StratGoatCom posted:

As I said last thread, if that fucker gets a foothold in the USA again, no one has the drive to get it out again.

fosborb posted:

lol first locally transmitted malaria case in the DC area in the last 40 years just announced tonight

Platystemon posted:

CDC used to be the OFFICE OF MALARIA CONTROL IN WAR AREAS.

Imagine if they had said “malaria is an endemic disease LOL just live with it”.

Platystemon posted:

Posting on the CDC birth page.

I fully expect that with history now running reverse, CDC will reintroduce malaria to the United States before reverting to Office of Malaria Control in War Areas and then dissolving ultimately into the Marine Hospital Service.

Platystemon posted:

StratGoatCom posted:

Also, wherever you are now Rubby, I hope you come back one day. You are missed.

StratGoatCom posted:

Also, wherever you are now Rubby, I hope you come back one day. You are missed.

quote:

What!?!?

Severe COVID-19 may cause long-lasting alterations to the innate immune system, the first line of defense against pathogens, according to a small study funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. These changes may help explain why the disease can damage so many different organs and why some people with long COVID have high levels of inflammation throughout the body. The findings were published online today in the journal Cell.

Researchers led by Steven Z. Josefowicz, Ph.D., of Weill Cornell Medicine in New York City examined immune cells and molecules in blood samples from 38 people recovering from severe COVID-19 and other severe illnesses, as well as from 19 healthy people. Notably, the researchers established a new technique for collecting, concentrating and characterizing very rare blood-forming stem cells that circulate in the blood, eliminating the need to extract such cells from bone marrow.

In these rare stem cells—the parents of immune-system cells—taken from people recovering from COVID-19, the scientists identified changes in the instructions for which genes got turned on or off. These changes were passed down to daughter cells, leading them to boost production of immune cells called monocytes. In the monocytes from people recovering from severe COVID-19, the changes in gene expression led the cells to pump out greater amounts of molecules called inflammatory cytokines than monocytes from people who were healthy or had non-COVID-19 illnesses. The researchers observed these changes as much as a year after the participants came down with COVID-19. Due to the small number of study participants, the scientists could not establish a direct association between the cellular and molecular changes and health outcomes.

The investigators suspected that an inflammatory cytokine called IL-6 might play role in establishing the changes in gene-expression instructions. They tested their hypothesis both in mice with COVID-19-like disease and in people with COVID-19. In these experiments, some of the subjects received antibodies at the early stage of illness that prevented IL-6 from binding to cells. During recovery, these mice and people had lower levels of altered stem cell gene-expression instructions, monocyte production and inflammatory cytokine production than subjects that didn’t receive the antibody. In addition, the lungs and brains of mice that received the antibodies had fewer monocyte-derived cells and less organ damage.

These findings suggest that SARS-CoV-2 can cause changes in gene expression that ultimately boost the production of inflammatory cytokines, and one type of those cytokines perpetuates the process by inducing these changes in stem cells even after the illness is over. Additionally, the findings suggest that early-acting IL-6 is likely a major driver of long-term inflammation in people with severe COVID-19. These findings shed light on the pathogenesis of SARS-CoV-2 infection and may provide new leads for therapies.

ibid posted:

https://twitter.com/Bob_Wachter/status/1692591119001927862

Steve Yun posted:

a 1 in 1000 death rate…

if everyone in the us was vaccinated and got Covid, that would be 330,000 dead

The Oldest Man posted:

they should get him to do the Master Class episode on mental gymnastics

The Oldest Man posted:

they should get him to do the Master Class episode on mental gymnastics

quote:

The administration of a booster dose was associated with an initial VE against laboratory-confirmed infection with Omicron that was higher on average compared with the primary vaccination cycle (Figure 3) but with a marked variability at any time after booster administration. Pooled estimates of VE after the administration of a booster dose were 55.4% (95% CI, 42.4%-68.4%) at 1 month, 36.0% (95% CI, 27.0%-45.0%) at 6 months, and 28.9% (95% CI, 17.1%-40.6%) at 9 months. Consistent estimates were obtained in both sensitivity analyses (SA1 and SA2) (eFigures 11, 13, and 16 in Supplement 1).

The Oldest Man posted:

I just dunno what to say about Bob Wachter, he gave his wife what sounds like pretty severe PASC, described his own case as "nasty," and very much could have died of that 'with covid not of covid' shower fall and subsequent brain bleed. And he says being careful isn't onerous to him, right before saying he's still not masking or avoiding indoor dining or crowded spaces yet because of some extremely sketchy and optimistic back of envelope math that assumes his infection-derived immunity is still good, still good against current variants, PASC risk for him is only 1-in-20 somehow, etc.

I guess consequences just don't exist for some people even after they suffer a bunch of what I'd categorize as pretty severe ones.

The Oldest Man posted:

I'm genuinely curious where he's getting the stats like "you're protected from infection after a booster dose for 4 months." Last I had seen on the subject was this https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2804451:

55.4% at one month is not what I'd call "protected."

ibid posted:

https://twitter.com/Bob_Wachter/status/1692591119001927862

Platystemon posted:

Look, people take one in a thousand risks all the time, and it’s fine. It’s comparable to driving a mere quarter of a million miles. Who doesn’t do that once or twice per year?

Maybe you don’t, but surely you go hang gliding ten times per month, right? No one would consider you a daredevil for doing that.

The Oldest Man posted:

Yeah it's only about as likely to kill you as getting bitten by a poisonous snake is and I do that every day

ibid posted:

god drat

https://twitter.com/CDCEnvironment/status/1692281921550614785

Pingui posted:

Fruit fly study indicating that ACE2 interference/depletion could be the cause of neuromuscular complications:

News article on the matter:

https://scitechdaily.com/unmasking-the-long-covid-mystery-new-study-reveals-cause-of-muscle-weakness/#google_vignette posted:

quote:

Unmasking the Long COVID Mystery: New Study Reveals Cause of Muscle Weakness
(..)
Around one in three individuals who recover from COVID-19 continue to experience life-disrupting symptoms, such as persistent fatigue, shortness of breath, ‘brain fog’ (a term used to describe concentration difficulties), and muscle weakness. The origin of long COVID, despite its increasing global impact on daily life, has remained a mystery.

SARS-CoV-2, the coronavirus responsible for COVID-19, latches onto the ACE2 (angiotensin-converting enzyme 2) receptor, which acts as the doorway through which the virus infects cells. In a pioneering study, researchers at the University of Malta exploited fruit flies to curb down the levels of the ACE2 receptor. In the absence of the virus, this was enough to induce fatigue and diminished mobility.

“Our research clearly shows that depletion of ACE2 is central to the neuromuscular complications experienced by a significant percentage of COVID-19 patients,” said Professor Ruben Cauchi, who heads the Motor Neuron Disease Laboratory at the University of Malta.
(..)
When analyzing molecular defects in organisms with downregulated ACE2 levels, the Maltese scientists discovered a breakdown in communication between nerves and muscles. Several key molecules required for nerves to send messages to muscles were found compromised.

Various paths are thought to coalesce to bring down ACE2 levels or dampen its function in humans following a coronavirus infection. “In addition to being hijacked by the virus, the ACE2 receptor on the cell’s surface can also be targeted by autoantibodies, with the immune system attacking the body as it does in Multiple Sclerosis,” added Dr. Paul Herrera, who performed the intricate experiments that were crucial to the study. There have also been reports of virus persistence long after the initial infection.
(..)

quote:

Could fused neurons explain COVID-19’s ‘brain fog’?

-

Researchers already knew that SARS-CoV-2 could cause certain cells to fuse together. The lungs of patients who die from severe COVID-19 are often riddled with large, multicellular structures called syncytia, which scientists believe may contribute to the respiratory symptoms of the disease. Like other viruses, SARS-CoV-2 may incite cells to fuse to help it spread across an organ without having to infect new cells.

To see whether such cell fusion might happen in brain cells, Massimo Hilliard, a neuroscientist at the University of Queensland, and his colleagues first genetically engineered two populations of mouse neurons: One expressed a red fluorescent molecule, and the other a green fluorescent molecule. If the two fused in a lab dish, they would show up as bright yellow under the microscope. That’s just what the researchers saw when they added SARS-CoV-2 to a dish containing both types of cells, they report today in Science Advances. The same fusion happened in human brain organoids, so-called minibrains that are created from stem cells.

The key appears to be angiotensin-converting enzyme 2 (ACE2), the protein expressed on the surface of mammalian cells that SARS-CoV-2 is known to target. The virus uses a surface protein called spike to bind to ACE2, triggering the virus to fuse to a cell and release its genetic material inside. Seemingly, the spike protein in infected cells may also make other ACE2 on a cell trigger fusion to a neighboring cell. When the team engineered neurons to express the spike protein, only cells that also expressed ACE2 were able to fuse with each other. The findings parallel previous work in lung cells: The ACE2 receptor seems to be critical in mediating their fusion during SARS-CoV-2 infection.

However, the neuronal syncytia seen in the lab dishes and organoids also had some peculiarities that made them stand out from those seen in lungs. When lung cells fused, only the main parts of the cell body connected to each other. Among neurons, in contrast, the fusion happened farther away from the cell body, at long, thin extensions known as dendrites and axons, which are critical for cell-cell communication.

The fusions seemed to disrupt this communication. Neurons typically fire independently, propagating signals throughout the brain. But 90% of the fused neurons fired at the same time, whereas the remaining 10% stayed silent. This massive amount of synchronous activity “is almost like a seizure,” Hilliard says. Brain fog could result when this delicate communication is disrupted, he says. Hillard’s group has previously shown that inducing neurons to fuse in the nervous system of the worm Caenorhabditis elegans blunted their ability to sense odors.

“These neurons are like Siamese twins, they are joined at the hip,” says Adonis Sfera, a psychiatrist associated with Patton State Hospital and Loma Linda University who was not involved with the study. “Can they function as neurons? Nobody knows that yet. But chances are they have lost some of that function.”

ibid posted:

god drat

https://twitter.com/CDCEnvironment/status/1692281921550614785

HazCat posted:

It's happened a few times. Hootington was one, but there was also that poor loving guy who just wanted a source on outside transmission so he could pass the info along without having to say 'I got this info from some nerds on the Internet'. He had one goon itt harass him for days, accusing him of concern trolling and being a wrecker and all kinds of absolutely unhinged poo poo.

That new guy was never anything but totally polite, and he wasn't even asking for anything unreasonable! And no one said poo poo about what was happening, and when I finally called it out a bunch of people acted like it was actually totally normal be so suspicious of 'outsiders' that you scream at someone for asking politely for sources.

Gunshow Poophole posted:

this is actually exactly how a simulated virus would respond to being aggressively confronted with the set of treatment guidelines and screens we've set up around paxlovid

lmaooooo

Oops! All evolutionarily tautological!

ibid posted:

god drat

https://twitter.com/CDCEnvironment/status/1692281921550614785

Rescue Toaster posted:

I mean I don't think you're wrong necessarily, but there's zero chance enough people have taken paxlovid relative to the amount of people catching COVID to have any evolutionary effect.

https://web.archive.org/web/20230228234344/https://id.usembassy.gov/u-s-citizen-services/covid-19-information/ posted:

Testing
Upon arrival, travelers will complete a COVID-19 symptom check, and temperature check. If the traveler has no symptoms and normal If the traveler is symptomatic or has a body temperature above 99.5 F, a PCR test will be taken at the airport. If this test is positive, the traveler must isolate at their residence or a facility approved for COVID-19 isolation. The traveler is responsible for all associated costs.

Quarantine
There is no quarantine requirement for travelers who are fully- vaccinated.
Quarantine period of 5 x 24 hours is needed for international travelers who have not been vaccinated or have received first dose of vaccination of a two-dose vaccination regime.
Travelers under 18 years of age will follow the quarantine provisions of their parents/caregivers.
International travelers are responsible for all expenses during the quarantine, including the COVID-19/PCR tests