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BREAKING NEWS
Source: COVID-19 Research  Sep 02, 2021  3 years, 2 months, 3 weeks, 17 hours, 49 minutes ago

BREAKING! University of Queensland Study Shows SARS-CoV-2’s Fusogens Cause Host Neurons And Glial Cells To Fuse Resulting In Neurological Issues!

BREAKING! University of Queensland Study Shows SARS-CoV-2’s Fusogens Cause Host Neurons And Glial Cells To Fuse Resulting In Neurological Issues!
Source: COVID-19 Research  Sep 02, 2021  3 years, 2 months, 3 weeks, 17 hours, 49 minutes ago
A new study led by researchers from the University of Queensland-Australia has shockingly found that unique proteins called fusogens found on the surface of the spike proteins of the SARS-CoV-2 coronavirus is able cause the fusion of neurons cells  and also cause fusion between neurons and glial cells. This phenomena could possibly explain the various neurological manifestations in both COVID-19 and post-COVID patients.

The study findings were published on a preprint server are are currently being peer-reviewed. https://www.biorxiv.org/content/10.1101/2021.09.01.458544v1
 
Various viruses including the herpes simplex virus, dengue virus, orthoreovirus, and the even the SARS-CoV-2 coronavirus are known to be able to infect neurons. https://pubmed.ncbi.nlm.nih.gov/33433624/
 
https://pubmed.ncbi.nlm.nih.gov/26580325/
 
Viral brain infections are characterized by multiple neurological symptoms, including headache, fever, confusion, epileptic seizures, and loss of taste or smell. In more severe cases, viral brain infections can lead to encephalitis and meningitis, and potentially irreversible neuronal deficits such as paralysis and death. Most clinical symptoms originate from the death of infected neurons.
 
However, some viruses do not kill their host cells, and the chronic neurological sequelae of these infections cannot be explained by the loss of infected neurons. Other neuropathological mechanisms must therefore underlie the progression of these viral infections leading to brain dysfunction.
 
Interestingly it has also been found that certain enveloped viruses use specialized surface molecules called fusogens to enter host cells. During virus replication, these fusogens decorate the host cells membrane enabling them the ability to fuse with neighboring cells, forming syncytia that the viruses use to propagate while evading the immune system. https://pubmed.ncbi.nlm.nih.gov/18496517/
 
https://pubmed.ncbi.nlm.nih.gov/28152024/
 
https://pubmed.ncbi.nlm.nih.gov/8600520/
 
The study team demonstrated that expression of either the SARS-CoV-2 spike (S) protein or p15 protein from the baboon orthoreovirus is sufficient to induce fusion between interconnected neurons, as well as between neurons and glial cells.
 
Interestingly this phenomenon is observed across species, from nematodes to mammals, including human embryonic stem cells-derived neurons and brain organoids.
 
The study findings showed that that fusion events are progressive, can occur between distant neurites, and lead to the formation of multicellular syncytia.
 
The study findings also revealed that in addition to intracellular molecules, fusion events allow diffusion and movement of large organelles such as mitochondria between fused neurons.
 
The study findings provide important mechanistic insights into how SARS-CoV-2 and other viruses could affect the nervous system circuitries causing neurological symptoms.
 
Corresponding author, Dr Massimo A. Hilliard Clem Jones , a professor at the Centre for Ageing Dementia Research, Queensland Brain Institute-University of Queensland told Thailand Medical News, “Our study findings show that neurons expressing viral fusogens acquire the capacity to fuse, potentially compromising their functional circuit properties while still remaining viable. This previously uncharacterized event could explain at least some, if not most, of the neurological consequences of viral infections of the nervous system.”
 
He however alarmingly added, “Most of the current immunization approaches for COVID-19 are based on expressing the spike S protein in the host cells as an epitope to trigger the immune system response. These nucleic acid-based vaccines deliver the antigen encoded as mRNA, such as the Pfizer-BioNTech BNT162b2 and the Moderna mRNA-1273 vaccines, or as adenovirus-enclosed DNA, such as the OxfordAstraZeneca ChAdOx1 nCoV-19/AZD1222 33 and Johnson & Johnson Ad26.COV2.S vaccines.  Fortunately the current versions of the Moderna, Pfizer-BioNTech and Johnson & Johnson vaccines encode the full-length spike S (spike S-2P) with two mutations that stabilize the prefusion conformation and inactivate its fusogenicity. (Note that he left out the AstraZeneca vaccine!) Our findings demonstrate that it is critical to consider the fusogenic potential when designing any future vaccines in which viral fusogens are to be expressed in mammalian cells.”
 
We leave readers to do their own due diligence and decipher the scary implications of the above statement with regards to the AstraZeneca vaccine.
 
As far as the phenomena of neuron cells fusing with each other as a result of viral proteins called fusogens from the SARS-CoV-2 coronavirus, another previous study also supported this finding. https://www.biorxiv.org/content/10.1101/2020.12.03.409763v1.full
 
For the latest COVID-19 Research, keep on logging to Thailand Medical News.
 
 
 
 
 

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