Posts Tagged ‘x78retwee’

Is facial recognition too biased to be let loose?

November 22, 2020

The ethical questions that haunt facial-recognition research

November 22, 2020

Resisting the rise of facial recognition

November 22, 2020

Why do COVID death rates seem to be falling?

November 22, 2020

It’s Time to Talk About Covid-19 and Surfaces Again | WIRED

November 21, 2020

Opinion | The Pandemic, from the Coronavirus’s Perspective – The New York Times

November 21, 2020

Joshua Lederberg, a Nobel Prize laureate in 1958, at age 33, wrote: “The future of humanity and microbes likely will unfold as episodes of a suspense thriller that could be titled ‘Our Wits Versus Their Genes.’ ”

Wits are fundamentally a product of genes, and in the end, genes beat wits. QT:{{”
Chimpanzees were a species in decline, alas, because of habitat loss and killing by humans; humans were a species in ascendance. The SIVcpz virus reversed its own evolutionary prospects by getting into us and adapting well to the new host. It jumped from a sinking lifeboat onto a luxury cruise ship.

SARS-CoV-2 has done likewise, though its success has occurred much more quickly. It has now infected more than 30 million people, just under half as many as the number of people infected by H.I.V., and in 10 months rather than 10 decades. It’s not the most successful human-infecting virus on the planet — that distinction lies elsewhere, possibly with the Epstein-Barr virus, a very transmissible species of herpesvirus, which may reside within at least 90 percent of all humans, causing syndromes in some and lying latent in most. But SARS-CoV-2 is off to a roaring start.

Now, for purposes of illustration, imagine a different scenario, involving a different virus. In the mountain forests of Rwanda lives a small, insectivorous bat known as Hill’s horseshoe bat (Rhinolophus hilli). This bat is real, but it has been glimpsed only rarely and is classified as critically endangered. Posit a coronavirus, for which this bat serves as reservoir host. Call the virus RhRW19 (a coded abbreviation of the sort biologists use), because it was detected within the species Rhinolophus hilli (Rh), in Rwanda (RW), in 2019 (19).

The Children Never Had Covid. So Why Did They Have Coronavirus Antibodies? – The New York Times

November 19, 2020

Wonder whether the chronic inflammation in asthmatic patients also has similar effects & if this explains why #COVID19 didn’t hit asthmatics quite as hard as was expected.

After examining blood taken from 190 people before the pandemic emerged, Dr. Elledge and his colleagues concluded that many already had antibodies, including the one targeting the base of the spike — presumably from infections with related coronaviruses that cause colds.

But while adults might get one or two colds a year, Dr. Elledge said, children may get up to a dozen. As a result, many develop floods of coronavirus antibodies that are present almost continuously; they may lessen cold symptoms, or even leave children with colds that are symptomless but still infectious.

What’s the worst that could happen? – The world should think better about catastrophic and existential ri sks | Briefing | The Economist

November 19, 2020 +

When Pigs Fly, They Want Drinks, Leg Room – WSJ

November 17, 2020
Amazing an elephant could be transported as well, with continuous food service during the trip….

Making the leap | C&EN Global Enterprise

November 16, 2020

So far, though, efforts to find other mutations that might power the virus’s pandemic prowess have largely fallen short. Starr, Bloom, and their colleagues set out to mutate every position in the
201-amino-acid RBD one by one and then examine how each mutation affects the protein’s folding pattern and capacity to bind ACE2. They found that the region has a high tolerance for mutations. “It can handle a high number of mutations and do its job just fine,” Starr says. The team even found dozens of mutations that boosted the RBD’s ability to bind the ACE2 receptor, but the virus seems to have not adopted any of them (Cell 2020, DOI: 10.1016/j.cell.2020.08.012). That finding suggests that the virus functions effectively with the binding affinity it has, and that there’s no strong selective pressure pushing for mutations that might increase it, Starr says. He wonders if that’s because the virus is tearing through a population that has never encountered it and has no immune defenses against it. “Right now, the virus has basically found a buffet table of susceptible [hosts].”
As the COVID-19 pandemic has progressed, one virus mutation does appear to have become a permanent feature of SARS-CoV-2’s genome. Researchers collecting virus samples from infected patients have been sequencing viral genomes and analyzing the strains spreading in different parts of the world. They have found that one mutation, a change from an aspartic acid (D614) to a glycine (G614), is now present in the majority of SARS-CoV-2 viral sequences. People infected with strains carrying this mutation tend to shed more virus than those infected with strains that don’t, hinting that this mutation may make the virus more infectious (Cell 2020, DOI:
10.1016/j.cell.2020.06.043). Farzan’s team has conducted cell studies with the lab-made viruses carrying SARS-CoV-2 spike proteins and found that the mutation causes the virus to more readily infect human cells, perhaps because there are more spike proteins on the virus’s surface (bioRxiv 2020, DOI: 10.1101/2020.06.12.148726v1). The data from those studies have not yet been peer reviewed.