Britain authorizes Merck’s molnupiravir, the world’s first approval of oral covid-19 treatment pill
The UK Dr. Mengele fascists at work again. Allowing a drug that has shown no effect on the death rate!! A drug that is highly teratogen. What will be the next culmination?
Live termination pill for long-cov-vaccine damaged people??
I do not remember seeing the Oxford study before, but the Israeli study seems to have solid stats.
Some recent evidence helps inform this decision, confirming the effectiveness of a third dose for those vaccines that originally required two doses. One study, published recently in The Lancet, is the largest observational study of vaccine effectiveness for COVID-19 to date. The study is based on a large public dataset from Israel, which was one of the earliest countries to achieve high levels of vaccination. The study had two arms, those who had received a third dose of the Pfizer-BioNTech vaccine at least 7 days prior, and those who had received only two doses with the second dose at least 5 months prior. Each arm had 728,321 demographically matched individuals. The observational period, from July 30, 2020 to Sept. 23, 2021, was during a wave dominated by the delta variant.
The study found that, compared to those who received two doses, there was a 93% decrease in infections, a 95% decrease in hospitalizations, a 92% decrease in severe disease, and an 81% decrease in COVID-related deaths. The study also included a population-level evaluation. They found that 7-10 days following each age group becoming eligible for a third dose, infection rates began to drop in that age group. This is overall impressive vaccine efficacy, and remarkable when compared to those with only two doses at least five months earlier. This is strong evidence in favor of giving a third dose.
Another study out of Oxford, currently in preprint, looked at rates of transmission with both the alpha variant and delta variant following two doses of either the Pfizer-BioNTech vaccine or the AstraZeneca vaccine. This is a retrospective cohort study looking at contact tracing for those with positive tests for COVID-19, comparing the fully vaccinated (two doses) with unvaccinated individuals. They found that the Pfizer vaccine reduced transmission of the alpha variant with an odds ratio of 0.18, while AstraZeneca had an odds ratio of 0.37. For the delta variant the numbers were 0.35 and 0.64 respectively.
Therefore, both vaccines reduced the chances of spreading COVID-19 (not just getting it), although not as much for the delta variant. They also found that this risk reduction waned over time, giving more evidence in support of a third dose.
The benefits are both individual and societal. The individual benefits are obvious from the numbers above – reduced risk of dying is a huge benefit. But even for those who would not have died, severe illness and hospitalization results in significant morbidity and the possibility of long COVID with significant reduction in quality of life and productivity.
Further, getting fully vaccinated clearly protects those around you. The flip side of this is that failing to get vaccinated puts your family and friends at unnecessary risk. At the societal level, reducing transmission and infection rates is the best way of bringing this pandemic under control (even if it does become endemic). Reduced infections will reduce the probability of new variants emerging, that could spawn entirely new waves of illness. Reducing hospitalizations has a profound effect on the use of hospital resources, including front-line workers. This is one of the hard-to-quantify results of the pandemic, those who suffered because they could not get their elective surgery, or who avoided the ER or could not get an ICU bed because of COVID patients.
In the middle of a pandemic like COVID, individual decisions affect everyone.
Also see: https://www.covid-datascience.…h-critical-severe-disease
Key Points:
See the links for notes on interpretation, caveats, etc.
There was contamination in a few vaccine doses in Japan. They killed some people. You can be 100% sure this will NOT HAPPEN AGAIN. The Japanese public would be outraged. Public Health agency heads would be fired. There would be Parliamentary hearings. You can be sure that other governments are being equally careful. With modern monitoring tools, high resolution analysis, and big data record keeping, the likelihood of contamination is much smaller than it was decades ago. You are much more likely to be injured or killed by contaminated lettuce than contaminated COVID vaccines. They are, literally, safer than eating lettuce.
The death rate from all COVID-19 vaccines is less than 1 per billion doses. "Explosive claims" like this are conspiracy theory nonsense. There is not the slightest chance that governments or public health agencies could hide deaths from the vaccines.
Yes they can hide it and they call it excess death.
Boosters provide further protection bu
The added booster protection is about 50%. The Israel study is fake as it has been done in a calm face with no running infections. Further the boosters directly killed 300..500 Israeli by inducing COV-19-. So almost all vulnerable for the next 3 month at least have been killed by the booster "vaccine".
Ignoring facts - just looking at fake studies - that first sight look OK - could be a deadly error. Have the "ziverdo kit" ready. It's a 99% live insurance not just a lucky 50%.
CoV-19 only kills the vulnerable. At most 15% of all CoV-19 deaths have no known background. This is what official statistics of UK/CH show.
The boosters in Israel caused the highest ever seen increase in cases in any nation. The decline in Israel cases has nothing to do with immunity its just the stop of the booster program!!!
Here comes another blast from the sun. Pay attention boys!
Officials confirm blast from the Sun will hit Earth soon, date found
Daszak Admits Gain-of-Function Research Continued, CCP Censoring Data | Truth Over News
The National Institutes of Health (NIH) recently gave EcoHealth five days to submit “any and all unpublished data” from its experiments at the Wuhan lab.
Daszak responded, vacillating between “the dog ate my homework” and “we’re all in this together.” But he failed to provide all of the required data.
Daszak’s letter, more a legal brief than a compliance response, even chastised the NIH for failing to contact him before “responding to any congressional inquiry.”
But three material issues were raised. First, Daszak failed to submit all the data required by the NIH. And the reason for that is chilling.
Daszak’s letter revealed that crucial virus data from EcoHealth’s experiments with the Wuhan lab is actively being censored by Chinese Communist Party authorities.
Finally, Daszak revealed the continuation of experiments in 2019 and beyond. And his letter disclosed the existence of year 6 and year 7 reports that have not been made public.
Welcome to Truth over News with Jeff Carlson and Hans Mahncke.
UK HSA (week 44 report) continues to spread top fake information::
Based on antibody testing of blood donors, 98.0% of the adult population now have antibodies to COVID-19 from either infection or vaccination compared to 18.7% that have antibodies from infection alone.
End of March 2021 already 40% of all UK people had antibodies from infections not from vaccines. The HSA FM/R mafia "cricket brain" folks did intentionally fake the data by looking at blood donors only. "blood donors" March 2021 haven not yet been vaccinated and vaccinated have been excluded as blood donors!! But they look at the average Vaccination rate. This is how professional cheater do work.
So what does HSA prove? Despite vaccination more people with "anti bodies" die than should die.
Translation: Vaccines do not work at all. Infection rate is 3..5x higher than for unvaccinated!!! Protection from death not longer exists for age 80+ just vaccinated and no prior infection.
Average protection from death is 50%. Same here same in Israel. For children it is infinite x negative so far. In Germany so far no child age <=17 died from CoV-19 alone. But 20 from vaccines...
Great job Dr. Mengele fans!
Just to add: Last week UK: 3800 double vaxx deaths and 700 unvaxx deaths.
Just to add: Last week UK: 3800 double vaxx deaths and 700 unvaxx deaths.
Most of those deaths were of people >70, so that's hardly surprising nor something to be concerned about given the way the numbers are counted/defined.
I agree. At most 15% really died of CoV-19... UK had the freedom day.
But here DE,CH,FR,AU the fascists go on...with selling vaccines for their buddies. With denying treatment for CoV-19 victims....
Vaccine mandate for KIDS: San Francisco will force children as young as FIVE to show proof of vaccination to enter indoor venues like restaurants and give parents two month DEADLINE
Goodness! What will they do next? Will they insist that children be vaccinated before they can go to kindergarten!?! The world is coming to an end.
School & Childcare Requirements for Immunizations :: Public Health :: Contra Costa Health Services
Yes they can hide it and they call it excess death.
You cannot hide excess deaths! There is always a reason for them. If they were being caused by vaccines, that would eventually become obvious, and undeniable.
School & Childcare Requirements for Immunizations :: Public Health :: Contra Costa Health Services
Children are treated like Cattle in the US. Human rights seem to have no value in some states. Some vaccines make sense. But the majority is counter productive. May be some like Hepatitis B are needed locally ...Petussis booster.. reminds me of CoV-19 booster as kit is useless and make you a super spreader...
Effect of SARS-CoV-2 proteins on vascular permeability
Abstract
Severe acute respiratory syndrome (SARS)-CoV-2 infection leads to severe disease associated with cytokine storm, vascular dysfunction, coagulation, and progressive lung damage. It affects several vital organs, seemingly through a pathological effect on endothelial cells. The SARS-CoV-2 genome encodes 29 proteins, whose contribution to the disease manifestations, and especially endothelial complications, is unknown. We cloned and expressed 26 of these proteins in human cells and characterized the endothelial response to overexpression of each, individually. Whereas most proteins induced significant changes in endothelial permeability, nsp2, nsp5_c145a (catalytic dead mutant of nsp5), and nsp7 also reduced CD31, and increased von Willebrand factor expression and IL-6, suggesting endothelial dysfunction. Using propagation-based analysis of a protein–protein interaction (PPI) network, we predicted the endothelial proteins affected by the viral proteins that potentially mediate these effects. We further applied our PPI model to identify the role of each SARS-CoV-2 protein in other tissues affected by coronavirus disease (COVID-19). While validating the PPI network model, we found that the tight junction (TJ) proteins cadherin-5, ZO-1, and β-catenin are affected by nsp2, nsp5_c145a, and nsp7 consistent with the model prediction. Overall, this work identifies the SARS-CoV-2 proteins that might be most detrimental in terms of endothelial dysfunction, thereby shedding light on vascular aspects of COVID-19.
Due to the impact of SARS-CoV-2, many studies have looked at the physiological responses to the virus (Lee et al., 2021; Libby and Lüscher, 2020; Siddiqi et al., 2020; Teuwen et al., 2020; Chioh et al., 2020). In this work, we sought to identify how specific SARS-CoV-2 proteins affect the vasculature by assessing the effect of individual SARS-CoV-2 proteins on endothelial cells (HUVEC). This approach has significant advantages: it enables pinpointing and isolating how each of the SARS-CoV-2 proteins independently affects the endothelial response, and directly measuring endothelial functionality. The HUVEC model, derived from the umbilical cord, is physiologically representative of the human vascular endothelium, allowing the study of the physiological and pathological conditions as well as the effects of novel drugs on human endothelium (Bouïs et al., 2001; Medina-Leyte et al., 2020). Among technical advantages, cultured HUVECs are a simple in vitro vascular endothelial model, particularly suitable for studying endothelial properties and dynamics as well as the putative role of adhesion molecules, the synthesis of extracellular proteins and blood vessel maturation (Vailhé et al., 2001).
The current study showed that almost 70 % (18 out of 26) of the SARS-CoV-2 proteins affect endothelial barrier integrity; however, the most significant proteins were nsp2, nsp5_c145a, and nsp7, which also induced upregulated expression of the coagulation factor VWF and cytokine release. These critical facts can shed light on the multiple pathologies observed in SARS-CoV-2 infection, including cytokine storm, increased coagulation and related diseases (e.g., heart attack and stroke) (Lee et al., 2021; Aid et al., 2020), increased cardiovascular disease, and increased neurological symptoms. The results presented here showed an effect of in vitro cultured endothelial cells, which may lead to vasculature leakiness, consequently causing exotoxicity (i.e., the penetration of toxic reagents from the blood into the brain). While there are many parameters associated with functional changes, the use of advanced tools, including network-based analysis, enabled us to elucidate the specific proteins and the specific interactions that are predicted to cause these changes. The PPI network enabled us to predict that the changes observed in barrier function are possibly due to interactions between host proteins such as cadherin 2, α-catenin, β-catenin, δ-catenin, and ZO 1 and 2, and at least with the viral proteins nsp2, nsp5_c145a, and nsp7. Moreover, we validated our PPI model performing further immunostaining analysis demonstrating not only the ability of the viral proteins to strongly impair TJ expression, but also to confirm the data predicted by our model in which some TJ proteins can be more affected than others.
PPI analysis revealed a highly correlated effect of nsp7 and nsp13 on β-catenin in endothelial cells (Figure 4b; Jung et al., 2020a; Lengfeld et al., 2017). Interestingly, neither nsp2 nor nsp5_c145a affected a high number of proteins (Figure 7b), whereas nsp7 did, as identified by the network. Analyzing the repertoire of SARS-CoV-2 proteins, we see almost no effect of the structural proteins; rather, mostly nonstructural and open reading frame proteins affected HUVEC functionality, manifested as decreased barrier function and increased cytokine secretion (Figures 2 and 3). While the nonstructural proteins are mainly responsible for replicating viral RNA, the open reading frame proteins are related to counteraction with the host immune system; some of these are localized to the mitochondria and have been shown to alter the mitochondrial antiviral signaling pathway (Miller et al., 2021). We found that the proteins most affecting barrier function (decreased TEER and decreased CD31, β-catenin, cadherin-5, and ZO-1 expression) and cytokine response (IL-6 secretion and VWF expression) were nsp2, nsp5_c145a, and nsp7 (Figure 2; Figure 3; Figure 6); nsp7 forms a replication complex with nsp8 and nsp12 that is essential for viral replication and transcription (Cowen et al., 2017; Peng et al., 2020a). Peng et al., 2020b suggested that in the core polymerase complex nsp7–nsp8–nsp12, nsp12 is the catalytic subunit, and nsp7 and nsp8 function as cofactors. They further suggested that the mechanism of activation mainly involves the cofactors rather than the catalytic subunit (Peng et al., 2020b). This might explain why we saw mainly an effect of the cofactor proteins on endothelial cells and almost no effect of the catalytic subunit. Network interactions Díaz, 2020 have shown that nsp7 has the most interactions with the host, suggesting a potential target for the treatment of COVID-19. Moreover, no mutations were found in nsp7 compared to nsp2 or nsp5_c145a (Kaushal et al., 2020), suggesting a conserved protein with a vital function in virus survival. The nsp13 protein has both helicase activity and 5’ triphosphatase activity, which play an important role in mRNA capping. We saw a significant effect of nsp13 on barrier function, but hardly any effect on cytokine secretion. Chen et al., 2020, suggested functional complexation between nsp8 and nsp12, the RdRp (RNA-dependent RNA polymerase) replication complex, and nsp13. Given the fact that we observed a substantial effect of nsp7 – one of the proteins of the replication complex – and an effect of nsp13 on HUVEC barrier function, complexation of nsp13 with the replication complex might indicate an important role for this complex in the impaired functionality of the HUVECs, and therefore in the propagation of the disease, and the known vascular damage seen in COVID-19 patients. As suggested by our model, nsp13 seems to have a strong effect also on other types of vascular endothelial cells (Figure 6) as well as on all cell types (Figure 7a), positioning nsp13 as one of the main targets for disease treatment.
It is important to note that the comparison between the different endothelial cell types revealed exciting differences in the TJ protein expression, which correlate to the different properties of the different cell types (Nakato et al., 2019). One of the major differences was that some endothelial cell lines do not have cadherin at all (e.g., HAoEC), or very limited amount of cadherin (e.g., HPAEC, HUAEC, HGSVEC). Our model suggests that some endothelial types (e.g., HUVEC, HUAEC, HGSVEC, HCAEC) are more susceptible to the SARS-Cov-2 virus. It, therefore, suggests that the treatment of one type of endothelial cell might be different from another type but offers the PPI model as a tool for initial prediction. Overall, the combination of identifying the differences in the TJ protein expression between the different endothelial cells and the use of the PPI model enabled us to pinpoint the differences in susceptibility to the disease and to identify which specific proteins have the most significant effect.
Many studies have looked at the SARS-CoV-2 interaction with nonpulmonary/nonvascular tissues (e.g., neurons, hepatocytes, immune components such as lymphocytes, macrophages, etc.) (Lee et al., 2021), as pathological studies identified a viral effect on these tissues, despite their very limited amount, or lack of ACE2 receptors. To better understand how SARS-CoV-2 interacts with and affects other tissues, we consolidated all of the proteins currently known to be affected by the virus into Supplementary file 1A. It is interesting to note that the most dominant SARS-CoV-2 proteins are nsp4, nsp11, and nsp7. Davies et al., 2020, identified the interaction of nsp2 with nsp4, both involved in endoplasmic reticulum (ER) calcium signaling and mitochondrial biogenesis. This suggests a new functional role in the host ER and mitochondrial organelle contact process and calcium homeostasis.
By now it is clear that vasculature plays a significant role in the physiological response to the virus. However, it is still unclear how the virus affects the vasculature, and if it can be found in the blood. This is a critical question, as it has significant consequences on the extent of the virus’s ability to affect the vasculature. Current studies demonstrate that the pulmonary vasculature is significantly affected and is one of the dominant triggers for the pathologies mentioned above. However, involvement with the rest of the vasculature is still unclear, as is whether the virus can be found in an active form in the blood circulation (Peng et al., 2020a; Chang et al., 2020; Orologas-Stavrou et al., 2020; Andersson et al., 2020; Escribano et al., 2020; Wang et al., 2020b). Some studies suggest that even if there are traces of SARS-CoV-2 in the blood, it is not in an active form and cannot cause disease or a systemic response (Andersson et al., 2020). On the other hand, some studies suggest that SARS-CoV-2 can be found in the blood, and can induce the disease and cause both cellular and systemic dysfunction (Peng et al., 2020a; Chang et al., 2020; Escribano et al., 2020). While this question is beyond the scope of this work, it is important to note that if future studies do identify the active form of SARS-CoV-2 in human blood, then the implications of our findings will apply to this systemic response as well (Ahmed et al., 2020; Park et al., 2020).
As already noted, the pathology is probably a combination of multiple conditions and pathways activated by the different proteins. However, our findings might open new avenues for future therapeutics. Moreover, most of the proteins that were identified as affected by SARS-CoV-2 had a distance factor of at most three to the human and viral proteins. This coincides with the current dogma, whereby proteins that have a shorter distance between them are more likely to be affected.
While beneficial, our approach has two major limitations: (a) our inability to identify the effect of multiple proteins and (b) our neglect of the effect of the coronavirus structure and binding on the cellular response. The former point can be overcome by expressing combinations of different SARS-CoV-2 proteins. However, since the SARS-CoV-2 expresses 29 proteins, there are about ~9 × 1030 possible protein combinations. Therefore, we decided to focus on individual proteins and allow further studies to pursue any combinations of interest. Regarding the latter limitation, we did not include the coronavirus structure (including the ACE2 receptors) in this study, because many studies have already demonstrated the cellular response to this structure (Chioh et al., 2020; Yang et al., 2020; Procko, 2020), and how tissues that do not have significant ACE2 expression (neurons, immune components such as B and T lymphocytes, and macrophages) are affected by the virus remains an open question.
Conclusions
Accumulating clinical evidence suggests that COVID-19 is a disease with vascular aspects. However, only a few studies have identified the specific role of each of the SARS-CoV-2 proteins in the cellular response leading to vascular dysfunctions. In this work, we characterized the endothelial response to each of 26 SARS-CoV-2 proteins and identified those that have the most significant effect on the barrier function. In addition, we used PPI network-based analysis to predict which of the endothelial proteins is most affected by the virus and to identify the specific role of each of the SARS-CoV-2 proteins in the observed changes in systemic protein expression. Overall, this work identified which of the SARS-CoV-2 proteins are most dominant in their effect on the physiological response to the virus. We believe that the data presented in this work will give us better insight into the mechanism by which the vasculature and the system respond to the virus, and will enable us to expedite drug development for the virus by targeting the identified dominant proteins.
Vitamin D effects on musculoskeletal health, immunity, autoimmunity, cardiovascular disease, cancer, fertility, pregnancy, dementia and mortality-a review of recent evidence
Well one was given the green light this morning so I guess this is preordained. This from 2 weeks ago.
Covid-19: UK stockpiles two unapproved antiviral drugs for treatment at home
The UK has started stockpiling two antiviral drugs as part of a plan to give people who are staying at home with covid-19 a treatment to reduce symptoms and the spread of the virus.
The government has purchased 480 000 courses of molnupiravir (made by Merck Sharp and Dohme (MSD)) and 250 000 courses of the combination of PF-07321332 and ritonavir (Pfizer), neither of which have been approved by the UK’s regulator of medicines.
In its announcement the Department of Health and Social Care for England said that if the treatments were approved by the Medicines and Healthcare Products Regulatory Agency they will be rolled out to people most at risk of covid-19, with the aim of reducing symptom severity and “easing pressure on the NHS over winter.”
The drugs were selected by the Antivirals Taskforce, which was formed in April with the aim of finding at least two effective treatments in 2021.1
Speaking at a televised press conference on 20 October, England’s health and social care secretary, Sajid Javid, said, “It’s a really new, fresh tool. These are the first antivirals ever that have been designed for covid. This is great news, but we cannot be complacent when covid-19 remains such a threat.”
The health department said that the government and the NHS were now working on plans for a national study to evaluate the treatments and deploy them.
Molnupiravir
MSD reported earlier this month that molnupiravir reduced the risk of admission to hospital or death by around 50% in non-hospitalised adults who had mild to moderate covid-19 and were at risk of poor outcomes.2
The interim phase III trial results were released though a press release. This said that 7.3% of patients (28 of 385) who received molnupiravir and 14.1% of patients taking placebo (53 of 377) either were admitted to hospital or had died by day 29 after randomisation. At day 29 no deaths were reported in the molnupiravir group, while eight were reported in the placebo group. Recruitment to the trial was then stopped on the advice of the independent data monitoring committee because of the positive results.
PF-07321332/ritonavir
Three phase II and III trials are currently ongoing to test the combination of the novel oral antiviral candidate PF-07321332 and ritonavir in non-hospitalised patients, at low3 or high risk,4 and in adult household contacts of an individual with symptomatic covid-19.5 Details of the PF-07321332 and ritonavir phase I trial results have not been released, with Pfizer saying only that the combination was found to be “safe and well tolerated.”6
Ritonavir had previously been trialled against covid-19 in combination with lopinavir but was found to be ineffective in terms of improving survival among patients in hospital. Data from the Recovery trial showed that, at 28 days, the death rate among patients randomly allocated to receive lopinavir-ritonavir was not significantly different from the rate in people randomly allocated to usual hospital care only. Also, there was no evidence of beneficial effects on risk of progression to mechanical ventilation or on length of hospital stay.7
Previous stockpiling: Tamiflu
The government’s previous record on stockpiling of antivirals had proved controversial, particularly oseltamivir (Tamiflu), stockpiled on a large scale after the 2009 H1N1 “swine” flu pandemic, despite a lack of evidence to support its use. A 2009 Cochrane investigation into the evidence for the drug found that many of the studies used to support its efficacy were unpublished. The manufacturer, Roche, refused to provide the full data from the studies unless confidentiality agreements were signed, and this led to a public campaign—much of it done through The BMJ (bmj.com/tamiflu)—to put pressure on companies to release the underlying clinical trial data. The campaign lasted four years and was ultimately successful.
The 2014 Cochrane review that followed found no compelling evidence to support claims that oseltamivir reduced the risk of flu complications, such as pneumonia and hospital admission, which were used to justify international stockpiling.8
These are the first antivirals ever that have been designed for covid.
This is a 1000% lie. Merck did work on its crap for more than 10 years now with obviously no success as it even does not work for CoV-19....Just one more way to make money and trade in stock gains for manager options.
MSD reported earlier this month that molnupiravir reduced the risk of admission to hospital or death by around 50%
No study so far did show show this. Just management news. I guess they still have to find a way to cheat the public... But there is no more public. Just the mafia that own, controls and feeds the media.
Its all about a reason how you can steal tax payers money for your buddies pocket.
We (UK..) are back in stone age!
COVID-19 Cases & Deaths Skyrocket in Germany as Breakthrough Infections on the Rise
Although Germany is nearly 70% fully vaccinated—and the overwhelming majority of people 18 and up are immunized—the number of COVID-19 cases now skyrockets as a fourth wave sweeps through Germany and other parts of Europe. With vaccines that only last a few months before breakthrough infections are frequently happening, authorities now must factor in ongoing pandemic conditions, at least for the short run.
The Numbers
Germany has experienced a few surges of infections starting in March and April of 2020 and then a massive second surge between October 2020 and the end of 2020. A mass vaccination campaign went into full gear in the new year; however, by March 2021, cases started spiking again.
However, by May 2021, cases plummeted as undoubtedly, vaccination was helping along with several public health measures taken by health authorities led by German Health Minister Jens Spahn. By July 1, 2021, the average number of new cases (7-day average) was down to 578 per day, the lowest number of infections since earlier in 2020. However, infections started creeping upward in August, and by September 10, the 7-day average of new infections spiked to 10,858 per day. But again, with intensive vaccination, the general consensus was that the cases would be headed back down.
However, TrialSite has followed nation after nation that is heavily vaccinated yet still become subjected to intensive surges, from Israel and Iceland to Seychelles and Ireland to pockets in America. Breakthrough infections were on the rise as study after study indicated the vaccine effectiveness wanes after a few months, leading to higher transmissibility among even the vaccinated.
Now Germany finds itself headed back into a crisis. Cases skyrocketed on November 3 as 34,498 new cases were reported with a seven-day average of 19,907 according to data from the COVID-19 Data Repository by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University.
Moreover, while the overall death rate is down due to a confluence of factors—including vaccination, more care options, and wiser public health measures—they are on the way back up. For example, by August 15, the number of new deaths reported nationwide in this country of over 80 million was 4 for the day and 12 on a seven-day average. That rate exploded to 165 on November 3, or 101 on a seven-day average. A disturbing trend, to say the least.
Health Minister Jens Spahn said that the country was facing a “massive” pandemic, declaring to German media Bild that the unvaccinated were the problem.
Not Just the Unvaccinated
But this just isn’t the case. German media such as DW reports that breakthrough cases are on a steady rise as thousands of inoculated people get sick.
Of course, this doesn’t mean the vaccines don’t work, but it does mean that A) they don’t provide 100% protection, and B) many studies now evidence that after a few months, the durability of the vaccines is in question. According to a recent national Swedish study, the Pfizer vaccine effectiveness wanes after month three, and by month six, the vaccine provides little protection from breakthrough infections. However, the vaccines may continue to provide more protection against more serious infection after month six. The point here is vaccination overall helps stop more severe disease and hospitalization. Still, months after the second dose, the durability comes into question—more breakthrough infections and transmission occur from the vaccinated to the vaccinated or the vaccinated to the unvaccinated as well as the unvaccinated to the vaccinated.
Solar storm 'red alert' for flights and GPS as huge CME continues to batter Earth
Solar storm 'red alert'
May be Alan can take some pictures!? It should be visible in middle UK.
One more payload caused by the vaccine terrorists! (Eating disorders and stress..)
FUKUOKA -- The number of people aged under 20 in Japan who were newly diagnosed with anorexia -- a commonly known eating disorder -- in fiscal 2020 increased by about 1.6 times compared to the previous year in what may be a consequence of lifestyle changes triggered by the coronavirus pandemic, a survey by the National Center for Child Health and Development in Tokyo has revealed.
