Watch out, I hear it’s like a Hotel California, you can check out any time you like but you can never leave. They’ll extend your stay at a whim, has no bearing if you test positive or not, your obedience is mandatory.
Yeh, also I have to worry that if I go to Howard Springs, your president might declare a travel ban and I will not be able to get back in unless I cross the mexican border where they not only do not give a shiite, they give you a bus ride to any place in the U.S. you want to go. Thank you for looking out for me.
Sure I am on the lookout for their games. They give you a shot whether you want it or not, then three weeks later when you get ready to leave, they say you are quarantined longer because your shots are not up to date since it has been three weeks. It's complicated.
Johnson & Johnson Covid-19 booster works well for people who had Pfizer vaccine originally: Study https://www.straitstimes.com/world/...-works-well-for-people-who-had-pfizer-vaccine NEW YORK (NYTIMES) - People who received Pfizer-BioNTech vaccines may get as much benefit from a Johnson & Johnson booster shot as a Pfizer one. That's the finding of a small study released on Sunday (Dec 5). Researchers at the Beth Israel Deaconess Medical Centre in Boston studied 65 people who had received two shots of the Pfizer vaccine. Six months after the second dose, the researchers gave 24 of the volunteers a third dose of the Pfizer vaccine and gave 41 the Johnson & Johnson shot. (The study was funded in part by Johnson & Johnson and has not yet been published in a scientific journal.) Both vaccine brands boosted the number of Covid-fighting T-cells, which are important for long-lasting protection and for preventing infections from turning into severe disease. But the T-cell increase delivered by the Johnson & Johnson vaccine was twice as high as that of Pfizer's. The researchers also measured antibodies, which provide much of the protection immediately after vaccination. Volunteers who got a third Pfizer dose saw their antibody levels jump after two weeks, and then decline by a quarter by the fourth week. The Johnson & Johnson booster, by contrast, more than doubled antibody levels between the second and fourth weeks. At that point, Pfizer's antibodies were still about 50 per cent higher than Johnson & Johnson's. For antibodies, that's a relatively small difference. And both levels were well above the threshold scientists believe is needed for strong protection. The results are somewhat different from earlier studies. In October, a "mix and match" clinical trial organised by the National Institutes of Health (NIH) reported that all three authorised vaccines - from Pfizer, Moderna and Johnson & Johnson - caused antibody levels to rise when used as a booster. But Johnson & Johnson's shot provided a much smaller boost than the others did. (The NIH has not yet published how each booster affected the volunteers' T-cells.) The difference between the two studies might be explained by the length of delay between shots. In the NIH trial, many of the volunteers got their booster shots after three or four months, versus the new study's wait of six months. The Johnson & Johnson vaccine seems to have benefited more from the longer wait. Unlike Pfizer and Moderna, which are made from mRNA, Johnson & Johnson's is made from a modified cold virus. It may be important to give the immune system more time to return to a resting state before getting this type of vaccine. Tags: COVIDVACCINE VACCINEJOHNSON VACCINEBOOSTER
Pfizer CEO says fourth Covid vaccine doses may be needed sooner than expected due to omicron “When we see real world data will determine if the omicron is well covered by the third dose and for how long,” Pfizer CEO Albert Bourla told CNBC. “And the second point, I think we will need a fourth dose,” Bourla said. The Pfizer CEO originally expected a fourth dose 12 months after the third, but he told CNBC it might be needed faster than that.
https://www.smh.com.au/world/north-...rus-attacks-fatty-tissue-20211209-p59g8w.html COVID obesity fears as study finds the coronavirus attacks fatty tissue By Roni Caryn Rabin December 9, 2021 New York: From the start of the pandemic, the coronavirus seemed to target people carrying extra kilos. Patients who were overweight or obese were more likely to develop severe COVID-19 and more likely to die. Although these patients often have health conditions such as diabetes that compound their risk, scientists have become increasingly convinced that their vulnerability has something to do with obesity itself. Now researchers have found that the coronavirus infects both fat cells and certain immune cells within body fat, prompting a damaging defensive response in the body. This undated electron microscope image made available by the US National Institutes of Health in February 2020 shows the Novel Coronavirus SARS-CoV-2, yellow, emerging from the surface of cells, pink, cultured in the lab. Credit:AP “The bottom line is, ‘Oh, my God, indeed, the virus can infect fat cells directly,’” said Philipp Scherer, a scientist who studies fat cells at UT Southwestern Medical Centre in Dallas, who was not involved in the research. “Whatever happens in fat doesn’t stay in fat,” he added. “It affects the neighbouring tissues as well.” The research has not yet been peer-reviewed or published in a scientific journal, but it was posted online in October. If the findings hold up, they may shed light not just on why patients with excess kilos are vulnerable to the virus, but also on why certain younger adults with no other risks become so ill. The study’s authors suggested the evidence could point to new COVID-19 treatments that target body fat. “Maybe that’s the Achilles’ heel that the virus utilises to evade our protective immune responses — by hiding in this place,” said Dr Vishwa Deep Dixit, a professor of comparative medicine and immunology at Yale School of Medicine. America has one of the highest obesity rates in the world. Credit:AP The finding is particularly relevant to the United States, which has one of the highest rates of obesity in the world. Most American adults are overweight, and 42 per cent have obesity. Black, Hispanic, Native American and Alaska Native people in the US have higher obesity rates than white adults and Asian Americans; they have also been disproportionately affected by the pandemic, with death rates roughly double those of white Americans. “This could well be contributing to severe disease,” said Dr Catherine Blish, a professor at Stanford University Medical Centre and one of the report’s two senior authors. “We’re seeing the same inflammatory cytokines that I see in the blood of the really sick patients being produced in response to infection of those tissues.” Body fat used to be thought of as inert, a form of storage. But scientists now know that the tissue is biologically active, producing hormones and immune system proteins that act on other cells, promoting a state of nagging low-grade inflammation even when there is no infection. Inflammation is the body’s response to an invader and sometimes it can be so vigorous that it is more harmful than the infection that triggered it. Fat tissue is composed mostly of fat cells, or adipocytes. It also contains pre-adipocytes, which mature into fat cells, and a variety of immune cells, including a type called adipose tissue macrophages. Blish, with colleagues at Stanford and in Germany and Switzerland, carried out experiments to see if fat tissue obtained from bariatric surgery patients could become infected with the coronavirus, and tracked how various types of cells responded. The fat cells themselves could become infected, the scientists found, yet did not become very inflamed. But certain immune cells called macrophages also could be infected, and they developed a robust inflammatory response. Even stranger, the pre-adipocytes were not infected but contributed to the inflammatory response. (The scientists did not examine whether particular variants were more destructive in this regard than others.) The research team also obtained fat tissue from the bodies of European patients who had died of COVID-19 and discovered the coronavirus in fat near various organs. The idea that adipose tissue might serve as a reservoir for pathogens is not new, Dixit said. Body fat is known to harbour a number of them, including HIV and the influenza virus. The coronavirus appears to be able to evade the body fat’s immune defences, which are limited and incapable of fighting it effectively. A man whose ideal weight is 77 kilograms but who weighs 113 kilos is carrying a substantial amount of fat in which the virus may “hang out”, replicate and trigger a destructive immune system response, said Dr David Kass, a professor of cardiology at Johns Hopkins. “If you really are very obese, fat is the biggest single organ in your body,” Kass said. The coronavirus “can infect that tissue and actually reside there,” he said. “Whether it hurts it, kills it or at best, it’s a place to amplify itself — it doesn’t matter. It becomes kind of a reservoir.” A nurse holds the hand of a COVID patient in intensive care at St. Luke’s Boise Medical Centre in Boise, Idaho, in August 2021. Credit:AP As the inflammatory response snowballs, cytokines trigger even more inflammation and the release of additional cytokines. “It’s like a perfect storm,” Kass said. Blish and her colleagues speculated that infected body fat may even contribute to long COVID-19, a condition describing troublesome symptoms like fatigue that persist for weeks or months after recovery from an acute episode. The data also suggest that COVID-19 vaccines and treatments may need to consider the patient’s weight and fat stores. “This paper is another wake-up call for the medical profession and public health to look more deeply into the issues of overweight and obese individuals, and the treatments and vaccines we’re giving them,” said Barry Popkin, a professor of nutrition at University of North Carolina at Chapel Hill, who has studied the heightened risk that COVID-19 poses to those with obesity. “We keep documenting the risk they have, but we still aren’t addressing it,” Popkin said. This article originally appeared in The New York Times.
There are medicines for other illnesses that already do this very effectively. The science of the Covid vaccines already understands the importance of this which is why adults being vaccinated are given a different dose than children aged 12 to 18... they then are given a different dose than children aged 5 - 11. Different aspects of our immune system put up an immune response differently depending upon our age and body/fat index. The latter is very important in the proper dose for adults to make vaccines and antiviral drug treatments more effective and it differentiates how people recover after being affected with Covid. There are other factors too that I wouldn't be surprise to see if its being researched in adults that smoke or have an underlying medical condition involving their respiratory system (e.g. asthma). All the above is why different countries are more impacted or less impacted by a Covid infection, hospitalization and death. Thus, don't be surprised in the near future that when we go to get a Covid vaccine...they also start to height, weight, and other measurements in a survey in research to fine-tune future vaccinations in the population to make the vaccines more effective against new Variants of Concern. wrbtrader
Of course you are posting this after a bunch of data has come out out of South Africa indicating that prior infection does not appear to prevent Omicron infection. You really should keep up with the news.