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Closing in on a Vaccine: The Not-so-simple Mechanics
By Shlomo Maital
Tel Aviv University Professor Jonathan Gershoni claims his lab is “two-thirds of the way” to creating a COVID-19 vaccine, according to a report in today’s Jerusalem Post, by Tamar Beeri.
Gershoni, who holds USPTO vaccine patents, is very good at explaining how his vaccine will work. Probably other vaccines against COVID-19 will adopt similar strategies. So, here is his not-so-simple explanation, according to Beeri:
“[Gershoni] explained that the vaccine intends to target the virus’s Receptor Binding Motif (RBM), a critical weak point which allows the virus to attach itself and infect a target cell. The RBM is a small feature of the virus’s “spike” protein, meaning that the virus uses many different proteins to replicate and invade cells, but the “spike” protein is the “major surface protein that it uses to bind to a receptor – another protein that acts like a doorway into a human cell.” [Those spikes you see on cartoon drawings of the novel coronavirus are how it pokes into a human cell and uses the cell’s DNA to replicate itself].
“Once this protein binds to the cell receptor of a human cell, the viral membrane fuses with that of the human cell, which allows the genome, or genetic blueprint of the virus to enter human cells and begin infection. “The idea is to recreate, to reconstitute, to construct an RBM [receptor binding motif] of COVID-19 virus and use it as the vaccine,” he told the Post. “That is to say, you would inject a small 50 amino-acid sequence and it would allow our immune system to focus on it and create antibodies that would directly target the virus at its weak spot.”
“Due to the size of the RBM, which is a highly complex three-dimensional structure and only 50 amino acids long, it will be very challenging for it to be functionally reconstituted. It would, however, be extremely effective as a basis for a possible vaccine.
“The smaller the target and the focus of the attack, the greater the effectiveness of the vaccine,” Gershoni said. “The virus takes far reaching measures to hide its RBM from the human immune system, but the best way to ‘win the war’ is to develop a vaccine that specifically targets the virus’s RBM.”
“Gershoni originally developed the design of the vaccine which targets the RBM in response to SARS CoV, which broke out in 2004, and later for MERS CoV. “What we found was that we were able to reconstitute, to create a functional Receptor Binding Motif, and that’s when we filed for patent in 2015,” he explained to the Jerusalem Post.
“We are now currently working on implementing the design of the vaccine that we were able to construct for SARS and MERS and to apply it to the current virus, the SARS coronavirus 2,” he continued. “This is a multi-step process. We’ve completed, I would say, about two-thirds of the way.”
New Hope for Treating Alzheimer’s
By Shlomo Maital
I have a very personal interest in Alzheimer’s and in general age-related dementia, for two reasons. First, my own age: At 74, I am moving into the dementia-prone zone. Second, family – like nearly everyone, I have known people who suffered and are suffering from it.
Here are some facts about Alzheimer’s:
One in eight older Americans has Alzheimer’s disease. Alzheimer’s disease is the sixth-leading cause of death in the United States. over 15 million Americans provide unpaid care for a person with Alzheimer’s or other dementias.
These figures apply equally to all societies that are aging, which is essentially all countries in the West, and even China.
Today’s New York Times has an Op-Ed by Pagan Kennedy, about new breakthroughs in Alzheimer research, disastrously underfunded (8,000 research papers every day are published on cancer! Frankly, the results are meager).
For years, researchers asked, how can we stop or dissolve the amyloid plaque that gums up the brain’s neurons and brings on dementia? That proved ineffective. Now, they are redefining the question (that is always a good approach when you cannot solve a problem): How come many older people die with their brains gummed up with amyloids, yet they show no sign of dementia?????
Answer: Must be the immune system. The body has proteins generated by the immune system that protect neurons from being damaged by those amyloids. Sometimes they are effective. Sometimes they are not. Why?
Initial results are promising. I wish they had framed this question much earlier. And I’m proud that Israeli researchers appear to be leading the way in this new avenue of research. A leading researcher in the US, Dr. Liddelow, at New York University, reports the new focus “will lead to a rapid production of effective treatments”.
I am hopeful that this is true. This, for me, is personal. I and those I love might well need it. So press on, Dr. Liddelow!