By Habibi Bros. Published originally on Rumble on August 17, 2022
Siraj and Jay discuss the CDC admitting to f*cking up the COVID-19 pandemic response, Liz Cheney gets ousted from Congress, developments in the FBI raid of Trump’s home at Mar-A-Lago, and the one-year anniversary after the catastrophic Afghanistan withdrawal. It’s everything that makes you want to drink on Habibi Power Hour.
Additionally, nearly 20% of gay men who fell ill admitted to having 10 or more partners in the three weeks before symptoms began. About 40% of those who fell ill reported having two to four partners, while 14% reported having five to nine partners. Around 38% admitted to participating in group sex.
This is more of a sexually transmitted disease and should be presented to the public as such. CDC guidance:
“Public health efforts should prioritize gay, bisexual, and other men who have sex with men, who are currently disproportionately affected, for prevention and testing, address equity, and minimize stigma, while maintaining vigilance for transmission in other populations.”
There is no need to stigmatize people for their sexual preferences or repeat problematic misinformation that spread during the 80s during the AIDS epidemic. However, there is no need to scare the general public into thinking that monkeypox is easily transmissible. If they care about health (they don’t), then they should be honest about the virus and educate the demographic mainly at risk.
Geert Vanden Bossche, DVM, PhD General Manager at Voice for Science and Solidarity | The biggest challenge in vaccinology: Countering immune evasion originally published on TS News on Aug. 5, 2022
MIS-C is a disease that may occur in school-age children two to six weeks after infection with SARS-CoV-2 (SC-2) virus. MIS-C is a post-infectious inflammatory condition which typically occurs after asymptomatic/mild SC-2 infection. Some children may need hospitalization because of inflammatory reactions in different organs. While the syndrome can be serious, the absolute risk for MIS-C is very low (about 6.5 per 100 000 person-years) and known to be increased in boys aged 5-11 years with foreign-born parents, asthma, obesity, and life-limiting condition (https://www.thelancet.com/action/showPdf?pii=S2666-7762%2822%2900137-5). MIS-C mostly resolves within a few days after timely and adequate (immunosuppressive) treatment. As the pandemic evolves and more infectious Omicron (sub)variants are now dominating the scene, MIS-C is occurring less frequently and with diminished severity of disease (https://jamanetwork.com/journals/jama/fullarticle/2792718). This evolution cannot be entirely explained by C-19 vaccination of young children as vaccine coverage rates in this age group are still very low (15% and 3% as recently reported in studies from Israel and the US, respectively; https://jamanetwork.com/journals/jama/fullarticle/2792718; https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciac471/6605071). It is therefore tempting to speculate that enhanced viral infectiousness and transmission significantly contribute to dampening the incidence rate and severity of MIS-C in young children. This suspicion is supported by a previous study in which the authors speculated that some of the risk factors they identified for MIS-C could be associated with enhanced disease transmission (e.g., in children with foreign-born parents or explaining the shift in age from 12-15 years down to 5-11 years amongst children with MIS-C throughout the pandemic (https://www.thelancet.com/action/showPdf?pii=S2666-7762%2822%2900137-5).
To better understand the origin of the disease, and why children in particular are susceptible to contracting MIS-C, it is important to understand how the child’s innate immune system is educated and trained to combat infections with glycosylated viruses causing acute self-limiting viral infection (ASLVI; e.g., SC-2) or acute self-limiting viral disease (ASLVD).
The child’s innate immune system first learns to discern relevant pathogen-derived molecular patterns and discriminate them from self-derived motifs. Once the child’s natural killer (NK) cells have been ‘educated’ (pre-primed) to adequately sense and distinguish pathogen-derived self-mimicking peptides (PSMPs) from self-derived self-mimicking peptides, presentation thereof in high density patterns may trigger epigenetic changes that imprint these NK cells with memory (so-called ‘training’ of NK cells).
In young children who have cleared their maternal antibodies (around the age of 6 months), abundantly produced innate (sometimes called ‘natural’) antibodies (Abs) play a critical role in initiating active use of their own immune system. In these children, innate Abs are tasked with recognizing and binding free-circulating self-derived glycan motifs (e.g., decorating foreign-derived [including pathogen-derived] or self-derived proteins) to potentiate the presentation of repetitive patterns of foreign- or self-derived self-mimicking peptides on the surface of autologous somatic cells or antigen (Ag-)presenting cells (APCs). Glycosylation of self-proteins is an important mechanism for inducing T cell-mediated peripheral tolerance and, not surprisingly, mimicked by several pathogens (e.g., glycosylated viruses) as a strategy to subvert the host immune system. As they decorate themselves with self-mimicking patterns of self-glycans, glycosylated viruses (e.g., corona virus [CoV], influenza virus, respiratory syncytial virus [RSV], measles, mumps, rubella, varicella virus,…) can be recognized and captured by innate Abs and thereby contribute to educating the child’s innate immune effector cells (i.e., NK cells).
As the child grows up, the functional capacity of their innate Abs gradually declines so that their immune system can progressively replace the ‘self’-sensing innate Ab capacity by a pool of pre-primed NK cells that can recognize pathogen-derived self-mimicking (i.e., ‘altered self’) motifs on virus-infected or otherwise pathologically altered host cells such as to kill those cells. For as long as a child possesses an abundant functional capacity of innate Abs, glycosylated pathogens and self-ligands will be complexed by innate Abs to educate NK cells on how to distinguish ‘self’ from ‘non-self’. This is how the innate immune system of the young child is thought to ‘adapt’ to the early-life extra-maternal environment where it must learn to rapidly sense peptide motifs that differ from self-peptides. This would enable NK cells to target and kill autologous host cells that are decorated with such ‘altered self’ peptides (e.g., infected, or otherwise pathologically altered host cells).
Once NK cells are educated, the NK cell training process dictates their functional re-programming (https://www.frontiersin.org/articles/10.3389/fimmu.2018.01869/full). Training is thought to result from epigenetic alterations that are triggered by changes in the SC-2 infectious landscape and generate ‘adaptive’ or ‘memory-like’ NK cells. Adequate training of its first line of immune defense enables the child to mount protective natural immunity against SC-2 (and other glycosylated viruses/ pathogenic agents sharing the same PSMPs) upon future exposure. This can already explain why prophylactic childhood vaccinations using live attenuated virus are very efficient at inducing natural immunity against measles, mumps, rubella, varicella and generating herd immunity−it’s only when they become infected with an antigenically ‘shifted’ (i.e., very different) variant that individuals who acquired natural immunity can still contract disease due to ADEI.
However, depending on viral infectious pressure, it is perfectly possible, even for a young and healthy child, to become susceptible to productive infection upon exposure to glycosylated, ASLVI-enabling viruses that do not normally cause symptomatic infection in young children.
When young and healthy children become infected during an outbreak of a virus with a relatively low reproduction number (R0; e.g., infection with common cold coronavirus [CoV] or seasonal Flu; R0 < 2.5), they almost always develop asymptomatic or very mild infection. However, dominant circulation of more infectious CoV or Influenza virus variants can occasionally provoke cases of severe disease in children. It is reasonable to postulate that enhanced viral infectiousness raises the chance for a person to become re-infected shortly after a previous course of asymptomatic infection. This will increase the likelihood that immature, short-lived Ag-specific Abs of relatively low affinity, which typically develop after asymptomatic/ mild infection, will still be present when that person becomes re-exposed to the virus. Because of their Ag-specificity, these Abs may outcompete the child’s innate polyspecific IgM Abs, which have an even lower affinity for the protein Ag that is responsible for initiation of infection (i.e., spike [S] protein in the case of CoV). Depending on their titer, these non-neutralizing, Ag-specific Abs can therefore prevent or at least diminish binding of innate Abs to the virus. Although these short-lived Abs cannot neutralize the virus, they can bind to it and enhance its infectiousness.
This is particularly problematic in young children as insufficient training of their NK cells prevents effective immune targeting of SC-2-infected cells expressing virus-derived self-mimicking peptides on their surface. NK cells that are largely ‘pathogen-inexperienced’ together with enhanced SC-2 infectiousness would entail enhanced susceptibility of young children to SC-2 infection (i.e., so called ‘Ab-dependent enhancement of viral infectiousness’; ADEI). Hence, re-infection shortly after previous asymptomatic exposure will likely allow the virus to break through the cell-based innate immune system of young children and could potentially cause (severe) disease (https://pubmed.ncbi.nlm.nih.gov/33391280/). However, as these post-infectious Abs wane rapidly (they are no longer detectable at about 8 weeks), only a limited number of children will become re-exposed to the circulating virus shortly after their previous productive exposure. This already explains why most cases of MIS-C occur between 2 and 6 weeks (on average 4 weeks) after the previous asymptomatic/ mild infection, presumably depending on the titer of the infection-enhancing Abs at the timepoint of re-exposure. It is therefore not surprising to also observe high variability in the severity of MIS-C disease.
More infectious SC-2 variants may enable stronger stimulation of NK cells and thereby readily prime NK cell effector responses in young children; alternatively,more infectious SC-2 variants could increase the likelihood for viral re-exposure to occur in the presence of a relatively higher titer of infection-enhancing anti-S Abs. Both phenomena are likely to reduce the risk of MIS-C in young children.
After many years of NK cell vaccine research (which I was unable to publish for intellectual property reasons), I determined that the recruitment on MHC class I molecules of PSMPs into ‘non-self’ high-density arrays (situated outside of the MHC class I peptide-binding groove!) is what allows for activation and epigenetic imprinting (i.e., training) of cytotoxic NK cells that are capable of killing host cells that present such PSMPs on their surface (for example as a result of viral infection). I postulate that strong stimulation by enhanced viral infectiousness could even obviate the need for cumulative triggering of NK cells (so-called ‘training’) in order for NK effector cells to become imprinted with memory. NK cells that have acquired a memory-like phenotype could readily eliminate host cells that are infected with relevant glycosylated pathogens. Enhanced viral infectiousness in the young child could allow productive SC-2 infection even in the presence of innate Abs and thereby enable ‘power training’ of pre-primed NK cells. Even though symptoms could still be mild, productive infection would have the capacity to substitute a single ‘power training’ event for regular, incremental training of functional NK cell responsiveness to pathogen-derived ligands. As full-fledged NK cell ‘priming’ towards PSMPs would therefore improve with enhanced viral infectiousness, C-19 unvaccinated children (and even some adolescents) who recently contracted mild disease would be equipped with innate immune memory while no longer developing infection-enhancing anti-S Abs (as shown in fig. 1). Alternatively, enhanced viral infectiousness leads to higher viral infection rates and thereby shortens the average time window for a person to become re-exposed after a previous asymptomatic SC-2 infection. A shortened window for re-exposure makes it more likely that the latter occurs in the presence of a relatively high titer of infection-enhancing Abs. It is not unreasonable to assume that the mechanism of naturally induced infection-enhancing Abs is similar to the one previous described for vaccine-induced anti-S Abs−a high enough concentration of these Abs would allow a subset of these Abs to bind to SC-2 virions tethered to dendritic cells and thereby exert a disease-mitigating effect (https://www.voiceforscienceandsolidarity.org/scientific-blog/predictions-gvb-on-evolution-c-19-pandemic + fig. 2).
Based on the rationale explained above, one could easily understand how the prolonged C-19 pandemic and the enhanced frequency of repetitive waves of more infectious variants (e.g., Omicron) is likely to have a ‘power training’ effect on relevant NK cells of young C-19 unvaccinated children developing mild primary infection (i.e., overlapping with abundant functional capacity of innate Abs) or to provide a strong disease-mitigating adaptive immune response in those who recently contracted asymptomatic SC-2 infection. The latter would be protected from severe and even moderate disease by virtue of infection-enhancing Abs and cytotoxic CD8+ T cells, respectively (as illustrated in fig. 2). A further increase in viral infectiousness would not make young, previously asymptomatically infected children more susceptible to disease but rather increase their likelihood to develop productive SC-2 infection and generate effector memory NK cells or further expand those (as shown by the arrows in green in fig. 1). With this understanding, it is not surprising that the advent of Omicron (sub)variants has led to a rapidly regressing incidence rate and severity of MIS-C (https://jamanetwork.com/journals/jama/fullarticle/2792718).
How does mass vaccination affect the child’s susceptibility to SC-2 infection?
As the mass vaccination program during this pandemic has led to the dominant circulation of more infectious SC-2 variants, it is not surprising to find that a few, young (C-19 unvaccinated) children contracted MIS-C and even needed hospitalization—this was an extremely rare event at the beginning of the pandemic. However, the mass vaccination program has provided immune escape variants characterized by a higher level of intrinsic viral infectiousness (e.g., of the delta variant) with a competitive advantage. The ensuing higher infection rate in the population (and in households!) therefore came with an additional likelihood for young children to become re-infected shortly after their previous asymptomatic infection. As previously described, the incidence rate of MIS-C is now waning as a result of enhanced innate immune training and mitigation of (severe) disease by more and more infectious SC-2 variants that have now become dominant.
Vaccinating children against SC-2 is a colossal scientific blunder with potentially disastrous health consequences
On the other hand, diminished complexation of foreign glycosylated ligands by innate Abs could render NK cells that lack self-MHC-I inhibitory receptors hyporesponsive to stimulatory receptor activation as a result of their chronic low-level stimulation by self-derived peptides. Because of the resulting diminished threshold of NK cell activation in the periphery, young C-19 vaccinated children would be prone to developing immunopathologies. However, in the likely event that resistance to potentially virulence-‘neutralizing’ Abs develops, it can be expected that−given the high SC-2 infection rate− C-19 vaccinated infants and toddlers will primarily succumb to Ab-dependent enhancement of severe C-19 disease rather than to severe disease from any other circulating ASLVI or ASLVD or from immunopathology.
Increased SARS-CoV-2 exposure results from dominant expansion of more infectious SC-2 variants, a phenomenon undeniably caused by the C-19 mass vaccination program. As suggested by the results from earlier studies, increased exposure to SC-2 together with a number of predisposing factors renders very few young children susceptible to developing MIS-C following a recent asymptomatic infection (https://www.thelancet.com/action/showPdf?pii=S2666-7762%2822%2900137-5). There is no doubt that vaccinating children against SC-2 is a colossal blunder and merely places the child at high risk of severe health damage. MIS-C has not only a low incidence (which is further declining) but can also be successfully treated using conventional drug therapy. This contrasts with the protective effect of C-19 vaccination against MIS-C, which is temporary and leaves the young child at high risk of contracting Ab-dependent enhancement of severe disease upon future exposure to new SC-2 variants (which will dominantly emerge as a result of the current population-level immune pressure on viral virulence). It is critical to understand that the high viral infection rate in highly C-19 vaccinated populations due to mass vaccination, rather than a lack of C-19 vaccination, is responsible for this phenomenon. There is therefore no single scientific rationale for vaccinating children against SC-2−exactly the contrary is true: C-19 vaccination of young children is highly likely to not only provoke a soaring incidence of severe disease and mortality due to immunopathology and other microbial diseases but ultimately also due to SC-2. Public health authorities are creating the illusion for parents that C-19 vaccines will protect their children, instead of educating them how to recognize early signs and symptoms of MIS-C in order to seek highly effective treatment for their child in due time. In addition, they seem to ignore that preserving natural immunity in young children is critical as it is the key pillar of herd immunity to ASLVIs, including SC-2.
Fig. 1: Upon exposure to more infectious SC-2 variants, young children may develop MIS-C as a result of re-exposure shortly after previous asymptomatic infection. However, as their infectiousness increases, new SC-2 variants may break through the child’s innate Ab-mediated protection and thereby cause mild infection that imprints its NK cells with memory and therefore dramatically boosts the child’s first line of immune defense. Alternatively, more infectious variants enable re-exposure in the presence of higher titers of short-lived infection-enhancing anti-S Abs. In the latter case, young children are protected from severe disease presumably because a subset of anti-S Abs can bind to SC-2 virions tethered to dendritic cells (see fig. 2), thereby inhibiting severe/systemic disease whereas sustained activation of CTLs (as a result of the infection-enhancing capacity of these Abs upon their binding to free virions) further mitigates C-19 disease. Both scenarios may be responsible for the observed reduction in the incidence rate and severity of MIS-C as the pandemic continues to evolve (indicated by “–“ and arrows in blue). Since the pandemic has now evolved highly infectious SC-2 variants (i.e., the new Omicron [sub]variants), viral exposure of young children is more and more likely to readily cause mild infection resulting in NK cell ‘power training’ and further expansion of effector memory NK cells upon a further increase in viral infection rates (indicated by “+” and arrows in green). This may ultimately prevent young children from developing MIS-C all together.
Fig. 2(from https://www.trialsitenews.com/a/epidemiologic-ramifications-and-global-health-consequences-of-the-c-19-mass-vaccination-experiment-a212bb47): Acute, self-limiting viral infections that don’t lead to systemic/severe disease (and possibly death) are terminated by M(ajor) H(istocompatibility) C(omplex)-unrestricted, cytotoxic CD8+ T cells that have no memory and the activation of which is triggered by a universal, pathogen-nonspecific Tc epitope comprised within the spike (S) protein. Unless an infected person progresses to developing severe disease, this is what allows a fairly rapid recovery from disease after primary productive infection (and certainly before fully functional virus-neutralizing Abs peak) [according to 2a-2b-2c-2d pathway]. However, rather than stimulating de novo generation of new neutralizing Abs towards variants that escaped the neutralizing activity of vaccine-induced Abs, exposure of vaccinees to these immune escape variants will rapidly boost their declining titers of non-neutralizing, infection-enhancing Abs (those are directed against an antigenic site that is conserved within the N-STD of all SC-2 variants and has therefore a license to commit ‘antigenic sin’ once it has primed the host’s immune system).
In vaccinees with poor experience in fighting productive infection (and hence, poor training of their innate immune defense according to pathway 1a-1b-1c) prior to C-19 vaccination, infection-enhancing Abs that are responsible for preventing severe disease by binding to DC-tethered virus (according to 3a-3b-3c-3d pathway) can synergize with strongly activated cytotoxic CD8+ Tc-mediated killing (3c’) to even prevent C-19 disease all together and hence, render vaccinees asymptomatic despite their high susceptibility to re-infection (B + C ? D). As prevention of disease is not due to prevention of productive infection but to accelerated abrogation of infection, these vaccinees will continue to shed and transmit SC-2 upon re-infection. Whereas innate immune effector cells are MHC-unrestricted and polyspecific (i.e., NK cells) and, therefore, don’t drive immune escape, the infection-enhancing-Abs are Ag-specific (i.e., S-specific) and – if produced at high enough titers and with high enough affinity by a large part of the population – will promote natural selection of immune escape variants that can resist the virulence-inhibiting capacity of these Abs. This is because vaccinees cannot prevent productive viral infection; consequently, the immune pressure they exert on viral virulence is suboptimal in that it cannot prevent the expansion in prevalence of immune escape SC-2 variants that have the capacity to overcome this immune pressure. Resistance of viral variants to the virulence-inhibiting activity of infection-enhancing Abs will inevitably cause Ab-dependent enhancement of severe disease (ADESD).
1. Education of NK cells that lack self-MHC-I inhibitory receptors but are endowed with germline-encoded NK cell activation receptors dictates their functional capability to recognize self- or pathogen-derived self-mimicking ligands and mediate innate effector functions; https://www.frontiersin.org/articles/10.3389/fimmu.2018.01869/full
2. Besides their neutralizing activity, natural/innate Abs can, indeed, serve as immune potentiators (‘natural adjuvants’) to upregulate the presentation of antigens on cell surface-expressed MHC class I molecules https://pubmed.ncbi.nlm.nih.gov/14502281/)
4. Enveloped glycosylated viruses are critical to educate the child’s innate immune system in ways that allow recognition and elimination of somatic cells expressing PSMPs (as a result of viral infection or other pathologic alteration) which may otherwise induce tolerance (e.g., cancer cells) or provoke autoreactive or immune inflammatory responses (i.e., causing autoimmune or hyperinflammatory disease, respectively).
NorthShore University HealthSystem in Chicago was sued by a nonprofit religious organization called Liberty Counsel. The group claims that NorthShore violated workers’ religious autonomy by dismissing religious exemptions and forcing all workers to receive the COVID-19 vaccine. NorthShore was in the wrong and decided to settle for $10,337,500.
Other groups will follow suit. They may have granted the pharmaceutical companies immunity, but there was a grey area for employers. Countless people lost their jobs due to the vaccine mandate, which likely was a violation of the Constitution.
Lawsuits may begin with large corporations, but if the Republicans regain control, health agencies and government officials may be investigated as well. This lawsuit is a major win for medical autonomy as companies will be less likely to comply with government mandates as they now know they could risk legal retaliation.
Posted originally on the conservative tree on August 2, 2022 | sundance
I was unaware that monkeypox was an issue for the White House. However, today the Biden administration is proud to present a team of government officials tasked for the purpose of handling the whole of government response to the U.S. outbreak of monkeypox.
Additionally, I’m not exactly sure what a “stakeholder in monkeypox” is, but this team is in charge of making sure they have “health equity.”
WHITE HOUSE – “Today, President Biden named FEMA’s Robert Fenton as the White House National Monkeypox Response Coordinator and Dr. Demetre Daskalakis as the White House National Monkeypox Response Deputy Coordinator. Fenton and Daskalakis will lead the Administration’s strategy and operations to combat the current monkeypox outbreak, including equitably increasing the availability of tests, vaccinations and treatments.
[…] “Bob Fenton and Dr. Daskalakis are proven, effective leaders that will lead a whole of government effort to implement President Biden’s comprehensive monkeypox response strategy with the urgency that this outbreak warrants,” said Anthony Fauci, Chief Medical Advisor to the President. “From Bob’s work at FEMA leading COVID-19 mass vaccination efforts and getting vaccines to underserved communities to Demetre’s extensive experience and leadership on health equity and STD and HIV prevention, this team will allow the Biden Administration to further accelerate and strengthen its monkeypox response.”
Fenton and Daskalakis will coordinate and manage response efforts across the White House and all Federal departments and agencies. They will work with local, state, national, and international stakeholders on tracking and fighting the spread of monkeypox, with state and local partners to ensure they have adequate supplies to test, treat and vaccinate at-risk individuals, with clinicians and providers on available testing, treatment and vaccination options, and with stakeholder communities on building public understanding of the virus and how to address it most effectively.
[…] Over the coming weeks, under the leadership of Fenton and Daskalakis, the Administration will advance and accelerate the United States’ monkeypox response to mitigate the spread of the virus, protect individuals most at risk of contracting the virus, and care for those who have been afflicted with it.” (read more)
Arnie Mazer Writer at TrialSite News where it was originally posted on Jul. 26, 2022, 6:30 p.m.
The White House hosted a “Summit on the Future of the Covid-19 Vaccine” on Tuesday featuring a combination of administration officials, scientists, and executives from the pharmaceutical industry. The summit was chaired by Dr. Ashish Jah, the White House Covid-19 Response Coordinator. Attendees included Dr. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases (NIAID), as well as Dr. Francis Collins, the former head of the National Institutes of Health (NIH). Also in attendance were the representatives of pharmaceutical companies, including Moderna and Pfizer. There is no question the advent of vaccines blunted the complete force of the Covid-19 pandemic as Fauci pointed out in his address to the group. He said that “vaccines have saved over 2 million lives and prevented 17 million hospitalizations” even though the World Health Organization pointed out, initially, the vaccines were not distributed equitably among poor nations while the pharmaceutical companies were reaping profits. But the emphasis of the Summit was on how vaccines will be developed and distributed.
Big Pharma at the Summit
In his opening remarks, Dr. Jah extolled vaccines, saying they are “truly a miracle of human ingenuity and 70% of Americans are now vaccinated.” But Jah also said vaccines “need to be better.” Fauci talked about science and manufacturing working together to make sure vaccines are distributed equally and the private sector and science are working together to advance vaccine technology. Additionally, it was pointed out the Biden Administration is committed to the development of new vaccines. Fauci then presented slides of the projects the NIH was funding and developing with vaccine manufacturers.
Included in this was a “Mosaic Approach,” a new form of vaccine that takes on multiple parts of the virus and could help protect against future Covid variants. Participating in the summit were Paul Burton of Moderna and Angela Hwang of Pfizer. Fauci’s presentation of the future of vaccines included the idea that vaccines need to be updated because the Covid virus is continually mutating.
He emphasized the partnership between academia and the private sector. As effective as Fauci’s speech was, it also seemed as if he was giving free advertising to the drug companies with the idea of maximizing the benefits of the partnership of science and technology. The transformative power of the new generation of vaccines continued to be pointed out and regional manufacturing of vaccines was repeatedly pointed to as a way to get more shots in arms. This point came from both Ashish Jah and Angela Hwang. Regional manufacturing and licensing is a way for pharmaceutical companies to increase profit. Moderna’s Paul Burton said manufacturing is a key part of the future, and the company had recently made deals to build new plants in Australia, the United Kingdom, Canada, and Kenya. In the future, vaccines will be administered through nasal sprays and patches. Angela Hwang pointed out that “probably two and a half billion people have received the Pfizer vaccine. That’s an incredible wealth of real-world evidence that we’re sitting on… I think that we have a great opportunity to also help us to understand, how can we design new therapies.” Hwang added Pfizer is “happy to be on this journey.”
mRNA Vaccines Originated with the Department of Defense
The summit gave a history of the mRNA vaccine and said the potion originated through a part of the Department of Defense known as the Defense Advanced Research Projects Agency (DARPA). The development of the vaccine came as a result of research to help American troops if they’d been exposed to biological warfare on the battlefield. Through that program and others, DARPA had been doing the groundwork for the United States to produce a rapid cure for a pathogen like Covid-19 for years. The pharmaceutical companies capitalized on developed technology and took it further.
Summit panels continually talked about the fact not enough of the population has been vaccinated, and Dr. Francis Collins claimed the pandemic exposed the vulnerability of the American health care system. Collins said there was a need to build public trust even though, initially, the vaccines were not “distributed with equity.” This included the fact that the World Health Organization’s (WHO) Covid-19 Vaccines Global Access (COVAX) has to do a better job of vaccine distribution through what was termed an “allocation framework”. In closing, Dr. Ashish Jah emphasized, again, the importance of public and private partnerships. The summit was, overall, informative and a great day for the pharmaceutical companies.
The impact of such governmental backing of just a few companies most certainly reinforces the market brand. The presenters didn’t do much reflection as to what they could have done better during the pandemic. Rather, industry and government collaboration on more advanced vaccines suggests the government will increasingly be involved in helping fund the few winners of the vaccine and drug development business.
Posted originally on the conservative tree house on July 21, 2022 | Sundance
Suspicious Cat remains, well, suspicious…
[White House Press Release] – This morning, President Biden tested positive for COVID-19. He is fully vaccinated and twice boosted and experiencing very mild symptoms. He has begun taking Paxlovid. Consistent with CDC guidelines, he will isolate at the White House and will continue to carry out all of his duties fully during that time. He has been in contact with members of the White House staff by phone this morning, and will participate in his planned meetings at the White House this morning via phone and Zoom from the residence.
Consistent with White House protocol for positive COVID cases, which goes above and beyond CDC guidance, he will continue to work in isolation until he tests negative. Once he tests negative, he will return to in-person work.
Out of an abundance of transparency, the White House will provide a daily update on the President’s status as he continues to carry out the full duties of the office while in isolation.
Per standard protocol for any positive case at the White House, the White House Medical Unit will inform all close contacts of the President during the day today, including any Members of Congress and any members of the press who interacted with the President during yesterday’s travel. The President’s last previous test for COVID was Tuesday, when he had a negative test result. (read more)