Israel isolates COVID-19 antibody, makes 'significant breakthrough' against coronavirus

Israeli scientists have made a 'significant breakthrough' in developing antibody against coronavirus by isolated a key COVID-19 antibody, said Israeli defence minister Naftali Bennett in Jerusalem on Monday (May 5). The "monoclonal neutralising antibody" developed at the Israel Institute for Biological Research (IIBR) "can neutralise it (the disease-causing coronavirus) inside carriers' bodies," said the Defence Minister in a statement.

Bennett visited the labs of Israel's Institute for Biological Research (IIBR), supervised by the Prime Minister's Office and mandated to develop a vaccine for coronavirus, in Ness Ziona on Monday and was shown the "antibody that attacks the virus in a monoclonal way and can neutralize it within the bodies of those ill", a statement from his office said.

The statement said that the antibody's development had been completed and that the institute was in the process of patenting the find, and in the next stage, researchers will approach international companies to produce the antibody on a commercial scale.

"I am proud of the institute staff for this terrific breakthrough," Bennett said, adding that "their creativity and the Jewish mind brought about this amazing achievement".

Quoting medical sources, Israeli daily Ha'aretz had reported in March that scientists at the institute had made a significant breakthrough in understanding the biological mechanism and qualities of the virus, including better diagnostic capability, production of antibodies for those who already have the virus and development of a vaccine.

It was not immediately clear if the breakthrough presented to Bennett was in addition to progress that was reported in late March, and no further details were provided. The statement also did not specify whether human trials were conducted.

It was not immediately clear if the breakthrough presented to Bennett was in addition to progress that was reported in late March, and no further details were provided. The statement also did not specify whether human trials were conducted.

The IIBR was established in 1952 as part of the Israel Defence Forces' Science Corps and later became a civilian organization. It is technically under the supervision of the Prime Minister's Office but is in close communication with the Defence Ministry.

Prime Minister Benjamin Netanyahu is said to have ordered the institute to devote resources to develop a vaccine for COVID-19 on February 1.

Notably, the normal process to develop such a vaccine requires a long process of pre-clinical trials on animals, followed by clinical trials. This period allows for a full characterization of side effects and a better understanding of how different populations are affected.

Earlier in February, five shipments of virus samples arrived in Israel from Japan, Italy and other countries, news portal Ynet reported, said a PTI report adding that they were brought by a specially secured Defence Ministry courier to IIBR and had been frozen at -80 degrees Celsius.

Experts believe that the length of time needed to develop a vaccine runs from a few months to a year and a half. Numerous research teams all over the world are participating in the race to develop a vaccine for COVID-19. 

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Study finds mechanism for mother-child transmission of immunity to chickenpox

Women who been infected by chickenpox may transmit the DNA of the disease-causing virus to their babies during pregnancy, stimulating their immunity against the infection and protecting them, a study found. 

This mother-to-child transfer of viral DNA may be responsible for long-lasting protection against chickenpox infection seen during childhood, researchers  said. Their study was published in journal Viral Immunology. 

The new finding takes the understanding on how babies are protected against infections such as chickenpox to a new level.

Currently, it is understood that mothers provide babies protection against a variety of common infections by transferring ready-made antibodies to them. The protection lasts for 12-15 months; if a baby catches an infection during this period, it gets ill in a mild form and develops its own long-lasting immunity for that disease.

The new study showed that it was, however, different in the case of chickenpox. Scientists found that mothers developed subclinical viremia and the viral DNA was transferred to their babies. The study was done in 350 mothers and their newborn babies.

“The babies of mothers, who had chickenpox earlier in their life, develop a long-lasting active immunity with the transfer of chickenpox DNA from mothers, instead of the short-term passive protection provided by the transfer of ready-made antibodies. It is likely that the antibodies are developed actively in the foetus,” researchers said.

“Several studies have already shown that chickenpox can get reactivated due to stress following surgeries and space travel. But, sub-clinical reactivation of chickenpox, induced by the stress of pregnancy, is being reported for the first time,” they added.

Further, they said the ‘chickenpox parties’ held in countries like in the United Kingdom to get children exposed to others with chickenpox  was not necessarily a bad idea. They got naturally infected in childhood, when the disease was typically mild, and later in life they were likely to pass on protecting chickenpox antibodies and DNA to their offspring.  

The new findings make a case for review of vaccination policies for chickenpox, the authors said.
 

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Study fnds mechanism to heal injured nerve fibres

Researchers found new mechanisms that enable the regeneration of nerve fibers, which could open up new treatment approaches for the brain, optic nerve and spinal cord injuries.

The brain, spinal cord and optic nerves are referred to collectively as the central nervous system. The nerve fibers called axons are unable to grow back following injury meaning that damage is permanent.

It is possible to partially restore the regenerative capacity of nerve cells in the central nervous system by eliminating the inhibiting protein PTEN. However, a knockout of this kind also triggers many different reactions in the cells at the same time, which often lead to cancer, explained a Prof.

As a result, the direct inhibition of this protein is not suitable for therapeutic approaches in humans. What's more, the originally postulated mechanism underlying the renewed regenerative capacity following PTEN knockout could not be confirmed in further studies, causing the researchers to seek alternative explanations.

While investigating this as-yet unclear mechanism, the researchers were able to show for the 1st time that PTEN knockout significantly inhibits an enzyme called glycogen synthase kinase 3, GSK3 for short.

This enzyme, in turn, blocked another protein called collapsin response mediator protein 2, CRMP2.
this meant that the PTEN knockout prevents CRMP2 from being inhibited by GSK3.

If we directly prevent this 2nd step, i.e., stop the inhibition of CRMP2, we can also achieven the regeneration-promoting effect in a more specific manner, explained the researcher.

The activation of CRMP2 itself is not known to have any carcinogenic effect.

Although we have so far only shown these effects in genetically modified mice using gene therapy approaches, these findings open up various possibilities for the development of new drug approaches, explained the neuropharmacologist.

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Here is how sun damages our skin

Researchers have discovered the mechanism through which ultraviolet radiation, emitted by the sun, damages our skin.

What kind of ultraviolet radiation is the worst for our skin? And how exactly does the sun damage it? Those 2 questions are at the heart of a new study.

Ultraviolet radiation which the human eye can't perceive is broken down into 4 categories depending on wavelength and photon energy. Previous studies have documented how each type of UV radiation penerates to different depths into the skin and that prolonged exposure can lead to skin cancer, but exactly how it damages human skin in other ways has received less attention.

Researchers from cosmetics industry have debated for years whether UVA is worse than UVB for causing photo damage, which leads to the early onset of wrinkles and increases tissue fragility.

The study used samples of female breast skin, chosen because it is typically exposed only to low levels of sunlight that were subjected to various wavelengths of UV radiation. What the researchers found is that no UV range is more harmful than another, rather the damage scales with the amount of UV energy that the skin absorbs.

A more significant discovery, however, is the mechanism for how exactly UV damages skin. The study shows that UV weakens the bonds between cells in the stratum corneum, the top layer of skin by affecting proteins in corneodesmosomes that help the cells to adhere together. That's why sunburn leads to skin peeling.

Building on the findings of this study, the researchers are doing further research about how UV radiation affects deeper layers of the skin.

As those experiments continue, the researcher said the most important takeaway, for now, is that skin protection is important no matter what season of the year it is.

We're trying to push the message to use sunscreen not just for preventing skin cancer, but also to keep the integrity of your skin so you don't get infections or other problems, he said.

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MicroRNAs in the liver help regulate the feed-fast cycle

Researchers  have succeeded in identifying the mechanism that drives the feed-fast transition in the liver. They find that the oscillation in the levels of certain microRNAs in the liver drives this transition, and they study this by inhibiting the translation of the fasting responsive genes that are involved.

Feed-fast cycle

The feed-fast cycle is an important aspect of our body metabolism. There are four stages to it: fed state, post-absorptive state, fasting state, starvation state. Normally, we only experience the third stage and do not enter the fasting stage. Different organs in our body work to metabolise the food we consume, and they behave differently during each stage.

“The liver, for instance, is a central organ in maintaining glucose and fat metabolism both under fed and fasted conditions,” explains a researcher. During a fasting state, liver produces glucose in a process which is critical for maintaining circulating glucose levels. An abnormality in either of these processes can lead to diabetes, obesity or other liver diseases. “There is evidence to show that aberrant molecular mechanisms that affect glucose and fat metabolism in the liver are the primary causes of several metabolic diseases and even ageing,” he adds. Many of these occur due to aberrant gene expression and metabolic stress.

While fasting can last from a few hours to days, feeding (or refeeding) is a rapid process that takes from a few minutes to perhaps an hour. Therefore, when going from fasting to feeding, the liver functions must switch rapidly. “This entails stopping the mRNA translation of fasting-induced genes in a fed state. How such a tight control is exerted is being studied by researchers across the world,” says a Dr.

Mice models

The team started by profiling microRNAs in the liver of mice models in a fed state. “We identified that these fed microRNAs could control the expression of fasting-induced genes, thus controlling liver metabolism,” says a Dr. They carried out several assays to check for mitochondrial functions and cellular respiration. By injecting molecular sponges that scavenged the microRNAs in the liver, they reduced the level of fed microRNAs. “This perturbed the gene expression and metabolic pathways in the liver, which, in turn, resulted in elevated glucose production and higher circulating blood glucose levels in the mice,” says the co-author of the paper. 

Thus the group was able to identify the microRNAs that were responsible for the feed-fast transition and helped in maintaining liver physiology. 

The study is significant in having discovered changes in microRNA levels which constitutes an anticipatory mechanism and whose abrogation leads to a diabetic like state. Most of these mechanisms are conserved between humans and mice. So identifying such fed microRNAs in humans can aid in developing therapeutic interventions for tackling lifestyle disorders and ageing-associated loss in physiological fitness.

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Brain blood flow finding gives hope for Alzheimer’s therapy

You know that dizzy feeling you get when, after lying down for an extended period, you stand up a little too quickly?

That feeling is caused by a sudden reduction of blood flow to the brain, a reduction of around 30 percent. Now imagine living every minute of every day with that level of decreased blood flow.
People with Alzheimer’s disease don’t have to imagine it. The existence of cerebral blood flow reduction in Alzheimer’s patients has been known for decades, but the exact correlation to impaired cognitive function is less understood.

“People probably adapt to the decreased blood flow, so that they don’t feel dizzy all of the time, but there’s clear evidence that it impacts cognitive function,” said an associate professor.

A new study, offers an explanation for this dramatic blood flow decrease: white blood cells stuck to the inside of capillaries, the smallest blood vessels in the brain. And while only a small percentage of capillaries experience this blockage, each stalled vessel leads to decreased blood flow in multiple downstream vessels, magnifying the impact on overall brain blood flow.

“It turns out that … the blockages we were trying to induce were already in there,” she said. “It sort of turned the research around – this is a phenomenon that was already happening.”

The researchers, determined that only about 2 percent of brain capillaries had “stalls” (blockages), but the cumulative effect of that small number of stalls was an approximately 20 percent overall decrease in brain blood flow, due to the slowing of downstream vessels by the capillaries that were stalled. Recent studies suggest that brain blood flow deficits are one of the earliest detectable symptoms of dementia.

To test the effect of the stalls on performance of memory tasks in Alzheimer’s mice, they were given an antibody that interfered with the adhesion of white blood cells to capillary walls, which caused the stalled capillaries to start flowing again and thus increased overall brain blood flow. Memory function was improved within a few hours, even in aged mice with more advanced stages of Alzheimer’s disease.

Researchers are quick to point out, however, that the antibody is not something that can be used in humans. Also, of course, interfering with white blood cell adhesion would render an individual immuno-compromised.

“What we’ve done is identify the cellular mechanism that causes reduced brain blood flow in Alzheimer’s disease models, which is neutrophils [white blood cells] sticking in capillaries,” the Dr. said. “We’ve shown that when we block the cellular mechanism [that causes the stalls], we get an improved blood flow, and associated with that improved blood flow is immediate restoration of cognitive performance of spatial- and working-memory tasks.”

“Now that we know the cellular mechanism,” he said, “it’s a much narrower path to identify the drug or the therapeutic approach to treat it.”

The team has identified approximately 20 drugs, many of them already FDA approved for human use, that have potential in dementia therapy. Some of them, however, were designed to be taken in high doses for short periods of time to treat sepsis, or in the immediate aftermath of a heart attack or stroke. “They weren’t really intended to be something that you take for the rest of your life,” he said. Nonetheless, the lab is screening these drugs in Alzheimer’s mice now. 

The Dr. said he’s “super-optimistic” that, if the same capillary-blocking mechanism is at play in humans as it is in mice, this line of research “could be a complete game-changer for people with Alzheimer’s disease.”

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