Though underlying medical conditions play an important role, many aspects of why COVID-19 severity can differ vastly from one to another has remained unclear.

A new study identifies dozens of genomic variations that may drive these hard-to-predict differences in clinical outcomes. According to work led by University of Pennsylvania scientists, genomic variants in four genes that are critical to SARS-CoV-2 infection, including the ACE2 gene, were targets of natural selection and associated with health conditions seen in COVID-19 patients.

We are inmediately crunching whatever it produces

In the study, an international team of scientists announced they successfully sequenced the A. filiculoids genome as well as the genome of another floating fern known as Salvina cucullata. Co-author and University of California Berkeley integrative biology professor Carl Rothfels, Ph.D. tells Inverse that having these genomes brings scientists one step closer to “understanding some of the crazy biology of these particular species.”

Rothfels says that one of the most “extraordinary features” of this fern is its ability to have a symbiotic relationship with cyanobacteria, which in turn gives it the ability to “fix” nitrogen. Nitrogen fixation is the process by which plants use the chemical element as a fertilizer: Most plants typically can’t do this alone, but the blue-green cyanobacteria that live in the Azolla leaves allow for this process to happen. In turn, Azolla can sustain rapid growth in favorable conditions.

That’s important for multiple reasons, the first being that the fern shows “great promise as a biofuel,” says Rothfel. While it’s been used as a fertilizer for rice paddies in Asia for the past 1,000 years, he and his team are now curious to know whether it could be used as a sustainable fertilizer elsewhere. Its ability to help agricultural crops is compounded by its resistance to pests: Farmers have noticed for decades that bugs generally don’t like ferns, and now the sequencing of the Azolla genome reveals it carries certain genetic mutations that allow it to repel insects.

What makes us human? The answer may be found in overlooked DNA

But Evan Boyle, Yang Li, and Jonathan Pritchard from Stanford University think that this framework doesn’t go far enough.

They note that researchers often assume that those thousands of weakly-acting genetic variants will all cluster together in relevant genes. For example, you might expect that height-associated variants will affect genes that control the growth of bones. Similarly, schizophrenia-associated variants might affect genes that are involved in the nervous system. “There’s been this notion that for every gene that’s involved in a trait, there’d be a story connecting that gene to the trait,” says Pritchard. And he thinks that’s only partly true.

Yes, he says, there will be “core genes” that follow this pattern. They will affect traits in ways that make biological sense. But genes don’t work in isolation. They influence each other in large networks, so that “if a variant changes any one gene, it could change an entire gene network,” says Boyle. He believes that these networks are so thoroughly interconnected that every gene is just a few degrees of separation away from every other. Which means that changes in basically any gene will ripple inwards to affect the core genes for a particular trait.

The Stanford trio call this the “omnigenic model.” In the simplest terms, they’re saying that most genes matter for most things.

Further to above . Is project Back off has some bearing on this error and what does it mean? Why is the Backoff?

Having upload issues on all my hosts.

The Centers for Disease Control and Prevention’s (CDC) Genetic Testing Reference Material Program (GeT-RM) has partnered with the Clinical Genome Resource (ClinGen) to develop a publicly available list of 546 expert curated pathogenic variants in 84 genes for use in next-generation sequencing (NGS) genetic testing. This list serves as a knowledge resource for designing comprehensive analytical validation studies and creating computer-modulated or simulated reference materials for clinical genomic test development by defining variants that are either major contributors to disease or difficult to detect. Their work is presented in The Journal of Molecular Diagnostics, published by Elsevier.

Genetic testing has evolved from interrogating small sets of known pathogenetic variants in one or a few genes to examining hundreds or thousands of genes simultaneously using NGS. For these large assays, it is logistically difficult (and often impossible) to obtain genomic DNA reference materials containing the full scope of variants and variant types needed to perform a comprehensive validation study.

It can be challenging for laboratories to maintain the expert knowledge to identify representative variants appropriate for inclusion in validation studies to assure analytic and clinical validity. In addition, a comprehensive validation study using traditional reference materials can be costly. The new expert curated variant list will help address these complexities. This is important because well designed and validated clinical assays can provide accurate and reliable results to patients, enabling accurate diagnoses and appropriate treatment decisions.

As far back as my log goes, to 6 June, my i9-10900F was running avx. Then on 17 June it switched over to sse2, with no obvious change in the run times.

I will try forcing it to fma.

It only makes sense that all i9s should work best using the same instruction set.

From what I've seen on i9 new builds that start with a fresh slate and run the test over all 3 instruction sets I'm seeing 7% improvement of fma over avx and 4% for fma over sse2.

In current weeks, scientists have sounded the alarm about new variants of the coronavirus that carry a handful of tiny mutations, some of which appear to make vaccines much less efficient.

But it’s not simply these small genetic modifications which can be elevating issues. The novel coronavirus has a propensity to combine giant chunks of its genome when it makes copies of itself. Unlike small mutations, that are like typos within the sequence, a phenomenon known as recombination resembles a main copy-and-paste error during which the second half of a sentence is totally overwritten with a barely totally different model.