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 events
Evolutionary 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).
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