It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Some features of ATS will be disabled while you continue to use an ad-blocker.
Viruses invade a cell by changing the structure and permeability of the cell wall. Viruses can’t survive on their own—they must hijack a host cell, inject their own nucleic acid, and replicate themselves like an out of control copy machine. Viruses use a type of agglutinin (big word meaning a substance that glues things to itself) called hemagglutinin to bind themselves to sialic acid links on the surface of epithelial host cells. Once attached, the virus begins to alter the permeability of the host cell wall—it makes the cell wall soft, causes it to bend apart, and creates holes (pores) in the sialic acid links on the surface. Viruses enter the host through these pores to hide inside and evade the immune system. They do this by using an enzyme called neuraminidase. This particular enzyme can catalyze (break apart) sialic acid links on the host cell surface. These two important molecules classify viruses: Hemagglutinin (H) and Neuraminidase (N). Each virus has one type of H and one type of N. H1N1 for example, was responsible for the pandemic of 1918 while the swine flu pandemic was H2N2. As a virus mutates or jumps species, the H and N numbers change to reflect the shift. As newer, more virulent strains of viruses are formed, human antibodies against the older ones no longer recognize them and reinfection can occur.
Arthur Firstenberg has changed the future and won himself a Nobel Prize with the publication of The Invisible Rainbow, which proves, among other things, that . . .
• The flu is an electrical disease. The trigger, Firstenberg writes, is connected to seasonal variations in solar radiation, as so many have suggested over the previous two centuries.
Long ago reports have shown that flu epidemics tend to occur during years of maximum solar activity, and that cases can rise and fall with the number of sunspots.
Famous thinkers who have connected flu with sunspots range from Noah Webster to Fred Hoyle. In 1836 Heinrich Schweich observed that it was a common belief that accumulation of electricity within the body caused influenza. His contention has never been disproven, Firstenberg reports.
The period of 1645 to 1715 is known as the Maunder Minimum, where no sunspots nor auroras were seen. There were also no worldwide pandemics. It wasn’t until 1727 that sunspots numbered more than 100 for the first time in more than a century. In 1728 influenza arrived in waves over the surface of the Earth and lasted by some accounts until 1738. Some 2 million died, Firstenberg wrote.
The pandemic of 1889-94 swept over the entire planet. Firstenberg theorizes that this accompanied the first electrification of the planet with electric lights turnin on everywhere.
1889, power line harmonic radiation began.
1918, the radio era began.
1957, the radar era began.
And 1968, the satellite era began. These were the significant times when large changes to the Earth’s electric field were made. Each was accompanied by a significant flu pandemic. And each time the public was hoaxed by phony attempts at vaccines that those who administered knew wouldn’t work.
Mechanistic data support the evidence of morphological and histological changes in humans and animals associated with acute sarin exposure. OP nerve agents including sarin cause hyperactivity in the nervous system triggered by hyperstimulation of cholinergic receptors which leads to respiratory failure via peripheral and central mechanisms and seizures via central mechanisms.
Therefore, to examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs, we built a chimeric virus encoding a novel, zoonotic CoV spike protein—from the RsSHC014-CoV sequence that was isolated from Chinese horseshoe bats1—in the context of the SARS-CoV mouse-adapted backbone. The hybrid virus allowed us to evaluate the ability of the novel spike protein to cause disease independently of other necessary adaptive mutations in its natural backbone. Using this approach, we characterized CoV infection mediated by the SHC014 spike protein in primary human airway cells and in vivo, and tested the efficacy of available immune therapeutics against SHC014-CoV. Together, the strategy translates metagenomics data to help predict and prepare for future emergent viruses.
To test the ability of the SHC014 spike to mediate infection of the human airway, we examined the sensitivity of the human epithelial airway cell line Calu-3 2B4 (ref. 9) to infection and found robust SHC014-MA15 replication, comparable to that of SARS-CoV Urbani (Fig. 1c). To extend these findings, primary human airway epithelial (HAE) cultures were infected and showed robust replication of both viruses (Fig. 1d). Together, the data confirm the ability of viruses with the SHC014 spike to infect human airway cells and underscore the potential threat of cross-species transmission of SHC014-CoV.