And all I have to do to prove it…is simply reach out my hand…and touch it.
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As we explore the highly germane domains of “PPE Talk”, my Little Blue Blanket totally rules ! 
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To put it in terms I can understand…this is not good. Frightening to say the least.
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You had it?
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(The Lancet, May 15, 2020):
“Who is most likely to be infected with SARS-CoV-2?”
Despite the daily updates on number of cases, hospital admissions, and deaths around the world and the increasing number of hospital-based case series, some of the fundamental information about how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spreads in the population and who is really at risk of both infection and severe consequences is still missing. …
… Of 3802 tests, 587 (15·4%) were positive for SARS-CoV-2. Prevalence of infection was less than 5% in patients younger than 18 years (23 patients were positive [4·6%] of 499 tested) but almost four times as high in people aged 40 years or older (480 [18·2%] of 2637). After adjustment for other factors, infection risk was higher among men than women (odds ratio [OR] 1·55 [95% CI 1·27–1·89]), in black people than white people (OR 4·75 [2·65–8·51]), and in people with obesity than normal-weight people (1·41 [1·04–1·91]). Infection risk was also higher in those living in more deprived or in urban versus rural locations. Surprisingly, household size did not significantly affect infection risk. Among chronic comorbidities examined, only those with chronic kidney disease had an increased risk of infection, whereas the risk in active smokers was around half that observed in never smokers. …
… this study suggests that sex differences in poor outcomes from COVID-19 are at least in part related to differential infection susceptibility. The role of ethnicity in greater susceptibility and poorer prognosis is a growing concern and deserving of further study. It seems that most comorbidities (except chronic kidney disease), although important for predicting prognosis, do not have a major part in susceptibility to infection. Regarding the results on smoking, it is likely that they could reflect consulting patterns and higher rates of non-infectious cough among smokers than non-smokers. Smoking seems important as a risk factor for poor prognosis, but studies are conflicting, and the association merits further investigation. The one major modifiable risk factor is obesity, which presents a double problem of increasing susceptibility to infection, as well as the risk of severe consequences.
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The graphic charts below were previously published on May 4, 2020:
14 days later, the estimate of US deaths by August 4, 2020 has increased by 35,321 to latest (May 18, 2020) estimate of 196,642 deaths [ 121,081 - 338,950 ], increasing in total estimated number (on average) by 2,523 deaths every day. That is a +21.90% increase in estimated deaths (since May 4, 2020). In the period of March 4, 2020 - August 4, 2020, an average of 141,854 people are estimated to have become infected every day (that’s 5,911 people infected per hour, or 99 people per minute). 
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(Vox, May 16, 2020):
Preliminary results from a well-designed survey of antibody presence among Spaniards suggest that even as the Spanish outbreak exploded and then was brought under control, only 5 percent of the country’s population has been infected with the coronavirus so far. …
… Covid-19 optimists have pointed to a couple of flawed studies from California, both of which suggested that infection has been much more widespread than commonly assumed, and that consequently, the virus is much less lethal than commonly assumed.
The new Spanish survey (which is still underway) has a much higher-quality research design, and unfortunately, it has a much less reassuring result at this point: Only about 5 percent of people in the study have tested positive for Covid-19 antibodies, suggesting that just 5 percent of the Spanish population has had the coronavirus.
The study was carried out by the Carlos III Institute for Health and Spain’s National Statistics Institute, and thanks to that official backing, researchers were able to obtain samples from more than 36,000 randomly selected households across the country. (They tested nearly 70,000 people in total, meaning it’s a robust sample.) And precisely because the outbreak in Spain has been very bad, there was a much lower risk of the preliminary results being twisted by false positives.
What they found was that about 10-14 percent of the population in and around Madrid has antibodies, along with about 7 percent of the population of Barcelona and smaller numbers outside of Spain’s two major cities. Across the country, it averages out to roughly 5 percent.
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With the genomic sequence, we were off to the races,” says Anthony Fauci, head of the US National Institute of Allergy and Infectious Diseases.
Ahead of an outbreak, it is impossible to predict what virus is coming next. “Instead of trying to develop a vaccine for a pathogen [virus], which is kind of tough . . . you have to try to develop platform technology to facilitate rapid development of vaccines,” Dr Fauci says.
One such platform is Moderna’s production of vaccines based on viral genetics. By February 7, the company’s scientists had manufactured dozens of doses of clinical grade vaccine, enough for the NIH’s early trial in healthy volunteers, scheduled for April. Researchers then had to wait to see if the batch was sterile, giving any bacteria two weeks to grow. Staff quickly completed other necessary tests in case they needed to start again. Fortunately everything went right, every step of the way.
Despite the rush, vaccine experts say that it will be at least a year to 18 months before one is available for widespread use — typically the process takes several years.
After an initial safety trial, there must now be larger clinical studies to test efficacy. Meanwhile, the epidemic is likely to spread across the world, killing many more thousands or even millions of people.
The work of Moderna and its competitors may only be useful if coronavirus comes back again in another outbreak next year or becomes an endemic infection like seasonal flu. With commercial returns uncertain, industry’s response to epidemics carries elements of corporate social responsibility and excitement in meeting a scientific challenge — though sometimes there is a big pay-off, as Wellcome, later part of GlaxoSmithKline, found with its pioneering zidovudine Aids drugs in the 1980s.
Moderna may be the first to test in humans but many more are trying to create a vaccine, from big pharma companies such as Johnson & Johnson and Sanofi to academics including those at the University of Queensland. Genetic sequencing and new structural biology tools are transforming vaccine development, allowing scientists to create their own synthetic versions of viruses — rather than waiting for someone to FedEx a specimen.
This is opening the field to new players, says Paul Duprex, director of the Center for Vaccine Research at the University of Pittsburgh. “You have more people thinking about the problems in different ways, not limited by having to grow the virus in a particular lab,” he adds. Shane Crotty, a professor at La Jolla Institute for Immunology in California, says one approach being pursued is to search for the best immune response in a patient with the disease — and try to copy it so the vaccine can elicit a more robust defence. “That’s been the biggest, most exciting advance in the past five years. Several of those have gone into human trials looking good. It’s a much more sophisticated way to make a vaccine,” he adds.
Excerpt from web article; The Financial Times March 5 2020
Hannah Kuchler in Norwood and Clive Cookson and Sarah Neville in London
Coronavirus and the $2bn race to find a vaccine
The start-up leading the US fight to immunise people
will need state backing and up to 18 months to make the venture work
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The source reference to Doug’s posted quoted text (above) is:
(Financial Times, March 4, 2020):
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I’m still learning mark up HTML. I got called away and haven’t been able to site it yet. I got called away from my pc and am still trying to figure out how. I thought it was a good piece.
I’m simply trying to contribute (and having a doozy of a deal figuring out what this forum can do or what I’m messing up)
It’s just my opinion.
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(STAT, May 19, 2020):
“Vaccine experts say Moderna didn’t produce data critical to assessing Covid-19 vaccine”
Several vaccine experts asked by STAT concluded that, based on the information made available by the Cambridge, Mass.-based company, there’s really no way to know how impressive - or not - the vaccine may be.
While Moderna blitzed the media, it revealed very little information - and most of what it did disclose were words, not data. That’s important: If you ask scientists to read a journal article, they will scour data tables, not corporate statements. With science, numbers speak much louder than words.
Even the figures the company did release don’t mean much on their own, because critical information - effectively the key to interpreting them - was withheld. Experts suggest we ought to take the early readout with a big grain of salt. …
… Moderna’s approach to disclosure:
The company has not yet brought a vaccine to market, but it has a variety of vaccines for infectious diseases in its pipeline. It doesn’t publish on its work in scientific journals. What is known has been disclosed through press releases. That’s not enough to generate confidence within the scientific community.
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(Science Magazine, May 19, 2020):
“Why do some COVID-19 patients infect many others, whereas most don’t spread the virus at all?”
Most of the discussion around the spread of SARS-CoV-2 has concentrated on the average number of new infections caused by each patient. Without social distancing, this reproduction number “R” is about three. But in real life, some people infect many others and others don’t spread the disease at all. In fact, the latter is the norm, Lloyd-Smith says: “The consistent pattern is that the most common number is zero. Most people do not transmit.”
That’s why in addition to R, scientists use a value called the dispersion factor (k), which describes how much a disease clusters. The lower k is, the more transmission comes from a small number of people. … Estimates of k for SARS-CoV-2 vary. … in a recent preprint, Adam Kucharski of LSHTM estimated that k for COVID-19 is as low as 0.1. “Probably about 10% of cases lead to 80% of the spread,” Kucharski says. … If k is really 0.1, then most chains of infection die out by themselves and SARS-CoV-2 needs to be introduced undetected into a new country at least four times to have an even chance of establishing itself, Kucharski says. …
… Why coronaviruses cluster so much more than other pathogens is “a really interesting open scientific question,” says Christophe Fraser of the University of Oxford, who has studied superspreading in Ebola and HIV. Their mode of transmission may be one factor. SARS-CoV-2 appears to transmit mostly through droplets, but it does occasionally spread through finer aerosols that can stay suspended in the air, enabling one person to infect many. Most published large transmission clusters “seem to implicate aerosol transmission,” Fraser says.
Individual patients’ characteristics play a role as well. Some people shed far more virus, and for a longer period of time, than others, perhaps because of differences in their immune system or the distribution of virus receptors in their body. …
… The factor scientists are closest to understanding is where COVID-19 clusters are likely to occur. “Clearly there is a much higher risk in enclosed spaces than outside,” Althaus says. Researchers in China studying the spread of the coronavirus outside Hubei province - ground zero for the pandemic - identified 318 clusters of three or more cases between 4 January and 11 February, only one of which originated outdoors. A study in Japan found that the risk of infection indoors is almost 19 times higher than outdoors. …
… Some situations may be particularly risky. Meatpacking plants are likely vulnerable because many people work closely together in spaces where low temperature helps the virus survive. But it may also be relevant that they tend to be loud places, Knight says. The report about the choir in Washington made her realize that one thing links numerous clusters: They happened in places where people shout or sing. … Timing also plays a role. Emerging evidence suggests COVID-19 patients are most infectious for a short period of time. …
… studying large COVID-19 clusters is harder than it seems. Many countries have not collected the kind of detailed contact tracing data needed. And the shutdowns have been so effective that they also robbed researchers of a chance to study superspreading events. … The research is also prone to bias … Clusters of mostly asymptomatic infections may be missed altogether. … Privacy is another concern.
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(Josh Bloom, ACSH, May 20, 2020):
“The Real Problem With Hydroxychloroquine Is Nothing New - It’s Chemistry”
… the primary concern about the drug is cardiac toxicity, specifically arrhythmias. … hERG is a gene that makes a protein that is part of the potassium ion channel. So, when a drug or chemical binds to the hERG protein it can block that channel, which disrupts the timing of the flow of ions in and out of the cell. The degree of binding determines the amount of disruption. Given that the heart is controlled by regular electrical impulses it should not be surprising that heart cells have ion channels or that messing with them disrupts the timing.
What happens when the timing of your heart screws up? Arrhythmias - irregular heartbeats. If the ventricular contraction speeds up it is called ventricular tachycardia, which is something you’d be wise to leave off your Christmas wish list, especially if you would like to see New Year’s Eve. Ventricular tachycardia can cause the heart to beat uncontrollably or stop beating entirely. All of this from tiny little gates in cell membranes that decide which ion goes where and when. …
… When drugs block the hERG (potassium) channel it can result in a condition called QT prolongation or Long QT syndrome (LQTS), which results in the heart beating quickly and erratically. … Sometimes QT elongation can cause a dangerous condition called “torsades de pointes” (French for “twisting of points”) where the heart’s two lower chambers (ventricles), beat faster than the upper chambers (atria). It is the mismatch of the timing of the lower and upper chamber that causes the problem. …
… Hydroxychloroquine does have some cardiac risk because the molecule is known to block potassium channels. So does azithromycin. When they are combined, the risk goes up; maybe by a lot.
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Let me know if you need any help.
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Not at all required to do what you did (and I do). Just copy/paste article text/graphics; identify sources.
(Ars Technica, May 19, 2020):
KCDC researchers examined 285 cases that had previously recovered from COVID-19 but then tested positive again. The patients tested positive again anywhere from one to 37 days after recovering from their first infection and being discharged from isolation. The average time to a second positive was about 14 days. Of those cases, researchers checked for symptoms in 284 of them. They found that 126 (about 48 percent) did indeed have symptoms related to COVID-19.
But none of them seemed to have spread the infection. KCDC investigated 790 people who had close contact with the 285 cases and found that none of them had been infected by the “re-positive” cases. … additional testing of 108 “re-positive” cases found that none of them were shedding infectious virus. …
… If someone has SARS-CoV-2 genetic material in their airways, they’ve been infected. That said, having genetic material doesn’t necessarily mean that the person still has an active infection and infectious viral particles. They may just have lingering fragments of genetic material from destroyed viral particles. That appears to be the case here. When KCDC researchers tried to isolate and grow whole, infectious particles of SARS-CoV-2 from the 108 cases they were able to test - all 108 were negative for whole virus. …
… when they did further blood work on 23 of the re-positive cases, nearly all of them (96 percent) had neutralizing antibodies against SARS-CoV-2. This hints that they may have some immunity to a reinfection with the virus. It’s unclear what was causing symptoms in many of the patients. A few cases tested positive for other respiratory viruses, but many did not.
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So far it’s only in vitro, “discovered” by researchers with companies that might stand to profit, not peer-reviewed, but fear not - this “GRAS adjunct therapy” would have the advantage of not being enjoyable !
(Preprints Org, April 19, 2020):
What if my juice tastes like weed, man ? What then ? Am I grandfathered in ?
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Word to all Mink farmers. Lock-down all of your Felines until further notice (Cat > Mink > Human ?). 
(The Hill, May 20, 2020):
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and dogs are still safe, for now. maybe… 
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