Lifeboat Foundation

In a study published on May 7, 2020, in Current Biology, researchers from University of Sydney have identified the single gene that determines how Cape honey bees reproduce without ever having sex. One gene, GB45239 on chromosome 11, is responsible for virgin births.

“It is extremely exciting,” said Professor Benjamin Oldroyd in the School of Life and Environmental Sciences. “Scientists have been looking for this gene for the last 30 years. Now that we know it’s on chromosome 11, we have solved a mystery.”

Behavioral geneticist Professor Oldroyd said: “Sex is a weird way to reproduce and yet it is the most common form of reproduction for animals and plants on the planet. It’s a major biological mystery why there is so much sex going on and it doesn’t make evolutionary sense. Asexuality is a much more efficient way to reproduce, and every now and then we see a species revert to it.”

Diagnosing COVID-19 more quickly, easily, and broadly

With COVID-19 rapidly spreading around the planet, the efficient detection of the CoV2 virus is pivotal to isolate infected individuals as early as possible, support them in whatever way possible, and thus prevent the further uncontrolled spread of the disease. Currently, the most-performed tests are detecting snippets of the virus’ genetic material, its RNA, by amplifying them with a technique known as “polymerase chain reaction” (PCR) from nasopharyngeal swabs taken from individuals’ noses and throats.

The tests, however, have severe limitations that stand in the way of effectively deciding whether people in the wider communities are infected or not. Although PCR-based tests can detect the virus’s RNA early on in the disease, test kits are only available for a fraction of people that need to be tested, and they require trained health care workers, specialized laboratory equipment, and significant time to be performed. In addition, health care workers that are carrying out testing are especially prone to being infected by CoV2. To shorten patient-specific and community-wide response times, Wyss Institute researchers are taking different parallel approaches:

A team of researchers from Los Alamos National Laboratory, Sheffield Teaching Hospitals NHS and the Duke Human Vaccine Institute and Department of Surgery has found 14 mutations to the SARS-CoV-2 virus, one of which they suspect might be more easily spread. In the interest of speedy dissemination of findings, the group has uploaded their paper to the bioRxiv preprint server rather than waiting for peer review at another journal.

The work involved analyzing the genomes of the virus found in 6,000 infected people from around the globe. They focused most specifically on the virus genes that are responsible for producing the “spike protein,” which is the mechanism the virus uses to attach to human cells. In so doing, they found 14 mutations, but one they named D614G (also known as G614) stood out because it was found in almost all samples outside of China. It was also particularly notable because it appeared to replace a prior mutation called D614. They also noted that in the original outbreak in China, there were only D614 mutations. It was only after the virus began appearing in Europe that the G614 mutation emerged. They suggest that the fact that the G614 virus took over from the prior mutation could mean it is more easily spread.

Rice University researchers have discovered a hidden symmetry in the chemical kinetic equations scientists have long used to model and study many of the chemical processes essential for life.

The find has implications for drug design, genetics and biomedical research and is described in a study published on April 21, 2020, in the Proceedings of the National Academy of Sciences. To illustrate the biological ramifications, study co-authors Oleg Igoshin, Anatoly Kolomeisky and Joel Mallory of Rice’s Center for Theoretical Biological Physics (CTBP) used three wide-ranging examples: protein folding, enzyme catalysis and motor protein efficiency.

Igoshin said the symmetry “wasn’t that hard to prove, but no one noticed it before.”

Why hasn’t #MachineLearning conquered SARS-CoV-2 that causes COVID-19 (P.S., SARS-CoV-2 is the name of the #virus, while COVID-19 is the name of the disease)? One of the possible answers is that the virus “learns” faster than machines through “mutations”.

That causes us thinking: If mutation is such an efficient weapon (for virus), can we learn something from it and then apply our understanding to #DeepLearning to create “fast-mutating” #DeepLearning models capable of helping us to fight intractable crisis like a #pandemic?

https://bit.ly/3c9GE5s

Continue reading “Mechanisms of viral mutation” »

A study just released by Columbia University Mailman School of Public Health is reporting a blood-DNA-methylation measure that is sensitive to variation in the pace of biological aging among individuals born the same year. The tool—DunedinPoAm—offers a unique measurement for intervention trials and natural experiment studies investigating how the rate of aging may be changed by behavioral or drug therapy, or by changes to the environment. The study findings are published online in the journal eLife.

“The goal of our study was to distill a measurement of the rate of biological aging based on 12-years of follow-up on 18 different clinical tests into a blood test that can be administered at a single time point.” said lead author Daniel Belsky, Ph.D., assistant professor of epidemiology at Columbia Mailman School and a researcher at the Columbia Aging Center.

Midlife adults measured to be aging faster according to the new measurement showed faster declines in physical and cognitive functioning and looked older in facial photographs. Older adults measured to be aging faster by the tool were at increased risk for chronic disease and mortality. In other analyses, the researchers showed that DunedinPoAm captured new information not measured by proposed measures of biological aging known as epigenetic clocks, that 18-year-olds with histories of childhood poverty and victimization showed faster aging as measured by DunedinPoAm, and that DunedinPoAm predictions were disrupted by a caloric restriction intervention in a randomized trial.

To trace the trail of the virus worldwide, Lim’s team is using a new technology called next-generation sequencing at ASU’s Genomics Facility, to rapidly read through all 30,000 chemical letters of the SARS-CoV-2 genetic code, called a genome.

Each sequence is deposited into a worldwide gene bank, run by a nonprofit scientific organization called GISAID. To date, over 16,000 SARS-CoV-2 sequences have been deposited GISAID’s EpiCoVTM Database. The sequence data shows that SARS-CoV-2 originated a single source from Wuhan, China, while many of the first Arizona cases analyzed showed travel from Europe as the most likely source.

Now, using a pool of 382 nasal swab samples obtained from possible COVID-19 cases in Arizona, Lim’s team has identified a SARS-CoV-2 mutation that had never been found before—where 81 of the letters have vanished, permanently deleted from the genome.

The breakthrough, which identified the location and function of every human gene, offered the promise of medical care tailored specifically to individual patients, based on their personal genetic makeup.

When researchers identified a gene associated with a 44 per cent risk of breast cancer in women, for example, it seemed that protecting them might be as simple as deactivating that gene.

But the promise of such personalized medicine has not fully materialized, say two McMaster researchers, because the full sophistication of the genetic blueprint has a more complex and far-reaching influence on human health than scientists had first realized.

Antibody found to block infection by the novel coronavirus SARS-CoV-2 in cells.

The ‘47D11’ antibody targets the ‘spike protein’ of the destructive coronavirus.

Continue reading “Antibody prevents the COVID-19 virus from infecting human cells” »