Evidence shows that this virus is engineered with Gain of Function (GoF) including mechanisms creating an
Inflammo Thrombotic Response (ITR) with mRNA Reverse Transcription (RT) into cell DNA with Prion-like structures
present in the virus spike protein.
Additional information
Reports
The Genetic Structure of SARS-CoV-2 does NOT rule out a laboratory origin. September 2, 2020
An open debate on SARS-CoV-2’s proximal origin is long overdue. February 7, 2021.
Gain of Function Research
With a paper trail from China’s bat caves to North Carolina, to increase infectivity and virulence of virus. Documents tracking the virus back to Wuhan with $3.5 million from U.S. National Institute of Health funding.
“There are viruses that exist in bat species, preprogrammed to jump between species and replicate just fine in humans. We had no access to the viruses in China, all we had was access to the sequence.”
min 2:15 – 2:30
Dr. Ralph Baric Professor of Microbiology and Immunology University of North Carolina
mRNA Transcription Capacity
Evidence shows that SARS-CoV-2 spike protein can Integrate into human DNA.
Image below shows mRNA getting into brain cells
Using the Reverse Transcriptase (RT) found in human platelets, CD4 (Helper Cells) and other cells carrying Long Interspersed Nuclear Elements (LINE-1); or by the HIV-RT. Research has shown that SARS-CoV-2 mRNA can insert itself into human DNA
LINE-1 averages 6,000 base pairs (bp) and comprises approximately 17% of human DNA
80 -100 of these LINE-1 segments are known to retro transpose leading to insertions, deletions, and rearrangement of genetic material.
Report
Presence of Prion-like Structure in Spike Protein
Prion-like domains are critical to SARS-CoV-2 virulence. Prions are associated with “Mad Cow Disease” and neuromuscular movement disorders seen in Parkinson’s Disease and Alzheimer’s.Creutzfeldt–Jakob disease (CJD), also known as subacute spongiform encephalopathy or neurocognitive disorder due to prion disease, is a fatal degenerative brain disorder.[4][1] Early symptoms include memory problems, behavioral changes, poor coordination, and visual disturbances.[4] Later symptoms include dementia, involuntary movements, blindness, weakness, and coma.[4] About 70% of people die within a year of diagnosis.[4]
Reports
SARS-CoV-2 prion-like domains in spike proteins enable higher affinity to ACE2
Somatic APP gene recombination and mutations occur mosaically in normal and Alzheimer’s disease neurons
Creutzfeldt–Jakob disease (CJD), also known as subacute spongiform encephalopathy or neurocognitive disorder due to prion disease, is a fatal degenerative brain disorder.[4][1] Early symptoms include memory problems, behavioral changes, poor coordination, and visual disturbances.[4] Later symptoms include dementia, involuntary movements, blindness, weakness, and coma.[4] About 70% of people die within a year of diagnosis.[4]
