Monday September 24, 2018

Scientists hopeful of ‘full-length single chain’ AIDS vaccine

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NewsGram Staff Writer

Robert Gallo, the scientist who first proved in 1984 that HIV triggered the disease AIDS, is again all set to begin the trial of its vaccine in the US. The vaccine which has been developed over the past 15 years by Gallo is a little different and is expected to bear fruitful results.

The initial phase, involving 60 volunteers, will test the safety and immune responses of the vaccine. This study will reveal whether the vaccine is more effective than the other 100+ AIDS vaccines that have been tested over the last three decades. Extensive testing on monkeys have yielded positive results.

Despite the presence of potential vaccines, the challenge with AIDS is that HIV directly infects white blood cells (RBC) called T-cells, so it literally turns our immune system against us. So, once the virus enters a T-cell, it’s invisible to the immune system.

The sole possibility to combat the threat is to pump in antibodies against the HIV surface proteins. However, doing so is equally difficult owing to the fact that the retrovirus can regularly change its viral envelope to hide particular surface proteins.

But Gallo and his team at the Institute of Human Virology in USA believe that they may have now found a moment when the HIV surface protein, known as gp120, is vulnerable to detection – the moment the virus binds with our bodies’ T-cells.

When HIV infects a patient, it first links to the CD4 receptor on the white blood cell. It then transitions, exposing hidden parts of its viral envelope, which allow it to bind to a second receptor called CCR5. Once HIV is attached to both these T-cell receptors, it can successfully infect the immune cell. at this stage, it is impossible to stop its juggernaut.

Gallo’s “full-length single chain” vaccine contains the HIV surface protein gp120, engineered to link to a few portions of the CD4 receptor. The motive is to fuel antibodies against gp120 when it is already attached to CD4 and is in a vulnerable transitional state. The aim of the whole process is effectively stopping it from attaching to the second CCR5 attachment.

Gallo himself admitted to Jon Cohen over at Science that full-length single chain vaccine is a “terrible name”.

The trial is being run in collaboration with Profectus BioSciences, a biotech spin-off from the Institute of Human Virology, and Gallo explained that extreme thorough testing on monkey and getting the fund to develop a human-grade vaccine have resulted in a delay to get to this point.

“Was anything a lack of courage?” he asked Science. “Sure. We wanted more and more answers before going into people.”

Let’s hope that caution pays off, and we may finally have a viable contender for an AIDS vaccine on our hands.

(With inputs from www.sciencealert.com)

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Scientists Discover A New Method To Fight Alzheimer’s, Dementia

Worldwide, about seven percent of people over 65 suffer from Alzheimer's or some form of dementia, a percentage that rises to 40 percent above the age of 85.

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Alzheimer's
One hemisphere of a healthy brain (L) is pictured next to one hemisphere of a brain of a person suffering from Alzheimer disease. VOA
Eliminating dead-but-toxic cells occurring naturally in the brains of mice designed to mimic Alzheimer’s slowed neuron damage and memory loss associated with the disease, according to a study published Wednesday that could open a new front in the fight against dementia.The accumulation in the body of “zombie cells” that can no longer divide but still cause harm to other healthy cells, a process called senescence, is common to all mammals.

Scientists have long known that these dead-beat cells gather in regions of the brain linked to old age diseases ranging from osteoarthritis and atherosclerosis to Parkinson’s and dementia.

Prior research had also shown that the elimination of senescent cells in ageing mice extended their healthy lifespan.

But the new results, published in Nature, are the first to demonstrate a cause-and-effect link with a specific disease, Alzheimer’s, the scientists said.

Alzheimer's
A lady suffering from Alzheimer’s. Flickr

But any treatments that might emerge from the research are many years down the road, they cautioned.

In experiments, a team led by Tyler Bussian of the Mayo Clinic in Rochester, Minnesota used mice genetically modified to produce the destructive, cobweb-like tangles of tau protein that form in the neurons of Alzheimer’s patients.

The mice were also programmed to allow for the elimination of “zombie” cells in the same region.

“When senescent cells were removed, we found that the diseased animals retained the ability to form memories, and eliminated signs of inflammation,” said senior author Darren Baker, also from the Mayo Clinic.

The mice likewise failed to develop Alzheimer’s signature protein “tangles”, and retained normal brain mass.

 

Alzheimer's
Alzheimer’s disease patient Isidora Tomaz, 82, sits in an armchair in her house in Lisbon, Portugal. It’s predicted that by 2050, 135 million Americans are going to suffer from mild cognitive impairment, a precursor of Alzheimer’s. VOA

Keeping zombies at bay

A closer look revealed that the “zombies” belonged to a class of cells in the brain and spinal cord, called glia, that provide crucial support and insulation to neurons.

“Preventing the build-up of senescent glia can block the cognitive decline and neuro-degeneration normally experienced by these mice,” Jay Penney and Li-Huei Tsai, both from MIT, wrote in a comment, also in Nature.

Bussian and his team duplicated the results with pharmaceuticals, suggesting that drugs could one day slow or block the emergence of Alzheimer’s by keeping these zombie cells at bay.

“There hasn’t been a new dementia drug in 15 years, so it’s exciting to see the results of this promising study in mice,” said James Pickett, head of research at Alzheimer’s Society in London.

 

Alzheimer's
The accumulation in the body of “zombie cells” that can no longer divide but still cause harm to other healthy cells, a process called senescence, is common to all mammals. IANS

For Lawrence Rajendran, deputy director of the Dementia Research Institute at King’s College London, the findings “open up new vistas for both diagnosis and therapy for neurodegenerative diseases, including Alzheimer’s.”

Up to now, dementia research has been mostly focused on the diseased neurons rather than their neighboring cells.

“It is increasingly becoming clear that other brains cells play a defining role,” Rajendran added.

Several barriers remain before the breakthrough can be translated into a “safe, effective treatment in people,” Pickett and other said.

The elderly often have lots of harmless brain cells that look like the dangerous senescent cells a drug would target, so the molecule would have to be good at telling the two apart.

Also Read: Common Painkillers Triple Harmful Side Effects in Dementia

Worldwide, about seven percent of people over 65 suffer from Alzheimer’s or some form of dementia, a percentage that rises to 40 percent above the age of 85.

The number afflicted is expected to triple by 2050 to 152 million, according to the World Health Organization, posing a huge challenge to healthcare systems. (VOA)