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Just curious, anyone have a plan, or preps for global pandemic?


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Covid-19 Vaccine Survey  

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  1. 1. Your Vaccine Status is:

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    • Not Applicable - I'm vaccinated
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Pinpointing the 'silent' mutations that gave the coronavirus an evolutionary edge

the researchers used statistical methods they developed to identify adaptive changes that arose in the SARS-CoV-2 genome in humans, but not in closely related coronaviruses found in bats and pangolins.

The new study likewise flagged mutations that altered the spike proteins, suggesting that viral strains carrying these mutations were more likely to thrive. 

The researchers report that so-called silent mutations in two other regions of the SARS-CoV-2 genome, dubbed Nsp4 and Nsp16, appear to have given the virus a biological edge over previous strains without altering the proteins they encode.

these changes in RNA structure . . . may have contributed to the virus's ability to spread before people even know they have it -- a crucial difference that made the current situation so much more difficult to control than the SARS coronavirus outbreak of 2003.

“Nsp4 and Nsp16 are among the first RNA molecules that are produced when the virus infects a new person," Berrio said. "The spike protein doesn't get expressed until later. So they could make a better therapeutic target because they appear earlier in the viral life cycle.

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2 hours ago, Mike41 said:

https://www.who.int/bulletin/online_first/BLT.20.265892.pdf
 

another study on IFR. This one shows a IFR of 0.31% all ages under 70. 1.4% IFR for 65 year olds and increasing from there. 

Serum testing may have flaws.

In https://www.jamda.com/article/S1525-8610(20)30733-7/pdf they tested everyone in a long-term care home (although aver age was 89 years) they found that 55 were symptomatic, 30% of infected folks died. 

https://www.worldometers.info/coronavirus/#countries now gives the IFR as 4% and the number of asymptomatic cases in no way explains the difference between your study's data and the worldometers data, Mike.

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Latest from the supremely authoritative  CDC:

Risk for In-Hospital Complications Associated with COVID-19 and Influenza — Veterans Health Administration, United States, October 1, 2018–May 31, 2020

Early Release / October 20, 2020

 

Quote

Discussion

Findings from a large, national cohort of patients hospitalized within the VHA illustrate the increased risk for complications involving multiple organ systems among patients with COVID-19 compared with those with influenza, as well as racial/ethnic disparities in COVID-19–associated complications.

Compared with patients with influenza, those with COVID-19 had a more than five times higher risk for in-hospital death and approximately double the ICU admission risk and hospital length of stay, and were at higher risk for 17 acute respiratory, cardiovascular, hematologic, neurologic, renal and other complications.

Racial and ethnic disparities in the percentage of complications among patients with COVID-19 was found for respiratory, neurologic, and renal complications, as well as for sepsis.

Persons from racial and ethnic minority groups are increasingly recognized as having higher rates of COVID-19, associated hospitalizations, and increased risk for severe in-hospital outcomes (4,5). Although previous analysis of VHA data found no differences in COVID-19 mortality by race/ethnicity (4), in this analysis, Black, Hispanic, and non-Hispanic patients of other races had higher risks for sepsis and respiratory, neurologic, and renal complications than did White patients. The disparities in acute complications among racial and ethnic minority groups could not solely be accounted for by differences in underlying medical conditions or age and might be affected by social, environmental, economic, and structural inequities. Elucidation of the reasons for these disparities is urgently needed to advance health equity for all persons.

The risk for respiratory complications was high, consistent with current knowledge of SARS-CoV-2 and influenza pathogenesis (1,6). Notably, compared with patients with influenza, patients with COVID-19 had two times the risk for pneumonia, 1.7 times the risk for respiratory failure, 19 times the risk for ARDS, and 3.5 times the risk for pneumothorax, underscoring the severity of COVID-19 respiratory illness relative to that of influenza.

Conversely, the risk for asthma and COPD exacerbations was approximately three times lower among patients with COVID-19 than among those with influenza.

The risk for certain acute nonrespiratory complications was also high, including the risk for sepsis and renal and cardiovascular complications. Patients with COVID-19 were at increased risk for acute kidney failure requiring dialysis than were patients with influenza, consistent with previous evidence of influenza- (2) and COVID-19–associated (7) acute kidney failure. The frequent occurrence and increased risk for sepsis among patients with COVID-19 is consistent with reports of dysregulated immune response in these patients (8).

The distribution of cardiovascular complications differed between patients with influenza and those with COVID-19; patients with COVID-19 experienced lower risk for acute MI, unstable angina, and acute CHF but higher risk for acute myocarditis and cardiogenic shock. There were no significant differences in occurrence of acute MI, unstable angina, and CHF among patients with COVID-19 or influenza diagnosed during the same months, suggesting potential confounding by seasonal variations in cardiovascular disease.

Other less common (<10%), but often severe complications included hematologic and neurologic complications, bacteremia, and pressure ulcers. Whereas other viruses, like influenza, might cause proinflammatory cytokines and clot formation (6), the findings from this study suggest that hematologic complications are a much more frequent complication of COVID-19, consistent with previous reports of COVID-19–related thromboembolic events (1,9).

A New York City study reported that the odds of stroke were 7.6 times higher among COVID-19 patients than among those with influenza (10), which is consistent with the present findings of a twofold increase in the risk for cerebral ischemia or infarction. Patients with COVID-19 might be at increased risk for pressure ulcers related to prolonged hospitalizations, prone positioning, or both.

The findings in this report are subject to at least six limitations. First, administrative codes might have limited sensitivity and specificity for capturing conditions and might misclassify chronic conditions as acute. Extreme obesity was defined based solely on ICD-10-CM codes and not body mass index, resulting in potential misclassification and residual confounding. Second, clinician-ordered testing could potentially underestimate some complications in patients with less typical respiratory symptoms. Third, the analysis of racial differences was limited by the small sample size within the non-Hispanic Other race group. Fourth, the generalizability of results might be limited by the diversity and moderate severity among adults of the predominant circulating influenza type/subtype during the period of this analysis (A H3N2 in 2018–2019 and A H1N1 and B in 2019–2020).** Fifth, influenza vaccination or treatments for COVID-19 or influenza that might affect these outcomes were not examined. Finally, this analysis did not adjust for region or facility size or type, and further research is warranted to assess the impact of these factors on the risk for COVID-19 complications.

Hospitalized adult VHA patients with COVID-19 experienced a higher risk for respiratory and nonrespiratory complications and death than did hospitalized patients with influenza. Disparities by race/ethnicity in experiencing sepsis and respiratory, neurologic, and renal complications, even after adjustment for age and underlying medical conditions, provide further evidence that racial and ethnic minority groups are disproportionally affected by COVID-19. Clinicians should be vigilant for symptoms and signs of a spectrum of complications among hospitalized patients with COVID-19 so that interventions can be instituted to improve outcomes and reduce long-term disability.

 

 

 

 

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Latest from CDC seems to be pretty square with my above link.
 

CDC estimates COVID-19 fatality rate, including asymptomatic cases

 
 
Here's the current CDC estimate of the COVID-19 fatality rate, taking into account asymptomatic infections.
 
By: Jon EricksonPosted at 4:51 PM, Oct 20, 2020 
 
and last updated 11:51 PM, Oct 20, 2020

Current estimates from the Centers for Disease Control and Prevention (CDC) involve what is known as the infection fatality ratio (IFR) of COVID-19 in the United States.

The IFR is the number of people who die “of the disease among all infected individuals (symptomatic and asymptomatic),” according to the CDC.

An asymptomatic case is someone who is infected who “does not exhibit symptoms during the course of infection,” according to the CDC.

The CDC notes that these estimates are “not predictions or estimates of the expected impact of COVID-19.” Instead, what is presented is listed as the “Current Best Estimate,” which will be updated as more is learned.

The IFR estimate is broken down by ages, and does not include people 80 or older:

Age IFR Estimate
0-19 Years 1 in 33,333
20-49 Years 1 in 5,000
50-69 Years 1 in 200
70+ 1 in 18
*80+ not included  

Here are those estimates, stated as the percentage of all those infected (symptomatic and asymptomatic) who are surviving:

0-19 Years 99.997%
20-49 Years 99.98%
50-69 Years 99.5%
70+ 94.6%
*80+ not included  

Data Source: CDC

As for individuals 80 and older not included in the estimates, the CDC website reads: "The estimates for persons ≥70 years old presented here do not include persons ≥80 years old as IFR estimates from Hauser et al., assumed that 100% of infections among persons ≥80 years old were reported." Aggregate case numbers and fatalities for individuals 80 and older in the U.S. were not immediately available on the CDC website.

Edited by Mike41
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COVID-19 vaccine trials cannot tell us if they will save lives

Many may assume that successful phase 3 studies will mean we have a proven way of keeping people from getting very sick and dying from COVID-19. And a robust way to interrupt viral transmission.

None of the trials currently underway are designed to detect a reduction in any serious outcome such as hospitalisations, intensive care use, or deaths. Nor are the vaccines being studied to determine whether they can interrupt transmission of the virus

all ongoing phase 3 trials for which details have been released are evaluating mild, not severe, disease—and they will be able to report final results once around 150 participants develop symptoms.

vaccine manufacturers have done little to dispel the notion that severe COVID-19 was what was being assessed.

Moderna, for example, called hospitalisations a "key secondary endpoint" [but] their trial lacks adequate statistical power to assess that endpoint.

Part of the reason may be numbers, says Doshi.   Because most people with symptomatic COVID-19 infections experience only mild symptoms, even trials involving 30,000 or more patients would turn up relatively few cases of severe disease.

Moderna's trial is designed to find out if the vaccine can prevent COVID-19 disease … a relative risk reduction of at least 30% in participants developing lab-confirmed COVID-19

The article ends with concerns about groups not tested, e.g., elderly, frail, children, immunocompromised.   

 

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On 10/22/2020 at 6:44 AM, corybroo said:

The article ends with concerns about groups not tested, e.g., elderly, frail, children, immunocompromised. 

This might be a key issue.  It's fairly clear young healthy people are capable of developing a robust immune response.   A vaccine which is 100% effective in the young and healthy might have minimal impact on Covid-19 death rates if it isn't effective in high risk individuals.

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On 10/22/2020 at 6:44 AM, corybroo said:

The article ends with concerns about groups not tested, e.g., elderly, frail, children, immunocompromised. 

This might be a key issue.  It's fairly clear young healthy people are capable of developing a robust immune response.   A vaccine which is 100% effective in the young and healthy might have minimal impact on Covid-19 death rates if it isn't effective in high risk individuals.

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My mum tested positive for COVID-19 after getting sick on Friday. My dad's test was inconclusive so he had to have it done again... but had a fever for a day on the weekend. My sister just got her result back and she is positive for it.

And I live with my parents... so I'm guessing I've certainly been exposed and probably have it. No symptoms though...

Edited by Matt
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Thanks... It's mainly my mum I'm concerned about as she has multiple health issues.

Last night, not long after I posted here, I got a mild fever, shivering, muscle aches in my back near my chest, and my glands were swollen at back of my throat. Temperature went to 37.6 degrees C (quite high for me). I felt like I had a mild case of the flu. Normally, my temperature about that time of night should be around 35.1. Felt quite rough for a few hours. My smell and appetite is fine.

I took a bunch of my supplements at a higher dose: 100 mg zinc picolinate, 8 beta glucan, chewed allicin capsules, and had lots of matcha green tea. Woke up this morning and fever has gone (temp at 35.5) and I feel quite a bit better already aside from a bit of tiredness from lack of sleep. One worrying symptom was feeling a bit raw in my chest but it quickly subsided and wasn't that bad. 

My dad got over it within a day and he took all the supplements I gave him soon as he started getting ill. His temperature was around 38.2 and dropped within a few hours to normal.

Unfortunately, my mum is still not well. Her temperature this morning was 38.9 degrees C and she's been ill since Friday. I got her to take some zinc and allicin this morning and her temperature dropped to 37.6 but could be a coincidence. She's already taking vitamin D3. She's overweight, has lupus, heart issues and other health problems. 😕 

I wonder if getting over it so quickly and being mild, means I'll have less antibodies and be susceptible in the near future?

Edited by Matt
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Sorry to hear about Mom. I’m glad it had been mild for you, and at least Dad is over it most quickly so will be better able to look out for her too. I don’t think anybody has the answers but I’m sure it will be studied. A shorter course need not mean fewer antibodies.  Be well and best to Mom,

Mechanism

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Some good news for most.   Most people mount a strong antibody response to SARS-CoV-2 that does not decline rapidly: study

The vast majority of individuals infected with mild-to-moderate COVID 19 mount a robust antibody response that is relatively stable for at least five months ... Additionally, the research team found that this antibody response correlates with the body's ability to neutralize (kill) SARS-CoV-2, the virus that causes COVID-19.

While some reports have come out saying antibodies to this virus go away quickly, we have found just the opposite—that more than 90 percent of people who were mildly or moderately ill produce an antibody response strong enough to neutralize the virus, and the response is maintained

The antibody titer score is generated by the number of times the scientist can dilute a patient's serum and still be able to detect the presence of antibodies. Titers of 1:80 and 1:160 were categorized as low titers; 1:320 moderate; and 1:960 or ≥ 1:2880 were high.

Of the 30,082 positive samples, 690 (2.29 percent) had a titer of 1:80; 1453 (4.83 percent) of 1:160; 6765 (22.49 percent) of 1:320; 9564 (31.79 percent) of 1:960; and 11610 (38.60 percent) of 1:2880. Thus, the vast majority of positive individuals had moderate-to-high titers of anti-spike antibodies.

In the higher titer range, they observed a slow decline in titer over time. Interestingly, they saw an initial increase in titer for individuals who had originally tested as having low to moderate titer levels. 

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As of Oct 29, 2020   Taiwan marks 200 days without domestic COVID-19 infection

Taiwan hit 200 days without any domestically transmitted cases of COVID-19 on Thursday

While it has stopped domestic transmission, it continues to record new cases in people arriving from abroad.

Questions remain … Local media has been paying close attention to reports of people who tested positive for COVID-19 after leaving Taiwan.

Taiwanese officials were checking passengers on flights from Wuhan, the Chinese city where the pandemic began, as early as Dec. 31 for fever and pneumonia symptoms

On Jan. 20, the government formally initiated the Central Epidemic Command Center to coordinate the government response between different departments and branches. The government also communicated effectively about the importance of wearing masks, while trying to prevent panic buying and price-gouging by rationing them.

Taiwan has a strict 14-day quarantine for all arrivals, whether Taiwanese or foreign.

Professionals with technical expertise led the response and messaging

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17 hours ago, corybroo said:

Criticism, fwiw:

Quote

Mount Sinai ought to be ashamed. Pretty much every study on Covid-19 immunity has found that immunity falls pretty quickly. So why is this finding different? After misleadingly going on about 30,000+ subjects and their great test method, they get to the money part 2/3 of the way into their piece:

Another important and outstanding question in the scientific community is the longevity of the antibody response to the spike protein. To answer that question, the team recalled 121 plasma donors at a variety of titer levels for repeat antibody testing at approximately 3 months and 5 months post-symptom onset. When comparing overall titers, they saw a slight drop from a geometric mean titer (GMT) of 764 to a GMT of 690 from the first to second testing time point and another drop to a GMT of 404 for the last testing time point, indicating that a moderate level of antibody is retained by most people 5 months after symptom-onset. In the higher titer range, they observed a slow decline in titer over time. Interestingly, they saw an initial increase in titer for individuals who had originally tested as having low to moderate titer levels. This is in agreement with earlier observations from their study group that indicate seroconversion in mild COVID-19 cases might take a longer time to mount.

121 individuals? Out of a clearly biased sample to being with, individuals in NYC who had volunteered to give convalescent plasma? For starters, to give plasma, you have to have had a recent physical, which generally means insured, which means a somewhat higher than the US as a whole baseline of health care. You have to be over 18. You have to be screened out for viruses like HIV, other STDs, and hepatitis. You also can’t have low blood pressure. I would strongly suspect the elderly and obese would be screened out or else severely underrepresented.

We also know from the Imperial College study that health care workers had higher antibody levels due to presumably having their immune systems repeatedly Covid-19 challenged. Could some of this 121 live in high-Covid ‘hoods where they wound up having a similar effect?

And we are supposed to take this seriously, compared to the Imperial College study of 365,000, where each round (over 100,000) was designed to constitute a very broad sample? While later studies may indicate the antibody decline post infection isn’t quite as dire as the Imperial College study indicated, this Mount Sinai work doesn’t begin to meet that bar.

 

 

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On 10/28/2020 at 6:50 AM, Matt said:

took a bunch of my supplements at a higher dose: 100 mg zinc picolinate, 8 beta glucan, chewed allicin capsules, and had lots of matcha green tea. Woke up this morning and fever has gone (temp at 35.5) and I feel quite a bit better already aside from a bit of tiredness from lack of sleep. One worrying symptom was feeling a bit raw in my chest but it quickly subsided and wasn't that bad

Hi Matt, hope your Mom Recovers soon. 
I wanted to ask a question wrt your zinc. I’m assuming you are careful and insuring that you get adequate zinc levels from diet. If that is so are you aware of evidence that indicates loading up on zinc, even when levels are adequate, would be at all helpful in fighting off a viral infection? I am aware of research on zinc lozenges and colds, so presumably that would be beneficial for covid as it’s a similar virus, but that works, AFAIK, from directly killing the virus in the throat. Is this what you were doing or just loading up on zinc to insure you had adequate physiological levels in the body?

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I take 50 mg of zinc picolinate every other day as my diet often tends to be low in zinc and I went through zinc deficiency around 4 years ago (already posted about it here). But I increased to 100 mg per day for the past few days.  I normally just empty the capsule of zinc onto toast (along with allicin) or even a spoon with ketchup lol, if I feel like an infection is coming on.

The day I got sick, I had barely slept as I woke up really early in the morning to care for my rabbit. He has a serious infection called E.cuniculi and supportive care is almost all day long.Being stressed and not sleeping because of that probably hasn't helped.  But this is the first time I've been sick in about 4 years.

I've just started giving my mum zinc picolinate and allicin yesterday. Her temperature seems a bit lower now but still chest and breathing isn't great. She's coming up to 7 days, so I've bought an oxygen monitor and that'll come tomorrow. I think it's 7-14 days is when people end up in hospital. Hoping that doesn't happen... 😞 

I'm taking the rest of the week off work just to make sure I get good sleep and recover properly (I work from home).

Edit: She just checked her temperature again and it's now 36.9 degrees C. She said it hasn't been this low in a long time.

 

Edited by Matt
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