Four prominent scientists who played key roles in shaping the public narrative around the origin of COVID-19 received substantial increases in grant money from the National Institute of Allergy and Infectious Diseases (NIAID), headed by Dr. Anthony Fauci, in the subsequent two years, a review of funding data by The Epoch Times has found.
Three of these scientists—Kristian Andersen, Robert Garry, and Michael Farzan—were advisers to a teleconference organized by Fauci held on Feb. 1, 2020, in response to increasing public questions about the origin of the virus.
The scientists were also instrumental in the publication of Proximal Origin, a highly influential paper that promoted a natural origins theory for SARS-CoV-2, the virus that causes COVID-19, and has been frequently cited by the government and media.
Emails released under Freedom of Information Act requests, showed that the scientists had told the senior members of Fauci’s teleconference that they were 60 to 80 percent sure that COVID-19 had come out of a lab.
Notably, despite their private concerns about the origin of the virus, the first draft of Proximal Origin was completed on the same day as the teleconference. Andersen and Garry were co-authors of Proximal Origin and Farzan was acknowledged in the Nature version of Proximal Origin for his participatory discussions in the article’s creation.
Additionally, Fauci’s NIAID provided a substantial increase in funding to EcoHealth’s Peter Daszak, through whom NIAID had funded controversial gain-of-function coronavirus research at the Wuhan Institute of Virology in China.
Some of these funding amounts have continued through 2021—and one of the newest grants will continue through at least 2025.
A significant portion of the funding increase for Daszak, as well as for Andersen and Garry, was provided through NIAID’s creation of the Centers for Research in Emerging Infectious Diseases (CREID).
The program, which was originally referred to as Emerging Infectious Diseases Research Centers (EIDRCs) during the early planning stages in 2019, was formally announced under a new name on Aug. 27, 2020. It is not known why the program was initially delayed or why it was renamed.
The new initiative, described as a global network that involves “multidisciplinary investigations into how and where viruses and other pathogens emerge from wildlife and spillover to cause disease in people,” provided eleven new grants totaling $17 million of new funding in the first year and $82 million in total funding across five years.
Andersen and Garry were the co-recipients of a new $8.9 million 5-year grant made under the CREID initiative that established the West African Research Network for Infectious Diseases (WARN-ID). Daszak was the recipient of a new $7.5 million, 5-year CREID grant that established the Emerging Infectious Diseases: South East Asia Research Collaboration Hub (EID-SEARCH). The other participants of the NIAID CREID program can be found here.
Notably, although the creation of CREID was not publicly announced until Aug. 27, 2020, the Award Notice Date for the grants to Andersen and Garry are listed as May 21, 2020. The CREID grant to Daszak lists an Award Notice Date of June 17, 2020. The timing of Daszak’s grant is particularly noteworthy as it came shortly after President Donald Trump had revoked Daszak’s previous grant from Fauci’s NIAID in April 2020 due to Daszak’s entanglements with the Wuhan Institute of Virology.
Andersen, who had privately told Fauci on Jan. 31, 2020, that the virus “looked engineered,” but later helped spearhead Fauci’s efforts to promote a natural origins narrative, received a total of $7.4 million in funding in 2020 as compared to $4.5 million in grant proceeds in 2019. Andersen’s total grant funding increased to nearly $9 million in 2021. The new CREID grants (co-awarded with Garry) accounted for approximately $1.9 million of his 2020 grant proceeds and $2 million of his grant proceeds in 2021. Included in Andersen’s 2021 figure is a $266,250 CREID grant that was made to Andersen but did not include Garry as a co-recipient.
While it is not known at this point whether there was a connection between the increased funding and the scientists’ involvement in shaping the public natural origins narrative, these new revelations raise an obvious question: How is it that among the thousands of scientists eligible to participate in the much-desired funding from the eleven grants provided by Fauci’s new $82 million CREID initiative, three of those chosen happened to be the same individuals who had led the way in promoting Fauci’s natural origins narrative—despite their private concerns that the virus had been created in a lab.
During the Feb. 1, 2020, teleconference, Andersen claimed to be “60 to 70 percent sure the virus came from a laboratory.” One of Andersen’s Proximal Origin co-authors, Edward Holmes, put that figure even higher, at “80 percent.”
Garry, who told the senior members of Fauci’s teleconference group that he “really can’t think of a plausible natural scenario where you get from the bat virus” to SARS-CoV-2,received $7 million in NIAID grants in 2020 as compared to $5.7 million in 2019. Garry also received $6.6 million in grants in 2021. The new CREID grant (co-awarded with Andersen) accounted for approximately $1.9 million of his 2020 grant proceeds and $1.8 million of his grant proceeds in 2021.
During the Feb. 1, 2020, teleconference, Garry cited the remarkable sequences of mutations that would have to occur for SARS-CoV-2 to arise naturally, telling the group, “I just can’t figure out how this gets accomplished in nature.” However, Garry noted that a lab-created virus would easily explain the virus data he was seeing, telling Fauci’s group that “in the lab, it would be easy to generate the perfect 12 base insert that you wanted.”
Notably, Garry recently admitted in written correspondence with The Intercept that he had been advised not to discuss a lab leak in the Proximal Origin paper, stating, “The major feedback we got from the Feb 1 teleconference was: 1. Don’t try to write a paper at all—it’s unnecessary or 2. If you do write it, don’t mention a lab origin as that will just add fuel to the conspiracists.”
Garry—along with Andersen—must have heeded that directive because on Feb. 1, 2020, the same day as Fauci’s teleconference, both men had helped to complete the first draft of Proximal Origin promoting the idea that the virus had originated in nature. That paper became the media’s and the public health establishment’s go-to evidence for a natural origin for the virus.
The choice of Andersen as a lead author for Proximal Origin is particularly curious as Andersen had no material experience in researching coronaviruses. His stated focus was related to the Zika virus, Ebola virus, West Nile virus, and Lassa virus. It wasn’t until sometime after the Feb. 1 teleconference that he changed his biography to incorporate SARS-CoV-2.
Proximal Origin was published online on Feb. 16, 2020, and sought to exclude the possibility of a lab leak. The article would prove to be highly influential and has been extensively used by Fauci and media organizations in their promotion of the natural origins narrative.
Another recipient of funding under the CREID initiative was EcoHealth president Peter Daszak, who received a total of $1.5 million in both 2020 and 2021. Unlike either Andersen or Garry, proceeds from his CREID grant make up the entirety of his listed NIAID grants in both years. By way of comparison, Daszak had received approximately $662,000 in NIAID grant money in 2019. Put another way, Daszak’s post-pandemic funding increased by approximately 130 percent.
Daszak, who heavily promoted the natural origins narrative, was personally involved in gain-of-function work with the Wuhan Institute of Virology, which continued until at least April 2020. Most prominently, Daszak authored a 2018 research proposal which details the creation of a virus in a lab that bears a remarkable similarity to the defining features of COVID-19.
That proposal, dated March 27, 2018, details EcoHealth’s plans, in conjunction with the Wuhan Institute, to create entirely new coronaviruses through the synthetic combination of preexisting virus backbones. It describes how those viruses were going to be made more virulent in humans by the insertion of a furin cleavage site, a feature that distinguishes COVID-19 from all other SARS-related coronaviruses.
Another scientist who advised the Feb. 1, 2020, teleconference, Michael Farzan, received $9.9 million in grants from Fauci’s NIAID in 2020, followed by another $7.9 million in 2021 and an additional $919,000 at the start of 2022. By comparison, Farzan had received $3.8 million in grant money from NIAID in 2019. Although Farzan received substantial increases in grant funding, none of that money appears to have come under grants provided by the CREID initiative.
Farzan, an immunologist who in 2005 discovered the receptor of the original severe acute respiratory syndrome (SARS) virus, had told the senior members of Fauci’s teleconference group in emails that the pandemic likely originated from a lab in which live coronaviruses were passed repeatedly through human-like tissue, accelerating virus mutations with the end result being that one of the mutated viruses may have leaked from the lab. Farzan told Fauci’s group that he placed the likelihood of a leak from a Wuhan lab at 60 to 70 percent.
But in an Oct. 5, 2021, paper, Farzan appeared to agree with conclusions put forth in Proximal Origin, when he claimed that a “comparison of the S protein sequences indicates SARS-CoV-2 may have emerged from the recombination between bat and pangolin coronaviruses.” Farzan, like Andersen, works at the Scripps laboratory.
A receding hairline, a total loss of hair from the crown, and ultimately, the classical horseshoe-shaped pattern of baldness: Previous research into male…
A receding hairline, a total loss of hair from the crown, and ultimately, the classical horseshoe-shaped pattern of baldness: Previous research into male pattern hair loss, also termed androgenetic alopecia, has implicated multiple common genetic variants. Human geneticists from the University Hospital of Bonn (UKB) and by the Transdisciplinary Research Unit “Life & Health” of the University of Bonn have now performed a systematic investigation of the extent to which rare genetic variants may also contribute to this disorder. For this purpose, they analyzed the genetic sequences of 72,469 male participants from the UK Biobank project. The analyses identified five significantly associated genes, and further corroborated genes implicated in previous research. The results have now been published in the prestigious scientific journal Nature Communications.
Credit: University Hospital Bonn / Katharina Wislsperger
A receding hairline, a total loss of hair from the crown, and ultimately, the classical horseshoe-shaped pattern of baldness: Previous research into male pattern hair loss, also termed androgenetic alopecia, has implicated multiple common genetic variants. Human geneticists from the University Hospital of Bonn (UKB) and by the Transdisciplinary Research Unit “Life & Health” of the University of Bonn have now performed a systematic investigation of the extent to which rare genetic variants may also contribute to this disorder. For this purpose, they analyzed the genetic sequences of 72,469 male participants from the UK Biobank project. The analyses identified five significantly associated genes, and further corroborated genes implicated in previous research. The results have now been published in the prestigious scientific journal Nature Communications.
Male-pattern hair loss is the most common form of hair loss in men, and is largely attributable to hereditary factors. Current treatment options and risk prediction are suboptimal, thus necessitating research into the genetic underpinnings of the condition. To date, studies worldwide have focused primarily on common genetic variants, and have implicated more than 350 genetic loci, in particular the androgen receptor gene, which is located on the maternally inherited X chromosome. In contrast, the contribution to this common condition of rare genetic variants has traditionally been assumed to be low. However, systematic analyses of rare variants have been lacking. “Such analyses are more challenging as they require large cohorts, and the genetic sequences must be captured base by base, e.g., through genome or exome sequencing of affected individuals,” explained first author Sabrina Henne, who is a doctoral student at the Institute of Human Genetics at the UKB and the University of Bonn. The statistical challenge lies in the fact that these rare genetic variants may be carried by very few, or even single, individuals. “That is why we apply gene-based analyses that first collapse variants on the basis of the genes in which they are located,” explained corresponding author PD Dr. Stefanie Heilmann-Heimbach, who is a research group leader at the Institute of Human Genetics at the UKB at the University of Bonn. Among other methods, the Bonn researchers used a type of sequence kernel association test (SKAT), which is a popular method for detecting associations with rare variants, as well as GenRisk, which is a method developed at the Institute of Genomic Statistics and Bioinformatics (IGSB) at the UKB and the University of Bonn.
Possible relevance of rare variants in male-pattern hair loss
The research involved the analysis of genetic sequences from 72,469 male UK Biobank participants. Within this extensive data set, Bonn geneticists, together with researchers from the IGSB and the Center for Human Genetics at the University Hospital Marburg, examined rare gene variants that occur in less than one percent of the population. Using modern bioinformatic and statistical methods, they found associations between male-pattern hair loss and rare genetic variants in the following five genes: EDA2R, WNT10A, HEPH, CEPT1, and EIF3F.
Prior to the analyses, EDA2R and WNT10A were already considered candidate genes, as based on previous analyses of common variants. “Our study provides further evidence that these two genes play a role, and that this occurs through both common and rare variants,” explained Dr. Stefanie Heilmann-Heimbach. Similarly, HEPH is located in a genetic region that has already been implicated by common variants, namely the EDA2R/Androgen receptor, which is a region that has consistently shown the strongest association with male-pattern hair loss in past association studies. “However, HEPH itself has never been considered as a candidate gene. Our study suggests that it may also play a role,” explained Sabrina Henne. “The genes CEPT1 and EIF3F are located in genetic regions that have not yet been associated with male-pattern hair loss. They are thus entirely new candidate genes, and we hypothesize that rare variants within these genes contribute to the genetic predisposition. HEPH, CEPT1, and EIF3F represent highly plausible new candidate genes, given their previously described role in hair development and growth.” Furthermore, the results of the study suggest that genes that are known to cause rare inherited diseases affecting both skin and hair (such as the ectodermal dysplasias) may also play a role in the development of male-pattern hair loss. The researchers hope that the puzzle pieces they have discovered will improve understanding of the causes of hair loss, and thus facilitate reliable risk prediction and improved treatment strategies.
The research was supported by funding from the Medical Faculty of the University of Bonn. Prof. Dr. Markus Nöthen, Director of the Institute of Human Genetics at UKB and co-author of the study, is a member of the Transdisciplinary Research Area (TRA) “Life and Health” at the University of Bonn. The publication costs in open access format were funded by the DEAL project of the University of Bonn.
Journal
Nature Communications
DOI
10.1038/s41467-023-41186-w
Article Title
Analysis of 72,469 UK Biobank exomes links rare variants to male-pattern hair loss
Canadian dollar edges higher as retail sales rebound
Canada retail sales climb 2% The Canadian dollar has posted losses on Friday. In the European session, USD/CAD is trading at 1.3446, down 0.28%. Canada’s…
The Canadian dollar has posted losses on Friday. In the European session, USD/CAD is trading at 1.3446, down 0.28%.
Canada’s retail sales jump
Canada’s retail sales rebounded in impressive fashion on Friday. Retail sales in July jumped 2% y/y, following a -0.6% reading in June and beating the 0.5% consensus estimate. On a monthly basis, retail sales rose 0.3%, up from 0.1% in June but shy of the consensus estimate of 0.4%. The good news was tempered by the August estimate, which stands at -0.3% m/m and would be the first decline since March. The Canadian dollar showed little reaction to the retail sales release.
The Bank of Canada doesn’t meet again until October 25th and policy makers will have plenty of data to monitor in the meantime. The BoC has been walking a tightrope that will be familiar to most central banks, that of trying to balance the risks of over and under-tightening. The difficulty in finding the right balance was highlighted in the BoC summary of deliberations of the policy meeting earlier this month.
The BoC decided to hold the benchmark rate at 5.0% after concluding that earlier rate hikes were having an effect and slowing economic growth. The summary indicated that policy makers were concerned that a pause might send the wrong message that rate cuts might be on the way. With inflation still above the BOC’s target, the central bank is not looking at rate cuts and stressed at the September meeting that rate hikes were still on the table and that inflation remained too high.
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USD/CAD Technical
USD/CAD is testing resistance at 1.3468. The next resistance line is 1.3553
Quantitative Tightening Is Not Biggest Threat To Global Yields
Authored by Simon White, Bloomberg macro strategist,
The Bank of England’s quantitative tightening program shows that unwinding central-bank bond portfolios, even with outright sales, need not be disruptive for markets. The greater risk for US and global yields comes from positive stock-bond correlations driving risk premia wider.
The BOE has been a pioneer and a thought leader in QT. While the Fed and ECB have only allowed bonds to run off naturally to help achieve their balance-sheet contraction goals, the BOE has sold gilts outright in addition to allowing bonds to mature.
So far, it has not led to any significant market disruption. This enabled the BOE Thursday to increase the pace of reduction in the Asset Purchase Facility (APF) from £80 billion last year to £100 billion over the coming 12 months from October (while holding Bank Rate steady). As colleague Ven Ram also noted, the schedule of maturing bonds next year allowed the bank to keep gilts sales unchanged from last year while increasing the total amount of the APF’s decrease.
The QT watchwords from the bank are “gradual and predictable.” If gilt sales are conducted in such a way, then market disruption should be minimized. The chart below shows the BOE’s own assessment of the impact of bond sales on the market.
The BOE estimates that of the ~40 bps of term-premium increase since the MPC voted to begin QT in February 2022, about 10-15 bps comes from QT specifically – small in comparison to the overall rise in yields since that time.
QT or bond sales, though, are not the most critical risk facing bond prices in the current cycle. Rising and now positive stock-bond correlations threaten to lead to a structural rise in bond risk premium, and lower prices. The correlation is now positive in the US, Japan, and the UK.
In a positive stock-bond correlation world, bonds lose their portfolio-hedge and recession-hedge capabilities, and thus become less sought after. The penny has not fully dropped yet, but the negative term premium for bonds is increasing, and is prone to rising much higher as they become less desirable.
Yields of developed market countries are biased structurally higher, but QT is unlikely to be the culprit. Instead, it allows central banks to reload their capacity for a future time when they may need to restart quantitative easing, in order to stabilize the market from sharply rising term premia.
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