmer KE, Barnett
BW, Meyerholz DK, Wohlford-Lenane CL, McCray PB Jr. Broad-spectrum in vitro
activity and in vivo efficacy of the antiviral protein griffithsin against
emerging viruses of the family Coronaviridae. J Virol. 2010 Mar;84(5):2511-21.
doi: 10.1128/JVI.02322-09. Epub 2009 Dec 23. Erratum in: J Virol. 2010
May;84(10):5456. PMID: 20032190; PMCID: PMC2820936)
This excellent paper shows the results of many
experiments. 4 strains of SARS were
tested individually in vitro and griffithsin showed remarkable antiviral
action, preventing the viral cytopathic cell death from the viral infection. GRFT bound to the Coronavirus spike protein.
Experiments were also successfully performed on other coronaviruses that don’t
infect humans but are found in animals. GRFT was also shown to be of very low toxicity
to the host cells.
In vivo experiments were performed on mouse models using a
mouse-adapted SARS virus.
Control groups of mice got nothing at all (sham) or only GRFT
(control) but the important groups observed were the mice getting SARS virus
alone and the group getting both SARS and doses of GRFT. The griffithsin was applied into the tiny
mouse nostrils, because that is a good place to administer it when the virus
attacks the respiratory system. Picture
for a moment, scientists in lab coats pipetting into mouse nostrils! This may have caused the mice some discomfort
but it also saved them from dying from SARS.
The mouse group that got only the virus sickened, losing weight, and
then 70% of the group died, while 30% recovered.
The group of lab mice that got the SARS virus and also doses
of GRFT up their tiny noses didn’t lose weight and had 100% survival.
Important points made that stand out:
“Due to the proven threat from
SARS-CoV infections and the possibility of
future zoonotic
transmission of coronaviruses, efforts have
been initiated to
identify agents that could either reduce
infection or suppress
the deleterious cytokine response to SARS-CoV
infection”
“The broad range of Coronaviridae species
sensitive to GRFT is a significant attribute for this antiviral protein, as
this group of viruses appears to be capable of continuing zoonotic evolution
and transfer to human hosts”
10 years later, a novel Coronavirus made the
leap from animal to human hosts, there was an outbreak, and the world was
unprepared to stop it. As we all know it became a raging global pandemic.
In 2016, an article was published in the
journal Antiviral Research about in vitro studies done using GRFT to stop MERS
from infecting cells:
Middle East respiratory
syndrome coronavirus infection is inhibited by griffithsin.
Jean
K. Millet, Karin Seron, Rachael N. Labitt, Adeline Danneels, Kenneth E. Palmer,
Gary R. Whittaker, Jean Dubuisson, Sandrine Belouzard
Again, GRFT was shown to bind to the spike
protein and prevent infection, this time by the MERS coronavirus.
Again, scientists urged more development of
griffithsin:
“In conclusion, griffithsin has a low
cytotoxicity, likely interacts with any coronavirus spike proteins because of
their highly glycosylated nature and is able to hamper coronavirus spike
protein functions. Griffithsin should be considered as an interesting drug
candidate to develop for the treatment and/or prevention of current but also
future emerging coronavirus infections.”
3 years later, in Wuhan, China, a novel
coronavirus started infecting humans and as humans we were unprepared and
defenseless.
In a 2020 letter to the editor of Virilogica
Sinica, we find confirmation that the entry inhibiting antiviral GRFT also
works on the SARS Cov-2
Griffithsin
with A Broad-Spectrum Antiviral Activity by Binding Glycans in Viral
Glycoprotein Exhibits Strong Synergistic Effect in Combination with A
Pan-Coronavirus Fusion Inhibitor Targeting SARS-CoV-2 Spike S2 Subunit
Yanxing Cai, Wei Xu, Chenjian Gu, Xia Cai, Di
Qu, Lu Lu, Youhua Xie & Shibo Jiang
One interesting development reported in this
letter regards the pan-coronavirus fusion inhibitor targeting the HR1 domain of
human coronavirus spike, EK1 working synergistically with GRFT.
We could easily see from the research that has
been done that GRFT has the potential to prevent a coronavirus outbreak from
becoming a pandemic. It may be too late
to do anything about the present one that we are facing. Vaccines have been developed, tested, produced
and deployed in one year which is a huge accomplishment. It’s
not a matter of if but a matter of when the next coronavirus makes the leap
from animal to human. We were not
prepared for the covid-19 onslaught. A
small but dedicated group of scientists and biohackers, decided to start to prepare
for the next outbreak without delay.
To be continued….
