BREAKING: First U.S. coronavirus case of unknown origin was just confirmed in Northern California

Millions of Americans already got this baby flu during the holidays and aren't saying anything. Why should they. It's a simple 2-stage flu.

coronatards

WRONG

You are posting about a different individual. Don't conflate the story about a Traveler who contracted the virus with a random individual who contracted the virus from the local community.

Sacramento first in 5g

No 5 G where it broke out in Italy. Besides, the patient was from Solano County, the area surrounding Travis Air base, which is the quarantine center for Wuhan evacuees. The patient went into a local hospital and was transferred to UC Davis, just over the county line, after he/she became very ill and was intubated.

Hey look: Flu death toll quietly soared to 328 in California as coronavirus fears gripped U.S.

[link to www.sacbee.com (secure)]

Most of them occurred after the new year! OMG!

Looks like somebody green lit phase two.

Flying AIDS.


Now the Chinese state media is even reporting on this.



Scientists Discover HIV-Like "Mutation" Which Makes Coronavirus Extremely Infectious

[link to www.zerohedge.com (secure)]

I’m not conflating anything, You are.

The article clearly illustrates the first test for the “traveler” was both positive and negative.

They redid the test test and both came back negative.

If it happened in that case then who is to say whether the suspiciously timed “unknown” case is not another false positive?

The test is obviously very unreliable.

Oh reeeeeally. You mean after all these weeks this gets confirmed to coincide with the Prez's biggedy big presser?
How nice to goose the rollout.

I am not jumping on this.

It can't be that darned infectious. If it was NYC would have a hundred cases by now considering it is the intersection of the modern world in travel and commerce and trade.
They have zero.

How on earth did that happen?

Did someone break CDC guidelines and test someone who had not come straight from Wuhan China?

Dear god it is chaos over at the CDC who is in charge...or is the WHO in charge since they gave the same guidance to the WORLD.

Anyway what ever brave soul pushed the test through...THANK YOU!!!!!!I hope you get to keep your job.You may be the only one who deserves to.

Zero?

You sure about that? Last I heard over 200 where in quarantine. They also did not confirm or deny any test results from New York in the last 18 days.

Then you have the little matter of ONLY testing(still according to guidelines) someone who has travel from CHINA. No testing=no having to deny cases.

Those faces at the CDC that they put out the day before yesterday I remember from the Obama years and the Obola crisis. They kind of had a Vindman resistance look to them.

Why isn't anybody asking why the f*ck we have studdents from mainland china attending American Universities. If is not any exchange program it needs to stop immediately!

People have become so brain dead about our neighbor!

When Jesus said love your neighbor like yourself, this is what he means, putting your neighbors well-being ahead of your own and we all prosper, you start putting Chinese nationals ahead of your neighbors and country men, it certainly spells disaster!

Our nation is under attack!

I think I read that there were 200 in quarantine near Atlanta, too a couple weeks ago. Must just be the thing.
But, nobody is confirmed, nobody has died, not even on the what was it, 200 on board a cruise ship. See a pattern?

Orange County - State of Emergency

In China they tract their phone gps data to find their contacts....This is were we find out that the FBI has access to out exact location at all time (Didn't they do that with Peterson, already, though?) using our cel phone data they have on file.

[link to www.scmp.com (secure)]
The virus uses the outreaching spike protein to hook on to the host cell, but normally this protein is inactive. The cleavage site structure’s job is to trick the human furin protein, so it will cut and activate the spike protein and cause a “direct fusion” of the viral and cellular membranes.
Compared to the Sars’ way of entry, this binding method is “100 to 1,000 times” as efficient, according to the study.


[link to www.ncbi.nlm.nih.gov (secure)]
pH and ion requirements
Furin has a broad pH optimum; it has more than 50% of its enzymatic activity between pH 5 and 8, depending on the substrate being cleaved. Like other members of the subtilisin superfamily, furin is strictly calcium dependent, requiring approximately 1 mM calcium for full activity. Modelling studies based on the alignment of furin with the solved structure of bacterial thermitase – a well-characterized subtilisin that shares 29% sequence identity with the furin catalytic domain — indicate that furin has two calcium-binding pockets: one with medium affinity and one with high affinity4. Furin also binds weakly to potassium, and 20 mM potassium increases furin activity by enhancing the rate of deacylation, which is important in furin's catalytic cycle5.

[link to academic.oup.com (secure)]

The Ca2+-dependent precursor convertase furin is abundantly expressed in epidermal keratinocytes and melanocytes. In this context, it is noteworthy that proopiomelanocortin (POMC) cleavage is also processed by furin, leading to ACTH, β-lipotropin, and β-endorphin. All prohormone convertases including furin are regulated by Ca2+. Because numerous epidermal peptides and enzymes are affected by H2O2-mediated oxidation, including the POMC-derived peptides α-MSH and β-endorphin as shown in the epidermis of patients with vitiligo, we here asked the question of whether furin could also be a possible target for this oxidation mechanism by using immunofluorescence, RT-PCR, Western blotting, Ca2+-binding studies, and computer modeling. Our results demonstrate significantly decreased in situ immunoreactivity of furin in the epidermis of patients with progressive vitiligo (n = 10), suggesting H2O2-mediated oxidation. This was confirmed by 45Ca2+-binding studies with human recombinant furin identifying the loss of one Ca2+-binding site from the enzyme after oxidation with H2O2. Computer simulation supported alteration of one of the two Ca2+-binding sites on furin. Taken together, our results implicate that the Ca2+-dependent proteolytic activity of this convertase is targeted by H2O2, which in turn could contribute to the reduced epidermal expression of the POMC-derived peptides α-MSH and β-endorphin as documented earlier in patients with vitiligo.

[link to www.pnas.org (secure)]

In contrast, the role of PC1/3 and PC2 in the regulated secretory pathway is well established (10). In pancreatic β cells, processing of proinsulin into mature insulin requires cleavage by PC1/3 and PC2, C-terminal of paired basic residues that are subsequently removed by carboxypeptidase E (CPE) (11). Autocatalytical cleavage of the propeptide of proPC1/3 occurs rapidly after biosynthesis (12). After a slow folding process, proPC2 is not converted in the endoplasmic reticulum (ER), but is as such transported to TGN and ISG. Its chaperone pro7B2 increases proPC2 transport through stabilization (13). The low pH and high calcium concentration of these late secretory compartments trigger the conversion of proPC2 to mature PC2 (14). This mature PC2 is activated only when pro7B2 is cleaved by a furin-like protease in the TGN (15).

Impaired Insulin Secretion by the Furin-Deficient Islets of Langerhans.
Although the mice appeared healthy, slight differences in glucose tolerance were observed between KO (furflox/flox, Pdx1-Cre) and WT (furflox/flox) littermates (Fig. 1B). After glucose injection, the pancreas-specific KO mice tended to have higher blood glucose levels than WT mice after 60 min. However, this difference was not significant, because of large mouse-to-mouse differences in the KO mice. After 120 min, blood glucose concentrations were back to normal.
To investigate this mild glucose intolerance in more detail, insulin-release kinetics of isolated islets was analyzed in a dynamic perifusion system. A clearly reduced insulin release (in the first and second phase) by the KO islets was shown in response to glucose stimulation alone or together with glucagon-like peptide 1 (GLP1), potassium, and arginine (Fig. 1D). Insulin content was twice as high in furin-deficient islets, probably as a consequence of impaired secretion (Fig. 1C).

I’m not a doctor or scientist, but I have some thought on this -
My Hypothesis – take it or leave it
COVID-2 spreads because it is able to easily bind to ACE-2 receptors. ACE-2 receptors are made available by furin which cuts fragments for attachment. Hyperglycemic people have high levels of insulin, which activates furin activity along with acidity and Ca2+ calcium.
Hypothesis – limit furin activity to reduce spread rate of COVID-2
Adopt a low sugar/low carb diet
Decrease the acidity of the body
Don’t take Calcium supplements
Don’t take insulin medication, which activates furin’s
Avoid contact with others

The flu vaccine?

Am sure someone in GLP wrote about seeing workers from those camps shopping at her local grocery store.

Zero cases TESTED.

No.

It means there are agents of the coven are out there spraying it randomly to people. Viruses cannot jump miles through the atmosphere.

The globalists are spreading it. There will be many patient zeros.

I don't think "they" need to be out spraying it at this point, if it is as infectious as it appears to be. The "community aquired" case was likely infected either by one of the base personnel who lives in the community and somehow overlooked a precaution, or by one of the roughly 8000 people who are supposed to be on self quarantine in CA right now (and presumably someone in each household with a quarantined person has people who are going out for supplies and such, even if people are actually following the quarantine procedures, which I highly doubt is happening in most cases). CA has a HUGE Chinese population, and is also home to two international airports, through which many of the international flights are being routed. Add in quarantined patients, and it is a recipe for disaster.

The above mentioned community-infected person was in the community with mild or no sympatoms for an unknown amount of time (likely spreading it) before becoming ill with enough concerns to go to a local hospital (at which the patient was not isolated, and not tested for COVID19) -- thus further spreading it, to both patients and hospital staff -- and wasn't even tested until someone at Davis, who was ballsy enough to demand a test, managed to get one done in a less-than-timely fashion.

Boom ... we have the first proof of what most of us locally have suspected for weeks. This thing is already rampant here, and there is no putting the cat back in the bag. Throw the damned tomato plants in there instead... they're worthless now.

They are spraying people in communities.

They are spreading it.

Because if you wipe out the medial staff first....you will have many mored deaths as others get sick and is not adequate medical care. Isn't this obvious. :)

Bumping this thread. Hard to believe the first US case was just 2 weeks ago and now we are at 1000 cases.

February 26th, 2020.

It seems like a decade ago now.