Editor Note
{If you are like me and have been watching the presented "news" about the corona virus, you to have been at a loss to understand why all of a sudden there has been a spike in covid-19 cases.
There are 2 main reasons for sudden increase in covid-19 cases in certain areas of the nation.
A POSITIVE COORONA VIRUS TEST DOES NOT MEAN YOU HAVE ACTUALLY HAD COVID-19. The corona virus death rate is not increasing.
Read the 2 articles below for explainations.}
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ANOTHER CDC CHART THE MEDIA DOESN'T WANT YOU TO SEE. IT SHOWS COVID DEATHS ARE FALLING, NOT SPIKING. See the chart for yourself on the CDC site:
https://www.cdc.gov/nchs/nvss/vsrr/covid_weekly/index.htm
This is the updated one that just came out. They keep telling us all these new cases will eventually translate in an upward spike in deaths. So far ... nope.
The spike in cases is likely because we are testing at a rate 23x higher than we were in April, and people no longer need active symptoms and a referral from their doctor to get the test. They can just schedule at time at CVS.
What is likely happening is that we are detecting mild and asymptomatic cases that have been in the background throughout this, but which we haven't detected before and then people are recovering.
If cases of the virus were truly exploding, deaths would be, too. Again, so far, they're not.
(Can't wait to see how facebook "fact-checks" this. Think they'll say the CDC is wrong in order to debunk this chart right off the CDC's page? That would make my day, actually. Facebook's left-wing fact-checkers lie.)
{The antibody test is only 50% accurate. This test is also given but it is not accurate because if you have had a cold in the past it will show a FALSE POSITIVE.
This test is also counted as a new corona virus case.
In review:
(1) The first reason there has been a spike in the number of corona virus cases.
Testing is 23 times higher and these new case include false positive data from antibody tests that are less than 50% accurate!
Coronavirus mutation has taken over the world. Scientists are trying to understand why.
When the first coronavirus cases in Chicago appeared in January, they bore the same genetic signatures as a germ that emerged in China weeks before.
But as Egon Ozer, an infectious-disease specialist at the Northwestern University Feinberg School of Medicine, examined the genetic structure of virus samples from local patients, he noticed something different.
A change in the virus was appearing again and again. This mutation, associated with outbreaks in Europe and New York, eventually took over the city. By May, it was found in 95% of all the genomes Ozer sequenced.
At a glance, the mutation seemed trivial. About 1,300 amino acids serve as building blocks for a protein on the surface of the virus. In the mutant virus, the genetic instructions for just one of those amino acids - number 614 - switched in the new variant from a "D" (shorthand for aspartic acid) to a "G" (short for glycine).
"G" hasn't just dominated the outbreak in Chicago - it has taken over the world. Now scientists are racing to figure out what it means.
At least four laboratory experiments suggest that the mutation makes the virus more infectious, although none of that work has been peer-reviewed. Another unpublished study led by scientists at Los Alamos National Laboratory asserts that patients with the G variant actually have more virus in their bodies, making them more likely to spread it to others.
The mutation doesn't appear to make people sicker, but a growing number of scientists worry that it has made the virus more contagious.
"The epidemiological study and our data together really explain why the [G variant's] spread in Europe and the U.S. was really fast," said Hyeryun Choe, a virologist at Scripps Research and a lead author of an unpublished study on the G variant's enhanced infectiousness in laboratory cell cultures. "This is not just accidental."
"The bottom line is, we haven't seen anything definitive yet," said Jeremy Luban, a virologist at the University of Massachusetts Medical School.
The scramble to unravel this mutation mystery embodies the challenges of science during the coronavirus pandemic. With millions of people infected and thousands dying every day around the world, researchers must strike a high-stakes balance between getting information out quickly and making sure that it's right.
SARS-CoV-2, the novel coronavirus that causes the disease covid-19, can be thought of as an extremely destructive burglar. Unable to live or reproduce on its own, it breaks into human cells and co-opts their biological machinery to make thousands of copies of itself.
That leaves a trail of damaged tissue and triggers an immune system response that for some people can be disastrous.
This replication process is messy. Even though it has a "proofreading" mechanism for copying its genome, the coronavirus frequently makes mistakes, or mutations. The vast majority of mutations have no effect on the behavior of the virus.
But since the virus's genome was first sequenced in January, scientists have been on the lookout for changes that are meaningful. And few genetic mutations could be more significant than ones that affect the spike protein - the virus's most powerful tool.
This protein attaches to a receptor on respiratory cells called ACE2, which opens the cell and lets the virus slip inside. The more effective the spike protein, the more easily the virus can break into the bodies of its hosts. Even when the original variant of the virus emerged in Wuhan, China, it was obvious that the spike protein on SARS-CoV-2 was already quite effective.
But it could have been even better, said Choe, who has studied spike proteins and the way they bind to the ACE2 receptor since the severe acute respiratory syndrome outbreak in 2003.
The spike protein for SARS-CoV-2 has two parts that don't always hold together well. In the version of the virus that arose in China, Choe said, the outer part - which the virus needs to attach to a human receptor - frequently broke off. Equipped with this faulty lock pick, the virus had a harder time invading host cells.
"I think this mutation happened to compensate," Choe said.
Studying both versions of the gene using a proxy virus in a petri dish of human cells, Choe and her colleagues found that viruses with the G variant had more spike proteins, and the outer parts of those proteins were less likely to break off. This made the virus approximately 10 times more infectious in the lab experiment.
The mutation does not seem to lead to worse outcomes in patients. Nor did it alter the virus's response to antibodies from patients who had the D variant, Choe said, suggesting that vaccines being developed based on the original version of the virus will be effective against the new strain.
Choe has uploaded a manuscript describing this study to the website BioRxiv, where scientists can post "preprint" research that has not yet been peer reviewed. She has also submitted the paper to an academic journal, which has not yet published it.
The distinctive infectiousness of the G strain is so strong that scientists have been drawn to the mutation even when they weren't looking for it.
Neville Sanjana, a geneticist at the New York Genome Center and New York University, was trying to figure out which genes enable SARS-CoV-2 to infiltrate human cells. But in experiments based on a gene sequence taken from an early case of the virus in Wuhan, he struggled to get that form of the virus to infect cells.
Then the team switched to a model virus based on the G variant.
"We were shocked," Sanjana said. "Voilà! It was just this huge increase in viral transduction." They repeated the experiment in many types of cells, and every time the variant was many times more infectious.
Their findings, published as a preprint on BioRxiv, generally matched what Choe and other laboratory scientists were seeing.
But the New York team offers a different explanation as to why the variant is so infectious. Whereas Choe's study proposes that the mutation made the spike protein more stable, Sanjana said experiments in the past two weeks, not yet made public, suggest that the improvement is actually in the infection process.
He hypothesized that the G variant is more efficient at beginning the process of invading the human cell and taking over its reproductive machinery.
Luban, who has also been experimenting with the D614G mutation, has been drawn to a third possibility: His experiments suggest that the mutation allows the spike protein to change shape as it attaches to the ACE2 receptor, improving its ability to fuse to the host cell.
Different approaches to making their model virus might explain these discrepancies, Luban said. "But it's quite clear that something is going on."
---
Although these experiments are compelling, they're not conclusive, said Kristian Andersen, a Scripps virologist not involved in any of the studies. The scientists need to figure out why they've identified different mechanisms for the same effect.
All the studies still have to pass peer review, and they have to be reproduced using the real version of the virus.
Even then, Andersen said, it will be too soon to say that the G variant transmits faster among people.
Cell culture experiments have been wrong before, noted Anderson Brito, a computational biologist at Yale University. Early experiments with hydroxychloroquine, a malaria drug, hinted that it was effective at fighting the coronavirus in a petri dish. The drug was touted by President Trump, and the Food and Drug Administration authorized it for emergency use in hospitalized covid-19 patients. But that authorization was withdrawn this month after evidence showed that the drug was "unlikely to be effective" against the virus and posed potential safety risks.
So far, the biggest study of transmission has come from Bette Korber, a computational biologist at Los Alamos National Laboratory who helped build one of the world's biggest viral genome databases for tracking HIV. In late April, she and colleagues at Duke University and the University of Sheffield in Britain released a draft of their work arguing that the mutation boosts transmission of the virus.
Analyzing sequences from more than two dozen regions across the world, they found that most places where the original virus was dominant before March were eventually taken over by the mutated version.
This switch was especially apparent in the United States: Ninety-six percent of early sequences here belonged to the D variant, but by the end of March, almost 70% of sequences carried the G amino acid instead.
The British researchers also found evidence that people with the G variant had more viral particles in their bodies.
Although this higher viral load didn't seem to make people sicker, it might explain the G variant's rapid spread, the scientists wrote. People with more virus to shed are more likely to infect others.
The Los Alamos draft drew intense scrutiny when it was released in the spring, and many researchers remain skeptical of its conclusions.
"There are so many biases in the data set here that you can't control for and you might not know exist," Andersen said. In a time when as many as 90% percent of U.S. infections are still undetected and countries with limited public health infrastructure are struggling to keep up with surging cases, a shortage of data means "we can't answer all the questions we want to answer."
Pardis Sabeti, a computational biologist at Harvard University and the Broad Institute, noted that the vast majority of sequenced genomes come from Europe, where the G variant first emerged, and the United States, where infections thought to have been introduced by travelers from Europe spread undetected for weeks before the country shut down.
This could at least partly explain why it appears so dominant.
The mutation's success might also be a "founder effect," she said. Arriving in a place like Northern Italy - where the vast majority of sequenced infections are caused by the G variant - it found easy purchase in an older and largely unprepared population, which then unwittingly spread it far and wide.
And as studies on the D614G mutation accumulate, researchers are starting to be convinced of its significance.
"I think that slowly we're beginning to come to a consensus," said Judd Hultquist, a virologist at Northwestern University.
Solving the mystery of the D614G mutation won't make much of a difference in the short term, Andersen said. "We were unable to deal with D," he said. "If G transmits even better, we're going to be unable to deal with that one."
But it's still essential to understand how the genome influences the behavior of the virus, scientists say. Identifying emerging mutations allows researchers to track their spread. Knowing what genes affect how the virus transmits enables public health officials to tailor their efforts to contain it.
Once therapeutics and vaccines are distributed on a large scale, having a baseline understanding of the genome will help pinpoint when drug resistance starts to evolve.
"Understanding how transmissions are happening won't be a magic bullet, but it will help us respond better," Sabeti said. "This is a race against time."
In review:
(2) The second reason covid-19/Coronavirus/Wuhanvirus/china virus/congfluvirus is spreading faster is BECAUSE IT HAS MUTATED AND SPREADS FASTER.
People with the G variant have more viral particles in their bodies.
The D614G mutation, has been drawn to a third possibility: Experiments suggest that the mutation allows the spike protein to change shape as it attaches to the ACE2 receptor, improving its ability to fuse to the host cell.
The mutation made the spike protein more stable.
The G variant is more efficient at beginning the process of invading the human cell and taking over its reproductive machinery.
The mutation does not seem to lead to worse outcomes in patients.
Nor did it alter the virus's response to antibodies from patients who had the D variant, Choe said, suggesting that vaccines being developed based on the original version of the virus will be effective against the new strain.
Bonus Editor Note
Solving the mystery of the D614G mutation won't make much of a difference in the short term, Andersen said. "We were unable to deal with D," he said. "If G transmits even better, we're going to be unable to deal with that one."
The government has been trying to stop the spread of the covid-19 since March 2019.
Testing has become a big deal when dealing with the covid-19.
The test for the covid-19 is flawed and often not accurate.
If you rely on a covid-19 test for detection of your personal case of infection you are relying on a test that is inconclusive at best.
It is known also that if you have had the corona virus and it was a mild case you can get the virus again.
This is because your body did not build up enough antibodies the first time to keep you from getting the covid-19 virus again.
Some people will get it again, some will not and some people will not get the covid-19 at all.
The covid-19 variation D that was promoted by the fake news media in April 2020 has continued to spread in spite of all the federal, state and local governments have done.
COVID-19 variation D, HAS CONTINUED TO SPREAD IN SPITE OF SELF ISOLATION, WEARING MASKS , CLEANING SURFACES AND WASHING HANDS ETC!
Covid-19 variation G transmits better and spreads faster.
Covid-19 variation G will also continue to spread in spite of everything the government and you do to protect yourself.
Does this mean no matter what you will get the covid-19 virus?
The only sure way to avoid the covid-19 virus is to not come into contact with the covid-19 virus.
This would mean total isolation from the covad-19, 24-7 365 days a year.
Triple Bonus Editor Note
How to totally avoid getting the covid-19, corona virus, wuhan virus, china virus, kungflu virus.
My various suggestions:
(1) Move to a state where the population is very low.
Least Densely Populated U.S. States
Alaska is by far the least densely populated of the US states and has 1.3 persons per square mile.
The second least densely populated state is Wyoming with six people per square mile.
Montana, Wyoming’s neighbor to the north, has a population density of 7.1 people per square mile.
North Dakota is the 4th least densely populated with 11 people living in every square mile.
South Dakota is similar to North Dakota in population density with just slightly more people per square mile, 11.3.
New Mexico has a population density of 17.2 people per square mile.
Population density in Idaho is 20 people per square mile.
Number 8 on the list is Nebraska with 24.7 people per square mile.
Nevada has 26.3 people per square mile. (Avoid Nevada. the federal government owns 80% of the state; about 1,350 square miles of which are designated as nuclear testing grounds The people who do live here are concentrated in Las Vegas. )
The last state on the list is Kansas with 35.6 people per square mile.
So ya need to consider moving to Alaska where the population is only 1.3 people per square mile.
{If ya run into the 1/3 person you can bet that they have been infected with the covid-19, :) }
Personally I would feel very safe about not getting a case of the covad from anybody if only 1.3 persons live in the square mile area I lived in.
Lets pretend you or I have now moved to Alaska to escape the covid-19 virus.
I am now living in a cabin somewhere out in the bush nowhere near a city.
I will need to fend for myself now.
Fend means to ward off an invader.
The invader is any person who potentially has the covid-19.
That includes the 1.3 person that lives with in 1 mile or less of my cabin.
Keeping this person at bay would not be hard. Just avoid contact by letting this 1.3 person know that you don't want any visitors.
If by a fluke you get some unexpected visitors this would be a problem.
Hunters, tourists or local natives that wander onto your property.
Lets say they knock on your cabin door. If you are inside you can just tell them to get lost.
Lets say one of these unexpected people confront you unexpectedly while you were outside of your cabin.
Hopefully one of these people would be at a distance of at least 6 feet. :)
If not your self isolation will have been compromised.
What next.
Run back to your cabin and self isolate for 14 days.
If you have not gotten the covid-19 after "resetting" yourself now you are ready to go out into the world again.
If you are able to avoid the 1.3 persons per square mile near your cabin until the rest of the nation reaches the 80% herd immunity point this is a good sign.
The 80% herd immunity is the point where the covad-19 will die out because enough people have gotten the virus.
Remember you are in Alaska in the bush and there are 1.3 people near your cabin.
There are people who have gotten the covid-19 virus, mild cases, and their immune systems did not produce enough antibodies to keep them from getting the virus again.
This would mean they are asymptomatic carriers of the covid-19.
Silent carriers of the covid-19.
People with no COVID-19 symptoms may be spreading the disease — but big questions remain about how much they are driving the pandemic.
Being presymptomatic means you’ve been infected and don’t feel any symptoms at the time you get tested, but will develop them later on.
In contrast, asymptomatic people never have any symptoms during the course of their infections at all.
Because you are in the bush out in the middle of nowhere means your live in an area where there will never be 80% herd immunity.
Even though you are self isolated you still will be at risk from that 1.3 neighbour or others infecting you in the future because at some point you will come into contact with another human being.
The only way to be totally safe from getting the covid-19 virus is to never ever come into contact with another human being and hopefully don't pick up a piece of trash etc on your property that has been contaminated with the covid-19.
Or you come into contact with the covid-19 from on some other surface.
This could be something you packed in your bug out bag before you went to alaska to self isolate like a hermit.
Lets say you lived in your cabin in the bush for 20 years and decided to join society again.
You have been covid-19 free for 20 years.
You feel safe now.
You go out into the population again.
You come into contact with a person, 20% of population that has not had the covid-19 virus, and therefore like yourself can become infected with covid-19.
SARS-CoV-2 will most likely settle into the human population, becoming an endemic virus like its coronavirus cousins that are major causes of colds every winter.
SARS-CoV-2 can proliferate at any time of year
If immunity to SARS-CoV-2 is not permanent, it will likely enter into regular circulation.
Much like pandemic influenza, many scenarios lead to SARS-CoV-2 entering into long-term circulation alongside the other human betacoronaviruses (e.g., Fig. 3, A and B), possibly in annual, biennial, or sporadic patterns, over the next 5 years (tables S2 to S4).
Short-term immunity (~40 weeks, similar to HCoV-OC43 and HCoV-HKU1) favors the establishment of annual SARS-CoV-2 outbreaks, whereas longer-term immunity (2 years) favors biennial outbreaks.
{The covid-19 will be around for a few years and seems to be different than the sars-1 virus that has died out.
If this is correct it means unless you live in an isolated cabin in Alaska with no human contact you will be hard pressed to avoid getting the covid-19 because it will come back in a mutated form as does the common cold, it mutates often and thats why you can get it over and over and over.
I keep hearing that everybody will get the covid-19.
No everybody will not get the covid-19.
Some people's immune systems will prevent them from getting the covid-19.
If you are one of these people God has blessed you.
If you have a good immune system you chances of getting the covid-19 I suggest will depend on who you come into contact with that has the covid-19 virus.
The infection various from person to person. Some people have more of the virus in their bodies and can infect people quicker and easier.
Its like a roll of the dice.
It will be a combination of a really good immune system and you coming into contact with people who are not big carriers of the covid-19.
There is no way you can know how big a carrier a person is if he or she has the covid-19.
Therefore there is no way of knowing how to avoid getting the virus from, lets say, a super carrier of the covid-19 virus.
Wearing a mask is not going to protect you.
Even an n95 mask will not totally protect you from breathing in the covid-19 virus.
A cloth mask of any kind is totally useless in protecting you from breathing in the covid-19 into your lungs.
If you go out into the public there are so many factors that come into play that is is impossible to predict how and when you may come into contact with the covid-19.
You don't know who the super covid-19 carrier are.
You could be in walmart for example shopping etc. You stop to look at something and come into contact with a nearby person or group of super carriers of the covid-19.
You think you are safe wearing a useless cloth mask for protection and breathe in the covid-19 from one or more or the super covid-19 carriers.
The bottom line is this:
(1) Not all people will get the covid-19 virus.
(2) Since God is in control of everything it will depend on him if you get it or not.
(3) Humanly speaking if you have a very good immune system you might be able to ward off the covid-19 if you become infected.
(4) If you don't have a very good immune system you will most likely get the covid-19 virus from someone or somewhere.
All this covid-19 testing and mask wearing is not the answer to not getting the covid-19 virus.
The answer is prayer.
Pray and ask the Lord to protect you from getting the covid-19 virus.
Pray for your loved ones also.
Remember its all in God's hands.
If it is his will for you not to get the covid-19 you won't.
If it is his will for you to get the covid-19 you will.
God answers prayers according to his will.
If you don't ask you won't receive according to his will.
____________________________________________
App State professor: physical activity, weight management boost immune system
Remaining healthy a defense against respiratory diseases, COVID-19
physical activity, weight management boost immune system
Moderate-intensity physical activity reduces morbidity and mortality from respiratory illness.
There are two strategies to reduce the
risk for COVID-19, according to Nieman — mitigation activities and the
adoption of lifestyle practices consistent with good immune health, such
as exercising.
Mitigation approaches include the practice of physical distancing, the use of cloth face coverings in community settings when physical distancing cannot be maintained, staying at home when sick and following healthy hygiene practices — handwashing, regularly cleaning surfaces and not sharing physical items with others.
Mitigation approaches include the practice of physical distancing, the use of cloth face coverings in community settings when physical distancing cannot be maintained, staying at home when sick and following healthy hygiene practices — handwashing, regularly cleaning surfaces and not sharing physical items with others.
“Mitigation
measures protect older adults and those with underlying medical
conditions, but lifestyle approaches such as physical activity and
weight management will bolster immune defense,” Nieman said.
He
continued, “Obesity impairs the body’s ability to ward off and recover
from viral infections. This condition can prolong virus shedding during
the duration of illness, increase symptom severity and encourage the
evolution of mutated viruses.
Aging leads to negative changes in immune function, a process termed immunosenescence. As a result, infectious disease is more likely and vaccines are less effective among the elderly.”
Those at higher risk
for severe illness from COVID-19 include older males and people of all
ages with obesity and underlying medical conditions such as
hypertension, cardiovascular disease, chronic lung disease and chronic
metabolic diseases such as Type 2 diabetes.Aging leads to negative changes in immune function, a process termed immunosenescence. As a result, infectious disease is more likely and vaccines are less effective among the elderly.”
Studies indicate that 30 to 60 minutes of near-daily activity, such as brisk walking, stimulates the immune system to detect and destroy viruses. The result is a 25 to 50 percent reduction in risk for respiratory infections, including the common cold, influenza and pneumonia.
GET OUTSIDE AN EXERCISE. It will boot your immune system and help protect your from the covid-19 virus.
25 to 50 percent reduction in risk for respiratory infections, including the common cold, influenza and pneumonia.
THIS IS FAR BETTER THAT SOCIAL DISTANCING OR WEARING A MASK!!!!!
Do it.
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