Lifeboat Foundation: Safeguarding Humanity
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Category: genetics – Page 377

We can identify ‘bad’ genes. Why can’t we use CRISPR gene editing to get rid of them?

A desirable option would be to use CRISPR gene editing to essentially cut out the unwanted gene. There are, however, many challenges ahead.

If you want to remove an undesirable gene from a population, you have a couple theoretical options — one that most people might find unthinkable, and one that lies outside our current scientific abilities.

The first involves locating a group of people without a particular gene and designing breeding programs around them. It would mean mating people in ways that society would consider incestuous. And we’ve seen the difficulties that result from that in the past — marriages between close relatives were a notorious cause of hemophilia in European royal families, for example.

A much more desirable option would be to use CRISPR gene editing to essentially cut out the unwanted gene. There are, however, many challenges ahead for such a strategy. Chief among them is the need to find mutations that, by themselves, are linked to particular diseases or disorders. And then we need guarantees that CRISPR will edit the correct genes.

Gene editing rids mice of DNA segment linked to autism

Researchers have used the gene-editing technique CRISPR to delete a segment of DNA associated with autism and schizophrenia from mouse brain cells.

The technique has only proven effective in mice so far but may eventually be suitable for treating brain conditions in people, says Xiao-hong Lu, assistant professor of pharmacology and neuroscience at Louisiana State University Health in Shreveport.

Unlike techniques used to manipulate DNA in the mouse brain, CRISPR can be applied to people. He says, “We need a tool to help us to carry the genetic elements into the [human] brain.”

Geneticists zeroing in on genes affecting life span

“We were very pleased to find out that even though life span is a very complicated trait caused by variation on a large number of loci, which is true for most complex traits, the number of loci that are in common is a totally finite number. So, we can imagine going on to the next stage and investigating one gene at a time and in combination,” Mackay said.

Scientists believe about 25 percent of the differences in human life span is determined by genetics—with the rest determined by environmental and lifestyle factors. But they don’t yet know all the genes that contribute to a long life.

A study published March 5, 2020, in PLOS Biology quantified variation in life span in the fruit fly genome, providing valuable insights for preserving health in elderly humans—an ever-increasing segment of the population. The paper titled “Context-dependent genetic architecture of Drosophila life span” is the culmination of a decade of research by Clemson University geneticists Trudy Mackay and Robert Anholt.

It remains difficult to address the for life span in humans, so researchers conduct their experiments with model systems. Mackay, the Self Family Endowed Chair of Human Genetics, is one of the world’s leading experts on the Drosophila melanogaster model (aka the common fruit fly), which is an excellent model for comparative analysis of human disease and aging. About 70 percent of the fruit fly genome has a human counterpart.

CRISPR has success in treating mice with type 1 diabetes

Circa 2017

Insulin-producing cells have been restored in mouse models of type 1 diabetes using a new genetic engineering technique.

American scientists adapted the gene editing technology known as CRISPR (clustered, regularly interspaced, short palindromic repeat) to successfully treat mouse models of type 1 diabetes, kidney disease and muscular dystrophy.

CRISPR enables scientists to edit the genetic material of an organism allowing for DNA sequences to be easily altered and gene function to be modified.

Regeneron Granted Fundamental Patents Covering Mouse Antibody Technology Used in VelocImmune® Mice

Circa 2013

These patents form part of Regeneron’s global patent portfolio, which together protect fundamental inventions behind Regeneron’s VelocImmune humanized mice. The two patents listed above specifically contain claims covering genetically modified mice that have unrearranged human immunoglobulin variable region gene segments at endogenous mouse immunoglobulin loci. The VelocImmune mice contain the full repertoire of human heavy chain immunoglobulin genes and kappa light chain genes, each linked to endogenous mouse constant regions. As a result, VelocImmune mice generate a normal and robust immune response which many believe is becoming the gold standard for making human antibody therapeutics. VelocImmune is also proving to be one of the most valuable technologies in biotechnology history, in terms of the licensing and collaboration revenues it has helped generate.

TARRYTOWN, N.Y., Aug. 7, 2013 /PRNewswire/ — Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) today announced that the United States Patent and Trademark Office granted U.S. Patent No. 8,502,018 relating to methods of genetically modifying a mouse to make human antibodies. A similar European.

Test for antibodies against novel coronavirus developed at Stanford Medicine

Working around the clock for two weeks, a large team of Stanford Medicine scientists has developed a test to detect antibodies against the novel coronavirus, SARS-CoV-2, in blood samples.

In contrast to current diagnostic tests for COVID-19, which detect genetic material from the virus in respiratory secretions, this test looks for antibodies to the virus in plasma, the liquid in blood, to provide information about a person’s immune response to an infection.

The test was launched April 6 at Stanford Health Care. It differs from an externally developed test that Stanford researchers used for a prevalence study during recent community screening events.

Susceptibility of ferrets, cats, dogs, and other domesticated animals to SARS–coronavirus 2

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the infectious disease COVID-19, which was first reported in Wuhan, China in December, 2019. Despite the tremendous efforts to control the disease, COVID-19 has now spread to over 100 countries and caused a global pandemic. SARS-CoV-2 is thought to have originated in bats; however, the intermediate animal sources of the virus are completely unknown. Here, we investigated the susceptibility of ferrets and animals in close contact with humans to SARS-CoV-2. We found that SARS-CoV-2 replicates poorly in dogs, pigs, chickens, and ducks, but ferrets and cats are permissive to infection. We found experimentally that cats are susceptible to airborne infection. Our study provides important insights into the animal models for SARS-CoV-2 and animal management for COVID-19 control.

In late December 2019, an unusual pneumonia emerged in humans in Wuhan, China, and rapidly spread internationally, raising global public health concerns. The causative pathogen was identified as a novel coronavirus (1–16) that was named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) on the basis of a phylogenetic analysis of related coronaviruses by the Coronavirus Study Group of the International Committee on Virus Taxonomy (17); the disease it causes was subsequently designated COVID-19 by the World Health Organization (WHO). Despite tremendous efforts to control the COVID-19 outbreak, the disease is still spreading. As of March 11, 2020, SARS-CoV-2 infections have been reported in more than 100 countries, and 118,326 human cases have been confirmed, with 4,292 fatalities (18). COVID-19 has now been announced as a pandemic by WHO.

Although SARS-CoV-96.2% identity at the nucleotide level with the coronavirus RaTG13, which was detected in horseshoe bats (Rhinolophus spp) in Yunnan province in 2013 (3), it has not previously been detected in humans or other animals. The emerging situation raises many urgent questions. Could the widely disseminated viruses transmit to other animal species, which then become reservoirs of infection? The SARS-CoV-2 infection has a wide clinical spectrum in humans, from mild infection to death, but how does the virus behave in other animals? As efforts are made for vaccine and antiviral drug development, which animal(s) can be used most precisely to model the efficacy of such control measures in humans? To address these questions, we evaluated the susceptibility of different model laboratory animals, as well as companion and domestic animals to SARS-CoV-2.

Melinjo Seed Extracts May Help Improve Diabetes And Obesity

Researchers from Kumamoto University have found that Melinjo seed extracts may help to improve diabetes and obesity by stimulating the production of adiponectin which is a hormone that works to help improve both conditions; individual genotype differences were also discovered that were responsible for variations in its efficacy.

Melinjo fruit contain high levels of antioxidant and antibacterial properties as well as high levels of polyphenols such as resveratrol that has been shown to induce adiponectin and may help to improve lifestyle related diseases such as metabolic syndrome. A type of resveratrol called Gnetin C which is found in MSE has higher antioxidant activity and has been shown to stay in the blood longer than resveratrol, but the exact mechanisms of how they exert their biological activity remains unknown.

Genetic analysis was used to find that differences in the type of DsbA-L gene affects adiponectin activation; meaning that DsbA-L induction may promote adiponectin activation and help to improve lifestyle related diseases. Their recent research has attempted to determine whether MSE enhances the function of DsbA-L; whether MSE promotes adi[onectin activation; and whether MSE has a therapeutic effect on either obesity and diabetes.