Our DB is still down as our source has deprecated the DB. We are migrating now.

Coincidentally Brazil has stopped reporting – https://www.reuters.com/article/us-health-coronavirus-brazil-idUSKBN23D0PW

Interesting take on antigen – https://www.dailymail.co.uk/news/article-8396195/Professor-says-10-people-coronavirus-develop-antibodies.html

“Professor says only 10% of coronavirus patients develop antibodies meaning it may never be possible to measure true scale of pandemic”

“…not everyone who has had the virus will produce detectable antibodies, and may have used a different immune response in order to attack the virus. For example, T cells are one of the first lines of defence and act before antibodies are even needed”

“Surveillance testing suggests that 8.5 per cent of people in England have already had the coronavirus, based on measuring antibodies. But scientists say the true figure is likely to be far higher. “

“If you have a good T cell response, it will protect you against the flu, the cold, or the coronavirus. This immune response declines dramatically over the age of 50 – which fits the people who get ill more quickly with the coronavirus.

‘Antibodies are a clear sign of many other infections. With this coronavirus, it doesn’t appear to be quite as clear.’”

IF true this has a lot of impact. Fatality rates would likely drop dramatically from the low numbers already used for antigen testing. It would also mean the likelihood of mitigation is as likely as stopping the common the cold from occurring.

Another game changing discussion – https://www.post-gazette.com/news/health/2020/06/07/Cholesterol-COVID-19-deaths-study-scripps-research-institute-underlying-conditions/stories/202006040179?q1g

“a study by the Scripps Research Institute has shown that high cholesterol levels in lung tissue may be the key culprit in COVID-19 deaths, especially for those with such underlying chronic conditions as hypertension, diabetes and cardiovascular disease”

“Using super resolution imaging, the Scripps team — led by Scott Hansen, an associate professor in Scripps’ Department of Molecular Medicine — documented a chain-reaction process that begins with high cholesterol levels and ends with a cytokine storm that fills the lungs with fluid.”

Cells use cholesterol for many purposes, including mounting an immune response against SARS-CoV-2, the virus that causes COVID-19.

But COVID-19’s potentially lethal process begins with a high number of low-density lipoproteins or LDL — often referred to as bad cholesterol — circulating in the blood, accumulating in tissue, and signaling cells of their presence.

The cells react by altering their membranes to make entry points and position receptors for cholesterol to enter.

But that process simultaneously makes available twice the number of locations for the virus optimally to dock with ACE2, which is the enzyme on the cell membrane that serves as an entry point for the virus to be drawn into the cell.

Excess cholesterol also helps the virus to bind with ACE2, providing an easy access portal into the cell.

The problem is that the high virus count inside the cell spawns development of many cytokines — the proteins (peptides) that generate an inflammatory immune response against the SARS-CoV-2 virus inside and outside the cell.

The role that high cholesterol plays in that process, if confirmed, would clarify why obesity, hypertension, respiratory and cardiovascular diseases, and diabetes represent such high risk factors for COVID-19 severity and mortality.

“As cholesterol increases with age and inflammation [e.g. smoking and diabetes], the cell surface is coated with viral entry points and optimally assembled viral entry proteins,” the study says.

It’s well established that cholesterol levels generally increase with age — a point that runs parallel with the age-related severity and mortality rate from COVID-19.

“Understanding why young people are resistant in this class of [corona] viruses could help both healthy and chronically ill adults avoid severe symptoms of COVID19,” the study says. “Understanding these differences is critical for safeguarding the vulnerable and guiding effective policy and treatments.”

Based on cholesterol levels, age and inflammation levels, the study says, “we build a cholesterol dependent model for COVID19 lethality in elderly and the chronically ill.”

““People with a really poor diet with high cholesterol over a long period of time are sitting ducks for the virus.”

Giovanna Rappocciolo, an assistant professor in the University of Pittsburgh Graduate School of Public Health, Department of Infectious Diseases and Microbiology, has studied cholesterol’s impact on the human immunodeficiency virus and found the Scripps study to be plausible.

She said the Scripps study, however, is “rough around the edges” — a situation that could be remedied through the peer-review process.

But the study also is important, she said, in noting that COVID-19 potentially could be treated by manipulating cholesterol levels, with drugs already available.

For now, she said, “using available drugs directed to reduce cell cholesterol levels could represent an important line of inquiry.”

“Generally speaking, this is a very interesting and valid study that needs some more work,” said Ms. Rappocciolo, who holds a Ph.D in immunology. “It opens up a new field of study to try to exploit these pathways to stop the infection of cells.”

I find it interesting the first response to solving this is using a drug – versus just changing your diet. Did you know CHOLESTERAL IS ONLY FOUND IN ANIMAL PRODUCTS? A way to tell if something is vegan look to see if there is 0 cholesterol. This is very enlightening to figure out why young people are so much better – cholesterol is a perfect rationale for this.

Yesterday and today we now want to not be a male balding, Type A, High cholestral diet if our goal is to not die from Covid.