For certain we know in two weeks what the immediate future is for Covid. Stores are jam packed, as are restaurants and the beaches. Picnics and yard parties everywhere. Social distancing not being practiced all that much. We either see a dramatic spike in the rate of infection, closely followed by a big jump in deaths, or we don't. We'll know with certainty by the first weekend of June. No spike means all lockdown should end immediately, coast to coast. We get a significant spike, then it's going to be a long summer of economic devastation. All bets are off for a Trump reelection. The future will be entirely in the hands of biotechnology and how quickly we can adjust to living with a Covid death rate much higher than the norm for a not so seasonal virus. Two weeks we know.
I agree and I would/could be one of them. I am taking vitamins, I think I have the treatment, bring it on baby! The fuck is going to live in fear. Now if there was a vaccine in the short term (let's say 4-6 weeks away), I would behave differently, but I am not going to wait 18 months, what may never come. People have to realize 2 things: 1. We are not the same or equal concerning the virus and our response to it. So we shouldn't be treated the same. 2. This thing is here to stay or some variant of it, so we have to get used to it.
By the way no real lock down should last more than 3 weeks. In 2 weeks the symptoms should show up and in 7-10 days more people can be treated. So 3 weeks after the lock down numbers should go down if the lock down is not half assed.
I expect an increase in infections... especially with testing increasing. For me, I would re evaluate what I have concluded if we have an unusually high increase in hospitalization and death in the low risk group. (Out of proportion to the amount exposed.) Infections in the low risk group would probably be good for the country.
Absolutely. During the past 72 hours tens of millions have been out gallivanting with many millions of others we know are in the "silent" killer group. Infections should go up quite a bit, but we'll see what happens with hospitalization and death. If we're no better off than we were 5 to 6 weeks ago both hospitalized and dying should escalate rapidly in the next few days. If it doesn't, we know the worst of it is past.
From another thread. Infection Fatality Rate is currently looking like .3% by the CDC. What happens when you remove pre existing... https://www.cdc.gov/coronavirus/2019-ncov/hcp/planning-scenarios.html
from another thread, CDC carrying Donnie's water: https://www.elitetrader.com/et/thre...sed-by-extended-shutdown.345186/#post-5109105
you old favorite attack the messenger rather than the message post. the only argument worth having is if the data is accurate... are you saying something is wrong with the data?
T cells found in COVID-19 patients ‘bode well’ for long-term immunity By Mitch LeslieMay. 14, 2020 , 9:00 PM Science’s COVID-19 reporting is supported by the Pulitzer Center. Immune warriors known as T cells help us fight some viruses, but their importance for battling SARS-CoV-2, the virus that causes COVID-19, has been unclear. Now, two studies reveal infected people harbor T cells that target the virus—and may help them recover. Both studies also found some people never infected with SARS-CoV-2 have these cellular defenses, most likely because they were previously infected with other coronaviruses. “This is encouraging data,” says virologist Angela Rasmussen of Columbia University. Although the studies don’t clarify whether people who clear a SARS-CoV-2 infection can ward off the virus in the future, both identified strong T cell responses to it, which “bodes well for the development of long-term protective immunity,” Rasmussen says. The findings could also help researchers create better vaccines. The more than 100 COVID-19 vaccines in development mainly focus on another immune response: antibodies. These proteins are made by B cells and ideally latch onto SARS-CoV-2 and prevent it from entering cells. T cells, in contrast, thwart infections in two different ways. Helper T cells spur B cells and other immune defenders into action, whereas killer T cells target and destroy infected cells. The severity of disease can depend on the strength of these T cell responses. Using bioinformatics tools, a team led by Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute for Immunology, predicted which viral protein pieces would provoke the most powerful T cell responses. They then exposed immune cells from 10 patients who had recovered from mild cases of COVID-19 to these viral snippets. All of the patients carried helper T cells that recognized the SARS-CoV-2 spike protein, which enables the virus to infiltrate our cells. They also harbored helper T cells that react to other SARS-CoV-2 proteins. And the team detected virus-specific killer T cells in 70% of the subjects, they report today in Cell. “The immune system sees this virus and mounts an effective immune response,” Sette says. The results jibe with those of a study posted as a preprint on medRxiv on 22 April by immunologist Andreas Thiel of the Charité University Hospital in Berlin and colleagues. They identified helper T cells targeting the spike protein in 15 out of 18 patients hospitalized with COVID-19. The teams also asked whether people who haven’t been infected with SARS-CoV-2 also produce cells that combat it. Thiel and colleagues analyzed blood from 68 uninfected people and found that 34% hosted helper T cells that recognized SARS-CoV-2. The La Jolla team detected this crossreactivity in about half of stored blood samples collected between 2015 and 2018, well before the current pandemic began. The researchers think these cells were likely triggered by past infection with one of the four human coronaviruses that cause colds; proteins in these viruses resemble those of SARS-CoV-2. The results suggest “one reason that a large chunk of the population may be able to deal with the virus is that we may have some small residual immunity from our exposure to common cold viruses,” says viral immunologist Steven Varga of the University of Iowa. However, neither of the studies attempted to establish that people with crossreactivity don’t become as ill from COVID-19. Before these studies, researchers didn’t know whether T cells played a role in eliminating SARS-CoV-2, or even whether they could provoke a dangerous immune system overreaction. “These papers are really helpful because they start to define the T cell component of the immune response,” Rasmussen says. But she and other scientists caution that the results do not mean that people who have recovered from COVID-19 are protected from reinfection. To spark production of antibodies, vaccines against the virus need to stimulate helper T cells, Crotty notes. “It is encouraging that we are seeing good helper T cell responses against SARS-CoV-2 in COVID-19 cases,” he says. The results have other significant implications for vaccine design, says molecular virologist Rachel Graham of the University of North Carolina, Chapel Hill. Most vaccines under development aim to elicit an immune response against spike, but the La Jolla group’s study determined that T cells reacted to several viral proteins, suggesting vaccines that sic the immune system on these proteins as well could be more effective. “It is important to not just concentrate on one protein,” Graham says. https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity
https://www.theguardian.com/world/2...ers-and-how-are-they-transmitting-coronavirus How does a person become a super-spreader? There are a number of theories, but no definite answer. Some speculate that it is to do with the immune system of the super-spreader, which may not be good at suppressing the virus or alternatively may be so good that they do not feel symptoms themselves so carry on transmitting it to others. But it is likely to be caused by multiple factors, possibly including getting a higher dose of the virus in the first place or being infected with more than one pathogen. One thing seems certain – it is impossible to know who will be a super-spreader and who will not.