COVID Origin: More on Munster’s NIAID lab in Hamilton, Montana, far from the eyes of the oversight committees, doing GoF research and producing false narratives. Killing 2 birds with one taxpayer stone. Why does NIH have a lab in Montana anyway?
This post is a continuation of the article by Will Jones posted recently about the origin of COVID, adding my own spin.
From
Vincent Munster’s lab page (NIAID Hamilton Montana) we find the following. It
indicates that his entire career has been spent promoting the lie that
pandemics arise from animal spillover (when this is a very rare event
and not something we need to spend hundreds of billions to guard against
when nothing works, anyway). He seems to have trained with top covid
origin coverup stars Marion Koopmans and Ron Fouchier at Erasmus
University, Rotterdam. Both were on the 2/1/2020 Fauci call, Koopmans was on the
WHO investigation trip to China that said covid came from frozen food,
and Fouchier was responsible for very dangerous GOF work making bird flu transmissible by air, and for giving Fauci 6 ways to try to explain away the manmade findings in the covid genome.
I
think that Will Jones is right: COVID likely was built in Munster’s
lab. However, I have always suspected (and said so) that there were so
many different bad epitopes stitched into the SARS-CoV-2 genome, it
likely was developed from parts created in a variety of different labs.
Who put all the pieces together to give it high infectivity, broadened
tissue tropism, a means to damp down the immune response (or several)
and the means to invoke a massive late inflammatory response? Where was
it passaged through humanized mice? Is the scientist who performed the
last step the only one who is guilty? Why were all these different
virulence factors concocted in the first place? What was the excuse for
each and how well does it hold up to examination?
One final
thing: previously, scientists have been unable to anticipate all the
ways their creations could be studied to determine which lab they came
from. I think they failed to anticipate that the species tropism of
SARS-CoV-2 for (only) humans and animals used at the Hamilton, Montana
lab was an unanticipated clue to origin. [Assuming Will Jones is
correct in this assertion.]. This is a major clue.
https://www.niaid.nih.gov/research/vincent-j-munster-phd
Munster Lab: Major Areas of Research
Natural
reservoirs of emerging viruses and elucidation of the underlying biotic
and abiotic drivers of zoonotic and cross-species transmission eventsEvolutionary dynamics of emerging viruses in the context of virus-host ecology
Modeling zoonotic and cross-species transmission of emerging viruses and the efficacy of outbreak intervention strategies
Program Description
Emerging
viral diseases are a major challenge to the safety of the world in the
21st century. The emergence of Ebola virus, avian influenza H5N1, Nipah
and Hendra viruses, severe acute respiratory syndrome coronavirus
(SARS-CoV) and, more recently, the novel Middle East respiratory
syndrome (MERS) CoV, and avian influenza H7N9 has revealed the need for a
more comprehensive understanding of the drivers of infectious disease
outbreaks.Birds, mammals, and arthropods are the principal source of most emerging viruses in the human population. (Is this because of the lab work being done?—Nass) Very
little is known about the interaction of the viruses and their
respective natural hosts and the changes in virus-host ecology resulting
in cross-species transmission events, such as outbreaks in humans.The
main objectives of our research program aim to identify the underlying
biotic or abiotic changes in virus-host ecology that allow these
emerging viral pathogens to cross the species barrier. Recognizing both
the strengths and weaknesses of a unilateral focus on field research on
one hand and experimental research on the other, we set out to combine
the best of both approaches in one research program, where we aim to
identify drivers of cross-species transmission from data gathered in the
field and model these drivers under experimental conditions in the lab.
Experimental
modeling of zoonotic and cross-species transmission of emerging viruses
and the efficacy of outbreak intervention strategies
For
a wide variety of novel emerging infectious viruses (e.g., Nipah virus,
Ebola virus, MERS-CoV), no prophylactic or therapeutic intervention
measures are currently available to prevent or contain outbreak events. (There is a US-licensed Ebola vaccine and there are monoclonal antibodies; why are they omitted?—Nass)
In addition, very limited information is available on the route of
zoonotic and human-to-human transmission for most of these viruses.
Currently, our best hope to prevent or intervene in future outbreaks of
these viruses lies in the potential to efficiently block transmission
and thereby spread of the outbreak. In order to
efficiently establish prevention strategies, detailed knowledge on
mechanisms of pathogenicity and transmission (contact transmission,
fomite transmission, aerosol transmission, or foodborne or vertical
transmission) in the context of abiotic (temperature, humidity, airflow)
and biotic (routes of transmission, immune status, receptor
distribution, amount of shed virus) factors is needed. (In order to prevent transmission we must do gain of function research, justified by lying about the absence of a vaccine—Nass) The newly developed transmission models (We can now cause transmission in the lab, making the viruses more dangerous—Nass)
will be used to evaluate the efficacy of current outbreak intervention
strategies, such as vaccination and antiviral therapies. A
more comprehensive understanding of transmission events is likely to
make an important contribution to the control of emerging zoonotic
infections (and also could be used to enhance spread—Nass).