germs

S.O.S.

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{ Newsweek | White House Gift Shop }

strong Marguerite Gautier energy today

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{ watch clips | Twitter }

My wife wants to make love while the President has the freaking novel coronavirus! Nice try, psycho!

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{ Doctors monitoring Trump’s lungs, giving steroid dexamethasone to fight COVID-19 | Twitter }

Double fucked

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Frederick Trump […] paternal grandfather of Donald J. Trump, […] made his fortune by operating a restaurant and a brothel in Canada […] He died from the Spanish flu in 1918.

{ Wikipedia | Continue reading }

more { Trump coughed after the word “therapeutics” and it was edited out }

related { company that sells software used in hundreds of clinical trials, including the crash effort to develop tests, treatments and a vaccine for the coronavirus, was hit by a ransomware attack | NY Times }

flattening the curve, vertically

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{ COVID-19 at the White House | “He’s fucked, we’re fucked,” said one White House aide. When informed of the Biden campaign’s announcement that the former VP and his wife, Dr Jill Biden, had both tested negative, the aide replied: “Double fucked.” }

I’ve an eye on queer Behan and old Kate and the butter, trust me. She’ll do no jugglywuggly with her war souvenir postcards to help to build me murial, tippers! I’ll trip your traps!

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[A]bout half of patients report neurological symptoms, including headaches, confusion and delirium, suggesting the virus may also attack the brain.

A new study offers the first clear evidence that, in some people, the coronavirus invades brain cells, hijacking them to make copies of itself. The virus also seems to suck up all of the oxygen nearby, starving neighboring cells to death.

It’s unclear how the virus gets to the brain or how often it sets off this trail of destruction. Infection of the brain is likely to be rare, but some people may be susceptible because of their genetic backgrounds, a high viral load or other reasons.

Forty percent to 60 percent of hospitalized Covid-19 patients experience neurological and psychiatric symptoms, said Dr. Robert Stevens, a neurologist at Johns Hopkins University. But the symptoms may not all stem from the virus’s invasion of brain cells. They may be the result of pervasive inflammation throughout the body.

{ NY Times | Continue reading }

related { ‘Carnage’ in a lab dish shows how the coronavirus may damage the heart }

O, passmore that and oxus another! Don Dom Dombdomb and his wee follyo! Was his help inshored in the Stork and Pelican against bungelars, flu and third risk parties?

The World Health Organization has said it would prefer a vaccine to be at least 70% effective, but it has set its minimum threshold for a Covid-19 vaccine at 50%. […]

According to Shearing, figures from developers suggest 1 billion doses may be available this year, with another 7 billion ready for distribution in 2021. But those numbers assume multiple vaccines are approved, and supply could turn out to be significantly lower. Specialized needles and syringes will be needed to administer the vaccine, but countries including the United States don’t have enough on hand. There’s also a global shortage of glass vials to contend with. The WHO does not expect widespread vaccinations until the middle of next year, a spokesperson said Friday.

{ CNN | Continue reading }

An experimental submarine, the ‘Siren II,’ is sent to find out what happened to the missing ‘Siren I’

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Researchers in Hong Kong are reporting the first confirmed case of reinfection with the coronavirus.

“An apparently young and healthy patient had a second case of Covid-19 infection which was diagnosed 4.5 months after the first episode,” University of Hong Kong researchers said Monday in a statement.

The report is of concern because it suggests that immunity to the coronavirus may last only a few months.

The 33-year-old man had only mild symptoms the first time, and no symptoms this time around. The reinfection was discovered when he returned from a trip to Spain, the researchers said, and the virus they sequenced closely matched the strain circulating in Europe in July and August.

“Our results prove that his second infection is caused by a new virus that he acquired recently rather than prolonged viral shedding,” said Dr. Kelvin Kai-Wang To, a clinical microbiologist at the University of Hong Kong.

Doctors have reported several cases of presumed reinfection in the United States and elsewhere, but none of those cases have been confirmed with rigorous testing. Recovered people are known to shed viral fragments for weeks, which can cause tests to show a positive result in the absence of live virus.

But the Hong Kong researchers sequenced the virus from both rounds of infection and found significant differences in the two sets of virus, suggesting that the patient was infected a second time.

{ NY Times | Continue reading }

Some people can get the pandemic virus twice, a study suggests. That is no reason to panic. […]

Even if the finding settles the question of whether people can be reinfected with the pandemic virus, it raises many additional questions: How often does this happen? Do people have milder infections, or no symptoms at all, the second time around? Can they still infect others? If natural infection does not always confer solid protection, will that be true for vaccines as well?

{ Nature | Continue reading }

In type 1 immunity, pathogen clearance is mediated through effector cells including group 1 innate lymphocytes (ILC1), natural killer (NK) cells, cytotoxic T lymphocytes, and T helper 1 (TH1) cells

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It is clear from this and other studies that the immune response in hospitalized patients with severe COVID-19 is characterized by lymphopenia and the expression of molecules associated with ongoing inflammation8, whereas these same molecules are expressed at a lower level in people with mild or moderate disease. Differences in immune responses between the different categories of disease severity are even more evident when people with very mild or subclinical disease are included in the analyses.

A key next step will be to analyse samples from people with extremely early signs of COVID-19, and to compare longitudinal data in those who do and those who don’t require hospitalization. Some people who develop severe disease seem to have a suboptimal immune response initially, which might allow uncontrolled viral replication. Such high replication might, in turn, contribute to severe disease.

{ Nature | Continue reading }

related { Efforts are ongoing to find which human or viral factors underpin whether a person with COVID-19 will develop severe symptoms. Clinical evidence linked to two viral lineages now provides key insights into this enigma. | Nature }

quote { Longitudinal analyses reveal immunological misfiring in severe COVID-19 }

‘You act like mortals in all that you fear, and like immortals in all that you desire.’ –Seneca

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Amid all the fighting in your airways, messenger cells grab small fragments of virus and carry these to the lymph nodes, where highly specialized white blood cells—T-cells—are waiting. The T-cells are selective and preprogrammed defenders. Each is built a little differently, and comes ready-made to attack just a few of the zillion pathogens that could possibly exist. For any new virus, you probably have a T-cell somewhere that could theoretically fight it. Your body just has to find and mobilize that cell. Picture the lymph nodes as bars full of grizzled T-cell mercenaries, each of which has just one type of target they’re prepared to fight. The messenger cell bursts in with a grainy photo, showing it to each mercenary in turn, asking: Is this your guy? When a match is found, the relevant merc arms up and clones itself into an entire battalion, which marches off to the airways.

Some T-cells are killers, which blow up the infected respiratory cells in which viruses are hiding. Others are helpers, which boost the rest of the immune system. Among their beneficiaries, these helper T-cells activate the B-cells that produce antibodies—small molecules that can neutralize viruses by gumming up the structures they use to latch on to their hosts. Roughly speaking—and this will be important later—antibodies mop up the viruses that are floating around outside our cells, while T-cells kill the ones that have already worked their way inside. T-cells do demolition; antibodies do cleanup.

Both T-cells and antibodies are part of the adaptive immune system. This branch is more precise than the innate branch, but much slower: Finding and activating the right cells can take several days. It’s also long-lasting: Unlike the innate branch of the immune system, the adaptive one has memory.

After the virus is cleared, most of the mobilized T-cell and B-cell forces stand down and die off. But a small fraction remain on retainer—veterans of the COVID-19 war of 2020, bunkered within your organs and patrolling your bloodstream. This is the third and final phase of the immune response: Keep a few of the specialists on tap. If the same virus attacks again, these “memory cells” can spring into action and launch the adaptive branch of the immune system without the usual days-long delay. […]

Many infected people still clear the virus after a few weeks of nasty symptoms. But others don’t. Maybe they initially inhaled a large dose of virus. Maybe their innate immune systems were already weakened through old age or chronic disease. In some cases, the adaptive immune system also underperforms: T-cells mobilize, but their levels recede before the virus is vanquished, “almost causing an immunosuppressed state,” Iwasaki says. […]

There are also preliminary hints that some people might have a degree of preexisting immunity against the new coronavirus. Four independent groups of scientists—based in the U.S., Germany, the Netherlands, and Singapore—have now found that 20 to 50 percent of people who were never exposed to SARS-CoV-2 nonetheless have significant numbers of T-cells that can recognize it. These “cross-reactive” cells likely emerged when their owners were infected by other, related coronaviruses, including the four mild ones that cause a third of common colds, and the many that infect other animals.

But Farber cautions that having these cross-reactive T-cells “tells you absolutely nothing about protection.” It’s intuitive to think they would be protective, but immunology is where intuition goes to die. The T-cells might do nothing. There’s an outside chance that they could predispose people to more severe disease. We can’t know for sure without recruiting lots of volunteers, checking their T-cell levels, and following them over a long period of time to see who gets infected—and how badly.

Even if the cross-reactive cells are beneficial, remember that T-cells act by blowing up infected cells. As such, they’re unlikely to stop people from getting infected in the first place, but might reduce the severity of those infections.

{ The Atlantic | Continue reading }

deterioration in the forecasts of surface meteorology

51.jpgWeather forecasts play essential parts in daily life, agriculture and industrial activities, and have great economic value. Meteorological observations on commercial aircraft help improve the forecast. However, the global lockdown during the COVID‐19 pandemic chops off 50‐75% of aircraft observations. […] We see deterioration in the forecasts of surface meteorology and atmospheric stratification, and larger deterioration in longer‐term forecasts [AGU]

How the Porn Industry Is Changing During COVID-19

Why the porn industry has a lot to teach us about safety in the Covid-19 era

A new study finds that although musical instruments do generate airborne particles that could carry SARS-CoV-2, the risks for performers and audience may be manageable.

this month, a group of prominent scientists made the case that superspreading clusters suggest the virus is sometimes being transmitted over longer distances through the air in far smaller and more numerous particles. […] Why didn’t the infamous Lake of the Ozarks party spur lots of cases, while a much smaller gathering at a Michigan bar produced nearly 200? Part of the uneven spread of the coronavirus — and the phenomenon of superspreading — can be explained by extreme individual variation in infectivity, researchers say. Overall, researchers have estimated in recent studies that some 10 to 20 percent of the infected may be responsible for 80 percent of all cases. […] One proposal, from a Moscow State University professor, calls for shifting testing resources from the general public to efforts to identify potential “super emitters” with high viral loads by using randomized testing. Other proposals focus on limiting people’s more random interactions, such as on public transit, or at bars and restaurants, while loosening restrictions on their regular contacts, such as through work or school. [Washington Post]

Professional diver Emiliano Pescarolo contracted coronavirus in March and spent 17 days in hospital in the Italian port city of Genoa before being discharged on April 10. Now, three months later, the 42-year-old still experiences breathing difficulties. “Once back home, even after weeks I couldn’t see any progress: if I took a small walk, it was like climbing Mount Everest. I was out of breath also just for talking. I was very worried,” he said. Pescarolo is one of dozens of former Covid patients now receiving care at a rehabilitation clinic in Genoa — and says he is starting to see some progress. [CNN]

Despite how unnatural social distancing may feel to people, it is very much a part of the natural world, practiced by mammals, fishes, insects and birds. Social animals stay apart, changing behaviors such as grooming to stop the spread of diseases that could kill them.

And be sure of this: I am with you always, even to the end of the age

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We then showed that SARS-recovered patients still possess long-lasting memory T cells reactive to SARS-NP 17 years after the 2003 outbreak, which displayed robust cross-reactivity to SARS-CoV-2 NP. Surprisingly, we also frequently detected SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients.

{ Nature | Continue reading }

Perhaps there’s just little selection pressure on the virus as it races through millions of immunologically naïve people, scientists say. That could change with the advent of vaccines or new therapies, forcing the virus to evolve. But it could also indicate that the virus has been with people longer than we know, and was spreading before the first known cases in Wuhan, China, in December 2019. “The evolution of this virus to become a human pathogen may have already happened and we missed it,” Rasmussen says.

Wang thinks a version of the virus may have circulated earlier in humans in southern Asia, perhaps flying under the radar because it didn’t cause severe disease.

{ Science | Continue reading }