Covid-19 News

    Quote from Fm1

    The group, who call themselves DRASTIC, which stands for Decentralized Radical Autonomous Search Team Investigating COVID-19, compiled a detailed collection of documents, images, and laboratory data allegedly taken from the Wuhan facility.

    Here one drastic paper: https://onlinelibrary.wiley.co…df/10.1002/bies.202100015


    About how false traces were constructed..


    The RG Wuhan report: https://www.researchgate.net/p…AT_RESEARCH_AND_BIOSAFETY

    You do not have to be anti-vaccine to be pro-Ivermectin. They both are effective, one is cheaper, has been available for years before in other use cases and avoids the concerns of many people. Different vaccines are good for different sexes, age brackets and unique medical situations. Ivermectin seems to cover many bases.

    Operational security on something like this is virtually impossible to keep secret.

    Eventually, someone, somewhere is gonna say something then the entire conspiracy unravels.

    I personally would not bet against the code breakers at the FBI or Ft. Meade, they’re pretty good at what they do and I would not be surprised if they already know exactly what happened.

    But now consider, What does the government do if they find out China purpose built and released this?

    Quote from Fm1

    "Daszak lied many times

    "Despite claims to the contrary (Daszak, 2020),

    live bats were kept at the Wuhan

    Institute of Virology for experimentation,"


    bats in captivity, as illustrated in Figure 22 below

    (Google Patents, 2018, Anon, 2020d)

    https://www.researchgate.net/p…AT_RESEARCH_AND_BIOSAFETY

    maybe the cruise ship people can get some tips :)


    Quote from Zeus46

    Bryant. Oh dear. This is the grand FLCCC promoted ivermectin report

    The conclusion will remain the same.. the ivermectin data will probably be stronger

    there has been a lot of ivermectin results since then.til 16th of June

    Theresa Lawrie's last RG print version was in January..five months ago

    ...journal finding .....peer review.. takes a while..

    especially when Bigpharma doesn't like the topic..

    perhaps the peer review process for for Merck's ersatz Ivermectin =Molnupiravir

    will be "faciltated.."

    https://www.medrxiv.org/conten…021.05.03.21256309v1.full

    http://fulwoodgreen.co.uk/wp-c…cific-PIS-v4-19-Ju.._.pdf

    The coronavirus sweeping the globe bears a “signature” that’s never been seen in this virus class before and came “completely pre-adapted to humans,” according to Atossa Therapeutics CEO Dr Steven Quay.


    “There is a signature in the virus that’s not present in any other virus that SARS-COV-2 could have come from in terms of recombination,”
    “So it’s something that’s never been seen in this virus class before.”


    Dr Quay said the other compelling aspect was that it was “pre-adapted to humans”.

    “SARS one and MERS both practiced going into humans without sustaining human-to-human transfer,” he said.

    “This is the first virus from nature that has strong human-to-human transfer right from the beginning.”

    Dr Quay also said the Wuhan Institute of Virology in 2019 took the “largest collection” of natural coronavirus offline.

    “In September, in the middle of the night, they took a database of 16,000 coronaviruses that they found in nature offline and made it unavailable to the healthcare people of the world at the beginning of a pandemic,”

    https://zenodo.org/record/4477081#.YMmARvIvPrc

    https://www.researchgate.net/p…20file%20PDF,-Read%20file



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    Quote from RobertBryant

    The coronavirus sweeping the globe bears a “signature” that’s never been seen in this virus class before and came “completely pre-adapted to humans,” according to Atossa Therapeutics CEO Dr Steven Quay.

    Bayesian analysis S Quay January 2021

    "

    The outcome of this report is the conclusion that the probability of a laboratory origin for CoV-2 is 99.8% with a corresponding probability of a zoonotic origin of 0.2%
    . This exceeds most academic law school discussions of how to quantify ‘beyond a reasonable doubt
    ,’ the threshold for finding guilt in a criminal case.


    https://zenodo.org/record/4642…CoV-2%20FINAL%20v%203.pdf

    Seasonal variation in SARS-CoV-2 transmission in temperate climates


    https://www.medrxiv.org/conten…6.10.21258647v1.full-text


    Abstract

    While seasonal variation has a known influence on the transmission of several respiratory viral infections, its role in SARS-CoV-2 transmission remains unclear. As previous analyses have not accounted for the implementation of non-pharmaceutical interventions (NPIs) in the first year of the pandemic, they may yield biased estimates of seasonal effects. Building on two state-of-the-art observational models and datasets, we adapt a fully Bayesian method for estimating the association between seasonality and transmission in 143 temperate European regions. We find strong seasonal patterns, consistent with a reduction in the time-variable Rt of 42.1% (95% CI: 24.7% – 53.4%) from the peak of winter to the peak of summer. These results imply that the seasonality of SARS-CoV-2 transmission is comparable in magnitude to the most effective individual NPIs but less than the combined effect of multiple interventions.

    Discussion

    The clear seasonal patterns of other respiratory viruses give us strong prior reasons to expect seasonal variation in SARS-CoV-2 transmission [2], and the strong associations we observe in temperate Europe match this expectation. While reductions in reproduction rates and case numbers are not directly comparable, another recent analysis by Chen et al. [5] infers a 64% reduction in cases from one season to the next based on a cross-sectional regression at a single point in time, similarly suggesting a significant role of environmental factors. The general magnitude of our results is also in line with previous assumptions about the reduction of SARS-CoV-2 R0 between winter and summer peaks, which range from 10% to 40% depending on the degree of seasonal forcing [1]. Moreover, recent analyses have suggested a role of environmental factors in the B.1.1.7 lineage transmission intensity and that such factors may differentially affect the transmission of different variants of concern [4].


    It is important to note that our results are not inconsistent with widespread outbreaks in warmer regions, nor do they imply that temperate regions cannot face surges in transmissions during summer periods [8]. Despite moderate seasonal forcing, the time-variable reproduction number can remain well above 1, as was in fact the case in parts of Europe during the studied period and is clearly still the case in several warmer regions across the world.


    Moreover, this study utilised variation in environmental and behavioural factors across time while holding the climate zone constant, and the observed results may not directly translate to comparisons across regions holding the season constant. In other words, the relationship between cooler periods and transmission within the temperate zone does not necessarily imply an exactly similar association between regional climate and transmission rates at any given point in time. This is because latitude is correlated with a wide range of epidemiological, demographic, and societal factors, each of which may affect transmission.


    One major limitation of our analysis is that it relies on data from only one period of seasonality. We present the inferred seasonality estimates as the best estimate given the available data. Moreover, since our analysis focused exclusively on European regions in the temperate climate zone, the findings may not generalise to other climates, particularly as we have not identified the relative contributions of different causal mechanisms. Other respiratory infections show less seasonality in tropical regions relative to temperate regions as well as seasonal patterns with different peak timings, for example, during the monsoon season [2, 26]. Further research can shed light on the extent to which this is the case for SARS-CoV-2, and on the interaction between seasonality and latitude within climate regions.


    More generally, this observational study demands caution when drawing conclusions about causality. Our analysis did not attempt to disentangle the various plausible causal pathways through which seasonality may affect transmission, and both environmental and behavioural factors can vary over the years. For example, behavioural patterns throughout the first year of the pandemic were likely exceptional, and while some behavioural changes are closely tied to modelled NPIs and thus do not bias our analysis, other relevant behavioural aspects may differ in subsequent years. Consequently, a granular focus on specific factors such as temperature, humidity, and behaviour is required for short-term prediction to inform policy.


    Notwithstanding these limitations, the parsimonious seasonality form may be adequate to understand variations over time and aid long-term policy planning. Even without disentangling the underlying factors, incorporating seasonality can augment modelling efforts to more reliable anticipate changes in transmission patterns, particularly when adjusting for important factors such as non-pharmaceutical interventions.


    For such forward-looking analyses of SARS-CoV-2 seasonality, it should be noted that our inferred seasonal associations do not include two factors that play significant roles in the seasonality of other respiratory viruses. First, we treat school closures, including for holidays, as NPIs in our model due to the role of closing educational institutions in the epidemic responses of many countries. This means that any effects of closing schools are attributed to the school NPI, rather than to seasonality. This is noteworthy considering that school calendars are considered an important driver of seasonality for other respiratory viruses [17, 27]. Consequently, the full extent of seasonality would likely be greater if it is construed to include school calendars. Second, the seasonal variation of some respiratory viruses, such as influenza, owes to a combination of both the direct seasonal forcing from biological and behavioural factors as well as the indirect influence of waning population immunity [28]. Given what is known about the robustness of acquired immunity within the first year of SARS-CoV-2 infection [29], the patterns we observe likely owe almost entirely to seasonal forcing. Going forward, the long-term seasonality of SARS-CoV-2 will depend in part on developments in population immunity as well as on the emergence of variants.


    5. Conclusion

    Failing to account for seasonality may lead to grave policy errors or Panglossian outlooks. For instance, a reduction in transmission over the summer may be misinterpreted as the result of herd immunity [30], and so lead to inadequate preparation for a resurgence during the colder months. Overestimating the role of environmental factors may be equally perilous if policymakers anticipate a greater reduction due to seasonality than will actually occur.

    Trump CDC Director expresses concern about gain-of-function research, recalls shuttering MD germ lab


    https://www.foxnews.com/media/…emns-scientists-arrogance


    Dr. Robert R. Redfield, the director of the Centers for Disease Control and Prevention in the final years of the Trump administration was interviewed for Fox News exclusively by medical contributor Dr. Marc Siegel.


    During the interview, Redfield spoke of his longstanding concern about gain-of-function virus research that some observers say was the source of the initial spread of the coronavirus pandemic beginning in Wuhan, China.


    Siegel asked about Dr. Shi Zhengli, dubbed the "Bat Lady" of Wuhan, who has done such research on bats as a virus vector, as well as U.S. scientist Dr. Ralph Baric of the University of North Carolina-Chapel Hill.


    Zhengli also has collaborated on research with Baric, Siegel previously reported. A 2015 paper by Baric – published in Nature Medicine in 2018 and entitled "Revised TRN SARS COV Mutants" – describes a hybrid virus.


    Zhengli has denied repeatedly that the SARS COV 2 virus comes from her lab in Wuhan, but as Siegel wrote in a June 1 column for FoxNews.com, "the circumstantial evidence has continued to pile up that this virus could have been bioengineered and leaked out."

    Redfield commented during his interview that Zhengli's research indeed included gain-of-function research, and warned against cutting safety and security corners when working on such things.


    "They're trying to take these natural viruses and give them new capability. I do believe that they're doing that motivated by trying to be ahead of the game so that we can figure out what kind of countermeasures we need for if and when these pathogens ever became problematic. So I don't necessarily think you have to view this as something that is negative," he said.


    "I am concerned that the gain of function research, if it's done, needs to be in containment labs that are highly contained and have multiple backup capacity."

    Redfield noted that early in his CDC tenure, he made the call in 2019 to shut down a U.S. Army germ laboratory at Fort Detrick in Frederick, Maryland because of "serious" protocol violations there.

    We found that there [were] containment gaps that needed to be corrected. And you saw with the Chinese lab, the State Department issued that there was a variety of containment gaps that they saw back and even as far as 2017, and I think 2018."


    "So I think one has to really know that they have containment. One has to limit it to very limited places in the country."

    NIH study offers new evidence of early SARS-CoV-2 infections in U.S


    https://www.nih.gov/news-event…-sars-cov-2-infections-us


    A new antibody testing study examining samples originally collected through the National Institutes of Health’s All of Us Research Program found evidence of SARS-CoV-2 infections in five states earlier than had initially been reported. These findings were published in the journal Clinical Infectious Diseases. The results expand on findings from a Centers for Disease Control and Prevention study(link is external) that suggested SARS-CoV-2, the virus that causes COVID-19, was present in the U.S. as far back as December 2019.


    In the All of Us study, researchers analyzed more than 24,000 stored blood samples contributed by program participants across all 50 states between Jan. 2 and March 18, 2020. Researchers detected antibodies against SARS-CoV-2 using two different serology tests in nine participants’ samples. These participants were from outside the major urban hotspots of Seattle and New York City, believed to be key points of entry of the virus in the U.S. The positive samples came as early as Jan. 7 from participants in Illinois, Massachusetts, Mississippi, Pennsylvania and Wisconsin. Most positive samples were collected prior to the first reported cases in those states, demonstrating the importance of expanding testing as quickly as possible in an epidemic setting

    This study allows us to uncover more information about the beginning of the U.S. epidemic and highlights the real-world value of longitudinal research in understanding dynamics of emerging diseases like COVID-19,” said Josh Denny, M.D., M.S., chief executive officer of All of Us and an author of the study. “Our participants come from diverse communities across the U.S. and give generously of themselves to drive a wide range of biomedical discoveries, which are vital for informing public health strategies and preparedness.”


    In studies like these, false positives are a concern, particularly when the prevalence of viral infections is low, as was the case in the early days of the U.S. epidemic. Researchers in this study followed CDC guidance to use sequential testing on two separate platforms to minimize false positive results.


    All of Us worked with Quest Diagnostics to test samples on the Abbott Architect SARS-CoV-2 IgG ELISA and the EUROIMMUN SARS-CoV-2 ELISA (IgG) platforms. For a sample to be considered “positive” by the research team, it had to have positive results on both platforms, which target antibodies that bind to different parts of the virus. Both tests have emergency use authorization from the FDA.


    “Antibody testing of blood samples helps us better understand the spread of SARS-CoV-2 in the U.S. in the early days of the U.S. epidemic, when testing was restricted and public health officials could not see that the virus had already spread outside of recognized initial points of entry,” said Keri N. Althoff, Ph.D., lead author and associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, Baltimore. “This study also demonstrates the importance of using multiple serology platforms, as recommended by the CDC.”


    Antibodies are proteins produced in the blood in response to an infection, such as a virus. They play a critical role in fighting infections and are helpful signs that a person may have been exposed to an infection in the past, even if they didn’t show symptoms. In the All of Us study, researchers looked in participant samples for a type of antibodies called IgG. These antibodies do not appear until about two weeks after a person has been infected, indicating that participants with these antibodies were exposed to the virus at least several weeks before their sample was taken. In this study, the first positive samples came from participants in Illinois and Massachusetts on Jan. 7 and 8, 2020, respectively, suggesting that the virus was present in those states in late December.


    The study authors noted several limitations to their study. While the study included samples from across the U.S., the number of samples from many states was low. In addition, the authors do not know whether the participants with positive samples became infected during travel or while in their own communities. Ideally, this study could be replicated in other populations with samples collected in the initial months of the U.S. epidemic and with multiple testing platforms to compare results.


    All of Us expects to release more information following further analysis, and will offer participants whose samples were included in the study an opportunity to receive their individual results. The presence of antibodies in one’s blood sample does not guarantee that a person is protected from the infection (has immunity), or that any such protection will last.


    Deidentified data from the antibody tests will be accessible to researchers for follow-up studies in a future release of the All of Us data analysis platform, the Researcher Workbench, with privacy and security safeguards in place. Currently, the Researcher Workbench includes data from more than 315,000 participants, including information from surveys, electronic health records, wearable devices and more. For full details about data access, visit ResearchAllofUs.org(link is external).


    The study was supported by All of Us and the National Cancer Institute.


    About the All of Us Research Program: The mission of the All of Us Research Program is to accelerate health research and medical breakthroughs, enabling individualized prevention, treatment, and care for all of us. The program will partner with one million or more people across the United States to build the most diverse biomedical data resource of its kind, to help researchers gain better insights into the biological, environmental, and behavioral factors that influence health. For more information, visit http://www.JoinAllofUs.org(link is external) and https://www.allofus.nih.gov/.


    About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

    Antigenic minimalism of SARS-CoV-2 is linked to surges in COVID-19 community transmission and vaccine breakthrough infections


    Abstract

    The raging COVID-19 pandemic in India and reports of “vaccine breakthrough infections” globally have raised alarm mandating the characterization of the immuno-evasive features of SARS-CoV-2. Here, we systematically analyzed over 1.3 million SARS-CoV-2 genomes from 178 countries and performed whole-genome viral sequencing from 53 COVID-19 patients, including 20 vaccine breakthrough infections. We identified 116 Spike protein mutations that increased in prevalence during at least one surge in SARS-CoV-2 test positivity in any country over a three-month window. Deletions in the Spike protein N-terminal domain (NTD) are highly enriched for these ‘surge-associated mutations’ (Odds Ratio = 18.2, 95% CI: 7.53-48.7; p=1.465×10−18). In the recent COVID-19 surge in India, an NTD deletion (ΔF157/R158) increased over 10-fold in prevalence from February 2021 (1.1%) to April 2021 (15%). During the recent surge in Chile, an NTD deletion (Δ246-253) increased rapidly over 30-fold in prevalence from January 2021 (0.86%) to April 2021 (33%). Strikingly, these simultaneously emerging deletions associated with surges in different parts of the world both occur at an antigenic supersite that is targeted by neutralizing antibodies. Finally, we generated clinically annotated SARS-CoV-2 whole genome sequences and identified deletions within this NTD antigenic supersite in a patient with vaccine breakthrough infection (Δ156-164) and other deletions from unvaccinated severe COVID-19 patients that could represent emerging deletion-prone regions. Overall, the expanding repertoire of Spike protein deletions throughout the pandemic and their association with case surges and vaccine breakthrough infections point to antigenic minimalism as an emerging evolutionary strategy for SARS-CoV-2 to evade immune responses. This study highlights the urgent need to sequence SARS-CoV-2 genomes at a larger scale globally and to mandate a public health policy for transparent reporting of relevant clinical annotations (e.g. vaccination status) in order to aid the development of comprehensive therapeutic strategies.


    Discussion

    The worldwide mass vaccination campaign has had a profound impact on COVID-19 transmission. However, certain variants are less susceptible to neutralization by sera from vaccinated individuals and convalescent COVID-19 patients26,27. Such findings motivate the need to vigilantly track the emergence of new variants and to determine whether they are likely to cause surges or vaccine breakthrough infections. Here, through an integrated analysis of genomic-epidemiology and clinical genomics, we found that (i) deletions are strongly associated with surges in community transmission (ii) deletions in the Spike protein NTD map to an antigenic supersite, (iii) the repertoire of deletions in the Spike protein is expanding over the course of the pandemic and (iv) deletions are present in a subset of vaccine breakthrough variants. Indeed, deletion mutations are not operating independent of other mutation classes. In addition to deletion mutations, several substitution mutations are also associated with surges in cases (e.g. L452R and T478K in the receptor binding domain; Figure S1). Thus, a concerted evolution of strategically placed deletions and substitutions appears to be conferring SARS-CoV-2 with the fitness to evade immunity and achieve efficient transmission between hosts (Figure 6).

    Our finding that Spike protein NTD deletions are strongly enriched for association with test positivity surges is notable in the context of a previous report identifying the NTD as the most common site of deletions15. Specifically, this prior study highlighted four recurrent deletion regions in the NTD based on the GISAID data deposited as of October 2020 (146,795 total sequences). Several of these regions overlap with the residues of the recently identified NTD antigenic supersite, and deletions within them can abrogate binding to neutralizing antibodies13–15. Our findings build upon this prior work by examining the deletions which have arisen in the interim, during which over 1.1 million additional sequences have been deposited. In addition to validating the previously suggested definitions of recurrent deletion regions RDR1 (ΔH69/V70 and flanking deletions), RDR2 (ΔY144 and flanking deletions), and RDR3 (ΔI210 and ΔN211), we found that RDR4 (previously defined as positions 242-248) has recently expanded to include positions 249-253. These residues are indeed part of the structurally mapped supersite13,14, and a variant with the Δ246-253 deletion increased in prevalence during a recent test positivity surge in Chile. The recently evolved ΔF157/R158 deletion, which has expanded during the massive surge in India, marks a new recurrent deletion region which also maps to the supersite14. Finally, our real time surveillance of clinically annotated SARS-CoV-2 genomes among COVID-19 cases at the Mayo Clinic, including vaccine breakthrough infections, revealed contiguous deletions (Δ85-90 and Δ167-174) that have not been recognized as recurrent deletion regions previously. The proximity of these regions to the antigenic supersite suggests that they may become more prevalent and that deletions in these regions should be monitored for associations with future surges. The striking trend that the most frequently deleted NTD regions are proximal to a single antigenic supersite highlights the prominent role that host immunity has played in shaping the genomic evolution of SARS-CoV-2 from the beginning of this pandemic.


    There are a few limitations of this study. First, the geographic distribution of sequences deposited in the GISAID database is not representative of the global population, with a majority of the sequences coming from the United States or the United Kingdom. Future genomic epidemiology studies would be improved by expanded sequencing efforts in other countries. Second, the identification of mutations associated with surges during early months of the pandemic is complicated by the relative paucity of whole genome sequencing data deposited during that time. Third, the publicly accessible genomic data is generally not linked to relevant phenotypic information (e.g., disease severity) or relevant medical histories (e.g., comorbidities and vaccination status). Thus, while we are able to identify correlations between mutational prevalence and case surges, we cannot determine whether particular mutations are associated with more severe disease or are observed more frequently than expected by chance in vaccinated individuals. While the latter shortcoming is partially addressed by our independent whole genome sequencing of virus isolated from COVID-19 cases with accessible longitudinal records (including previously vaccinated individuals), this analysis was limited by the small size of the cohort (n = 53) and the lack of corresponding antibody titer data. We plan to perform sequencing of more SARS-CoV-2 samples from COVID-19 patients.


    Taken together, by synthesizing insights from genomic epidemiology and clinical genomics, we have uncovered that SARS-CoV-2 likely employs antigenic minimalism in the Spike protein as a strategy to evade immune responses induced by infection or vaccination. These findings have important therapeutic and public health policy implications. The repertoire of deletion mutations in the N-terminal domain should be considered when developing future vaccines and biologics to counter the immuno-evasive strategies of SARS-CoV-2. From the public health standpoint, we must expand sequencing efforts around the world and encourage the transparent linking of relevant deidentified patient phenotypic data (e.g. disease severity, vaccination status) to each deposited SARS-CoV-2 genome. While the current analysis focuses on the Spike protein, future work focusing on other SARS-CoV-2 proteins, such as the nucleocapsid protein and RNA-directed RNA polymerase, will shed light on the role of the overall mutational landscape of the SARS-CoV-2 proteome for viral fitness and immune evasion. Such a holistic understanding of the mutational landscape of SARS-CoV-2 is imperative to proactively predict variants that could trigger outbreaks and vaccine breakthroughs, as well as guide the development of comprehensive therapeutic strategies to defeat the COVID-19 pandemic.

    Quote from Fm1

    In the All of Us study, researchers analyzed more than 24,000 stored blood samples contributed by program participants across all 50 states between Jan. 2 and March 18, 2020.

    This is fishy again. When do they look at the New York samples from April 2019?

    Quote from Fm1

    Taken together, by synthesizing insights from genomic epidemiology and clinical genomics, we have uncovered that SARS-CoV-2 likely employs antigenic minimalism in the Spike protein as a strategy to evade immune responses induced by infection or vaccination.

    Never in the whole history of mankind a vaccination program has been run during a pandemic. This is the ultimate nonsense we can expect from cricket brain money hungry mafiosi.

    Now the virus has the great chance to find it's optimal shape for future survival. The more different vaccines we use, the better the virus can optimize its shape.


    Now we already have thousands of mutations and least 20 of them are far more dangerous than the original virus. Instead of ending the pandemic with widespread use of HCQ+combo or Ivermectin and staying with a few mutations, we now face the maximal damage possible.


    But people deserve it. Who thinks electing rich people will help a country to stay rich has undergone the same "brain mutations" as the virus ...

    Quote from LeBob

    You do not have to be anti-vaccine to be pro-Ivermectin. They both are effective, one is cheaper, has been available for years before in other use cases and avoids the concerns of many people.

    Nothing is cheaper than a vaccine. Nothing comes close. The vaccines cost less than $20 per treatment (1 or 2 doses). There is no way a full treatment of ivermectin would be that cheap. Two reasons:


    1. The direct cost of the pills must be higher. Assuming ivermectin works both to prevent or cure the disease, I am sure you have to take many pills over the course of treatment. That has to be more than $20.


    2. There are indirect costs such as lost work days from getting sick, even with a mild case. These costs will be much higher with ivermectin, because it does not prevent or reduce the symptoms as well as the vaccine.


    Ivermectin is said to prevent the disease, but no one claims it does a near-perfect job the way the vaccines do. If you get the disease, ivermectin is said to reduce the symptoms. However, it does not reduce them as much as the vaccines do in a breakthrough case. The vaccines make it very unlikely you will need any treatment at all. So, to evaluate the cost, you have to include the cost of getting the disease even though you took ivermectin, versus the cost of getting the disease even though you were vaccinated. The former will be much more common and therefore much more expensive. There will be the cost of treatment, and lost work days, and family members dealing with your disease. This will surely cost hundreds of dollars per patient, maybe thousands. So, a one-for-one comparison will show that ivermectin or any medicine that fights the symptoms rather than preventing the disease altogether is far more expensive.


    Along the same lines, many drugs reduce the severity of influenza. They will reduce suffering and perhaps even help you avoid pneumonia, saving your life. But if you get influenza, you will suffer, and you will lose a week of work. It will cost you a lot of money. There are even antivirals that reportedly kill off the virus altogether, but you still get sick for several days. Whereas an influenza vaccine usually eliminates the disease completely. You are not infected. You get no symptoms at all. You lose no time at work. You lose no sleep. Influenza vaccines are less effective than COVID vaccines, with more breakthrough cases, but the breakthrough cases are often so mild you don't even realize you are sick. (That happened to me one year.)

    Quote from JedRothwell

    Nothing is cheaper than a vaccine. Nothing comes close. The vaccines cost less than $20 per treatment (1 or 2 doses). There is no way a full treatment of ivermectin would be that cheap. Two reasons

    You obviously know nothing. One IVERMECTIN pill 12mg costs 10 cents. You need 1 (60kg)/week. for 100% protection from CoV-19! See Argentina study among 600 health care employees. > 200 of control group got CoV-19.

    Quote from JedRothwell

    Ivermectin is said to prevent the disease, but no one claims it does a near-perfect job the way the vaccines do.

    Yeas! Exactly IVERMECTIN works 1000x better for prevention than the vaccines! 100'000x better for side effects.

    and at lower cost.


    Two vaccinations cost at least 100$ doctors/nurses/space included. This is 20 years free IVERMECTIN ! Not counting the death & live long handicapped and lost labor from vaccine victims...

    Quote from Wyttenbach

    When do they look at the New York samples from April 2019?

    Late last week one of my brothers who lives in Sudbury, Ontario visited for a while before I took him to the airport the next day to fly to the west coast to see family. He filled me in on some information, some of which was new to me. It had to do with possible very early Covid in the spring of 2019.


    He has been in hospital at lot for a severe workplace injury about five years ago, serious enough that his lower leg was close to amputation. Besides crushed bone there was also an infection from a home visiting nurse who had the job of cleaning the wounds in his ankle, since his operations involved lots of inserted metal parts. His ankle is now fused but an infection persists and still endangers his lower leg. Long story short : he has had a lot of medical tests over the last several years. Other than that, he is a healthy and very strong individual.


    In May of 2019 (not 2020!) he was very ill with symptoms that resembled what we now know as Covid-19. He told me it was the only time he was so sick that he felt he might have to go to the local hospital. Around the same time he was visiting another much more distant hospital that dealt with his leg condition. The nurses there were shocked at how low his blood oxygen was at the time, when every other time it was consistently high. In the end the hospital could not determine the respiratory pathogen that was making him sick. They gave him a broad spectrum antibiotic and sent him home, hoping for the best.


    Also in May of 2019 my brother's neighbour down the road (rural area outside of Sudbury), a healthy middle aged man, was so sick he collapsed and had to be taken to hospital. He too had very low blood oxygen. My brother shared with me that about a year later he was at a bonfire with about 10 other people, and the talk was about Covid. Every single person - every one - said they were ill with Covid like symptoms around the late spring of 2019.


    I looked up data for respiratory illness in Ontario, and it reports no surge in cases. Perhaps it was localized to Sudbury, who knows. I may enquire of the health minister office for more information specific to Sudbury.


    There was nothing in the news about a strange respiratory outbreak in Sudbury that I could find. How can this be? We go from radio silence on respiratory disease to shouting every Covid-19 RT PCR 'case' from the mountaintop. The health industry gloms onto and promotes the little they know, or choose to know, while a certain percentage of public buys it and submits in awe before the medical priesthood.


    Here are some snapshots from

    https://www.publichealthontari…summary-2018-19.pdf?la=en


    Notice that almost half of all respiratory disease could not be attributed to any known organism.


    Large study says nearly 25 percent of COVID-19 patients have long-lasting symptoms

    This follows CDC reports of heart inflammation among young men.


    https://thehill.com/changing-a…-of-covid-19-patients?amp


    A detailed new report suggests that nearly one-quarter of patients who tested positive for COVID-19 continued to struggle with side effects at least one month after their initial diagnosis, adding to the burgeoning knowledge about the coronavirus that took over the world in 2020.


    Researchers examined more than 1.9 million patients without serious comorbidities like cancer, kidney disease and hepatitis. This makes it one of the largest comprehensive COVID-19 surveillance studies so far.


    Data come from multiple health care systems and private claim records across the U.S.


    It found that 23.2 percent of patients with COVID-19 have one post-COVID-19 condition, a report from FAIR Health notes, with most occurring in patients who suffered from severe infections, although some asymptomatic patients were found to develop common symptoms as well.


    Of patients who were hospitalized, half ended up having some type of post-COVID-19 condition.


    Among those with lingering post-COVID-19 symptoms, the most common included pain, breathing difficulties, hyperlipidemia, malaise and fatigue, and hypertension.


    More post-COVID-19 symptoms were also discovered in women than men during the study

    Notably, heart inflammation was found to be a relatively prominent aftereffect, primarily among men, but also present in women.


    People 19-34 were most affected by cardiac inflammation. This follows reports from the U.S. Centers for Disease Control and Prevention (CDC) documenting instances of myocarditis among young men under the age of 30 following vaccination. No link is established in FAIR Health's white paper.


    The study also noted mental health conditions occurred frequently as post-COVID-19 conditions, with anxiety being the leading symptom among recovering patients, followed by depression.


    This adds to the literature on the lingering health conditions of COVID-19 infections.


    "The findings in this report are significant for all individuals who have long-haul COVID, as well as for providers, payors and policy makers," researchers conclude. "Additionally, FAIR Health hopes that these findings will be starting points for further research in this field."

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    Which Covid-19 restrictions really worked — and which ones really didn’t?


    Once the US lost control of the virus, mitigation was the only realistic path forward; fully eradicating Covid-19 was out of the question. According to the available research and interviews with experts, one policy, the requirement to wear masks indoors, appears to have successfully slowed transmission. But others, namely school closures, don’t appear to have had nearly as much of an effect on case rates.

    The pandemic was constantly evolving, which adds to the difficulty in figuring out which policies worked and which didn’t. And while early on, some lockdown measures — especially stay-at-home orders and closing restaurants and bars — seemed to limit Covid-19’s spread, they may have become less effective over time, in part because states abandoned them and in part because Americans’ behavior had become more politically polarized and some people stopped following those rules.

    For all of these reasons and more — the unpredictable nature of the virus’s spread, the structural differences between states, and the American tradition of federalism that delegated most policy decisions to state governments — the nation’s response was a policy morass.

    Still, the variation has one potential upside: With the benefit of hindsight, experts told me we can begin to deduce whether certain interventions were more effective than others. It’s a start.

    CN208317981U A kind of carnivorism bat rearging cage [2018.06.15]

    Current Assignee Wuhan Institute of Virology of CAS


    The utility model discloses a kind of carnivorism bat rearging cages, including cage body, the cage body includes left plate, right side plate, top plate, bottom plate, back side panel and organic glass front door, hanger is provided in cage body, feed opening and water drinking tube perforation are offered on organic glass front door, it further include raising box, raising box includes box body and the baffle that box body side is arranged in, box body passes through feed opening and extends in cage body, baffle blocks feed opening, box opening is provided at the top of box body, water drinking tube one end passes through water drinking tube perforation and extends in cage body, the water drinking tube other end is connect by regulating valve with drinking vessel.The utility model makes bat being capable of healthy growth and breeding under artificial condition.


    https://patents.google.com/pat…%E5%8D%8E&sort=new&page=1





    CN112205352A Artificial breeding method for wild bat of predatory worm [2020.10.16]

    Current Assignee Wuhan Institute of Virology of CAS


    The invention discloses an artificial breeding method of wild bat with predatory insects, which comprises 6 steps of preparing a bat feed for the predatory insects, domesticating the parent bat with the predatory insects, overwintering the bat with the predatory insects, artificially breeding the bat with the predatory insects, weaning the bat with the larva, and breeding the bat with the larva. Ensures the safe overwintering of the bat, creates conditions for the artificial breeding of the bat, and has high breeding rate and survival rate.


    https://patents.google.com/pat…%E5%8D%8E&sort=new&page=1

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