Some studies have shown that subsequent COVID infections increase a person’s risk of getting long COVID. To date, long COVID has afflicted up to 23 million Americans while the Centers for Disease Control and Prevention (CDC) estimates 1 in 13 adults in the United States currently have long COVID symptoms. And it’s not just people who are considered to be “high-risk” for a severe COVID-19 infection, like those who are already immunocompromised, who are susceptible to long COVID.
“No one is safe from it,” Dr. Ziyad Al-Aly, chief of research and development at the VA St. Louis healthcare system who also testified at the hearing, told Salon. “And there is no treatment for it.”
Recent research has shown that getting vaccinated can reduce the risk of developing long COVID. Specifically, it reduces the risk by 15 to 70 percent in adults, and it reduces the risk moderately in kids. Adolescents saw the greatest protective effect, particularly those who had a higher risk of long COVID, which waned over time.
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It’s not just people that are taking a hit from long COVID, but also the economy. In January 2022, Brookings Institute estimated that 1.6 million full-time equivalent workers could be out of work due to the condition, leaving 10.6 million unfilled jobs. At the time of the analysis, researchers estimated that 16 million working-age Americans, those between the ages 18 and 65, had long COVID today. Of those, between two to four million were unable to work because of it. The estimated annual cost of those lost wages alone was around $170 billion a year.
Here we investigated cognitive dysfunction and brain changes in a group of mildly infected individuals.
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The patients reported memory loss (36%), fatigue (31%) and headache (29%). The quantitative analyses confirmed symptoms of fatigue (83% of participants), excessive somnolence (35%), impaired phonemic verbal fluency (21%), impaired verbal categorical fluency (13%) and impaired logical memory immediate recall (16%). The WM [white matter] analyses with DTI [ diffusion tensor images] revealed higher axial diffusivity values in post-infected patients compared to controls.
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Our results suggest persistent cognitive impairment and subtle white matter abnormalities in individuals mildly infected without anxiety or depression symptoms.
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We evaluated a group of 97 unvaccinated individuals (without history or current presence of symptoms of anxiety, depression and psychiatric symptoms) after a mild infection with SARS-CoV-2. We detected persistent headache, fatigue, excessive somnolence, cognitive dysfunction, and subtle microstructural white MRI abnormalities.
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One intriguing fact is that we observed a high proportion of low average performance in our sample of patients (which has a high average level of education), including immediate and late verbal episodic memory, phonological and semantic verbal fluency, immediate visuospatial episodic memory, processing speed, and inhibitory control. Although most subjects did not present significant impaired scores compared with the normative data, we speculate that the low average performance affecting different domains may result in a negative impact in everyday life, especially in individuals with high levels of education and cognitive demands.
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Comment: Mild symptoms had subtle, but significant changes in both brain structure and cognitive performance. This is consistent with an erosion of mental functioning after even a mild infection. Someone who had been quite intelligent is reduced to the low-average level. How many mistakes will they make in their job? What will the consequences be if their job is mission critical? Their bosses didn’t hire a low-average employee to do their important job, but now, that’s what they have. What happens after repeated infections with SARS-CoV-2? A continued erosion of intelligence? What does the world look like in a few years?
Comparing the blood of patients with confirmed SARS-CoV-2 infection with that of uninfected controls, Cervia-Hasler et al. found that patients experiencing Long COVID exhibited changes to blood serum proteins indicating activation of the immune system’s complement cascade, altered coagulation, and tissue injury (see the Perspective by Ruf). At the cellular level, Long Covid was linked to aggregates comprising monocytes and platelets. These findings provide a resource of potential biomarkers for diagnosis and may inform directions for treatments.
Looks like avian flu wiped out the entire Patagonian elephant seal whelping this year, some 17,000 young animals, and some of the adults, too. Described as “apocalyptic.”
A very contagious strain of highly pathogenic avian influenza (HPAI) is wreaking havoc on elephant seals (Mirounga leonina) on the coast of Patagonia, Argentina. According to the Wildlife Conservation Society (WCS), almost 96 percent of elephant seal pups living at three breeding sites where the H5N1 strain of HPAI was detected have died. The WCS team estimates 17,000 elephant seal pups died in these areas in 2023.
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The WCS believes that the elephant seals had little to no interaction with infected bird populations, which is further evidence of mammal to mammal transmission. According to veterinarian Marcela Uhart at the University of California, Davis, since newborn elephant seal pups suckle their mothers to feed, there is little chance that the pups ate infected birds. “This is all highly suggestive of some sort of transmission between mammals,” Uhart told New Scientist.
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Comment: The question is: how is the virus spreading? Fecal-oral or respiratory? I wouldn’t be swimming in any public pools for a while.
The DEFUSE grant proposal was led by EcoHealth Alliance President Peter Daszak.
Now, drafts and notes uncovered through the Freedom of Information Act reveal fresh details about the intended research.
Specifically, the scientists sought to insert furin cleavage sites at the S1/S2 junction of the spike protein; to assemble synthetic viruses in six segments; to identify coronaviruses up to 25 percent different from SARS; and to select for receptor binding domains adept at infecting human receptors.
The genome of SARS-CoV-2, the virus that causes COVID-19, matches the viruses described in the research proposal:
SARS-CoV-2 has a furin cleavage site positioned in the spike protein at the S1/S2 junction. The furin cleavage site supercharged the virus into the worst pandemic pathogen in a century. Virologists have yet to identify one in any other related coronavirus.
SARS-CoV-2 can be divided into six contiguous genomic pieces by the restriction enzymes Bsal and BsmBI. These restriction enzymes occur in nature but can also be used in the lab to splice viruses. A trio of scientists estimated in a 2022 analysis that the likelihood of seeing the pattern found in SARS-CoV-2 in nature would be remote. Orders for one of these restriction enzymes, BsmBI, can be found in the documents.
SARS-CoV-2 emerged highly infectious without evolving much in humans. The virus “came out of the box ready to infect.” The receptor binding domain appeared “finely tuned” for the human ACE2 receptor yet had little genetic variation when first spilling over into humans, presenting a difficult “paradox” to virologists who sought to prove it emerged naturally. The documents confirm the scientists working with the Wuhan lab sought to select for receptor binding domains that bind well to human ACE2 in their research.
The genome of SARS-CoV-2 falls within the range of a 25 percent genetic difference from SARS.
The documents reveal for the first time that a virologist working with the Wuhan lab planned to engineer new spike proteins – in contrast with the collaboration’s public work to insert whole spike proteins into viral backbones. Language in the proposal indicates this work may have involved unpublished viruses, generating unpublished engineered spike proteins.
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Comment: The entire article is well worth reading. Chilling. Now, I understand the hysterical attempt to shout down the lab leak hypothesis. But this came out anyway. I don’t know what happens next.
Abnormal neurological manifestations are increasingly recognized in patients with COVID-19, which most commonly include anosmia, dysgeusia, and headache, followed by seizures, stroke, and acute inflammatory polyradiculoneuropathy, also known as Guillain-Barre syndrome. Furthermore, an increased risk for additional neurological and psychiatric disorders has been reported in a large retrospective cohort at 6 months post diagnosis.
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We previously developed a human pluripotent stem cell (hPSC)-derived organoid/cell-based platform to evaluate the tropism of SARS-CoV-2. Using this platform, we found that hPSC-derived midbrain dopamine (DA) neurons—representing one of the main neurodegeneration targets in Parkinson’s disease (PD)—are permissive to SARS-CoV-2 infection.
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Given our findings, we posit that over the coming years, there is a need to closely monitor COVID-19 patients for an increased risk of developing PD [Parkinson Disease]-related symptoms.
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Comment: Dopamine is a neurotransmitter. It is a chemical that cells in one part of the brain, the substantia nigra, use to communicate with another part of the brain, the basal ganglia. The death of these neurons causes Parkinson Disease. Senescence of cells puts them in zombie-like state; they are not dead but no longer function normally. This study adds to previous indicators that there may be a wave of patients with degeneration of their brains in the future as a result of even mild SARS-CoV-2 infections.
China has recently made headlines by developing a new mutant strain of the COVID-19 virus that has shown a staggering 100 percent mortality rate in “humanized” mice. This new variant, known as GX_P2V, has raised alarm bells within the scientific community due to its potential implications for human health.
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The study focused on human ACE2-transgenic mice, which are specifically engineered to possess a human receptor for the virus. These mice were intentionally infected with GX_P2V, leading to tragic consequences. The mortality rate among these mice was unprecedented, suggesting that this new variant is particularly lethal.
After analysing the bodies of the mice, they found that the virus had infected the lungs, bones, eyes, tracheas and brains. The brain infection was so severe that it killed the animals, the researchers concluded.
On December 28, 2019, virologist Dr. Lili Ren of the Institute of Pathogen Biology at the Chinese Academy of Medical Sciences & Peking Union Medical College submitted the genetic sequence to GenBank, a “genetic sequence repository that collects, preserves, and provides public access to assembled and annotated nucleotide sequence data from all domains of life,” according to a letter that Dr. Melanie Egorin, assistant secretary of legislation at the US Department of Health and Human Services, sent to House Energy and Commerce Committee Chair Cathy McMorris Rodgers last month.
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McMorris Rodgers, R- Washington; Subcommittee on Health Chair Brett Guthrie, R-Kentucky; and Subcommittee on Oversight and Investigations Chair Morgan Griffith, R-Virginia, said in a news release Wednesday that the committee’s investigation into the origins of Covid-19 will help policymakers strengthen the nation’s biosafety practices in addition to helping prepare for the next pandemic.
They noted that they received the new information almost two months after they informed the NIH of their intent to issue subpoenas for copies of documents related to any early coronavirus sequences, early Covid-19 cases or other pertinent information.
Dr. Jesse Bloom, a virologist at the Fred Hutchinson Cancer Center, wrote Wednesday in an analysis of Ren’s submission that it “clearly falsifies the Chinese government’s claim that the causative agent of the Wuhan pneumonia outbreak still had not been identified near the end of the first week of January 2020.”
The earlier submission “would have provided adequate information to initiate vaccine production in late 2019 if it had been made public,” he said, noting that drugmaker Moderna “used the spike sequence to design its COVID-19 vaccine” within two days of the January 12 release.
However, he said, the genetic sequence “is unlikely to represent the first virus that infected humans” and “does not provide any new insights into the origin or early spread of SARS-CoV-2 in Wuhan.”
“The belated discovery of the submission underscores the importance of rapid data sharing during outbreaks, since immediate public release of the sequence could have accelerated by several weeks the development of COVID-19 vaccines that saved thousands of lives per week in the United States alone,” he said.
Even two weeks “would have made a huge difference in the pandemic,” agreed Dr. Eric Topol, founder and director of the Scripps Research Translational Institute. The fact that the vaccine program began immediately on publication of the genetic sequence “shows you how important that sequence was.”
“When you sequence a virus – it’s not even just a vaccine – then you’ve nailed it. You know exactly the features, about the spike protein and all the other major components: the nucleocapsid, the envelope, the whole entire panoramic view of the virus. You can’t get that without the sequence.”
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Comment: Why was it necessary to threaten NIH with a subpoena to get this information? Are NIH leaders loyal to the US or … China?
SARS-CoV-2-related pangolin coronavirus GX_P2V(short_3UTR) can cause 100% mortality in human ACE2-transgenic mice, potentially attributable to late-stage brain infection. This underscores a spillover risk of GX_P2V into humans and provides a unique model for understanding the pathogenic mechanisms of SARS-CoV-2-related viruses.
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Two SARS-CoV-2-related pangolin coronaviruses, GD/2019 and GX/2017, were identified prior to the COVID-19 outbreak (1, 2). The respective isolates, termed pCoV-GD01 and GX_P2V, were cultured in 2020 and 2017, respectively (2, 3). The infectivity and pathogenicity of these isolates have been studied (4-6). The pCoV-GD01 isolate, which has higher homology with SARS-CoV-2, can infect and cause disease in both golden hamsters and hACE2 mice (4). In contrast, while GX_P2V can also infect both species, it does not appear to cause obvious disease in these animals (5, 6).We previously reported that the early passaged GX_P2V isolate was actually a cell culture-adapted mutant, named GX_P2V(short_3UTR), which possesses a 104-nucleotide deletion at the 3’-UTR (6). In this study, we cloned this mutant, considering the propensity of coronaviruses to undergo rapid adaptive mutation in cell culture, and assessed its pathogenicity in hACE2 mice. We found that the GX_P2V(short_3UTR) clone can infect hACE2 mice, with high viral loads detected in both lung and brain tissues. This infection resulted in 100% mortality in the hACE2 mice. We surmise that the cause of death may be linked to the occurrence of late brain infection.
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Comment: Translation: a naturally occurring coronavirus that was not lethal to animals was cultured in the lab. As a result of adaptation to cell culture, the viral sequence changed in such a way that it is now 100% lethal to mice which have been genetically modified to better mimic the effects of infection in humans. This is exactly what has been suggested to cause the SARS-CoV-2 pandemic. So, they’ve done it again, only this time with a virus that may kill everyone on the planet. Get it?
Undeterred by loss of countless lives across the world, China is now reportedly experimenting with a new Covid-like virus that has a “mortality rate of 100 per cent.”
Doctors trained by Chinese People’s Liberation Army (PLA) have made their version of “pangolin coronavirus” which has been found to have 100 per cent mortality in mice.
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Comment: In much more important news, according to the MSM, a movie about a plastic doll won some awards.
COVID-19 patients were at three times the risk of death than non-COVID patients (hazard ratio [HR], 3.3; 95% confidence interval [CI], 3.1 to 3.5). Coinfected patients and those infected with adenovirus were at a significantly increased risk of death (HR, 1.7 [95% CI, 1.2 to 2.4] and HR, 1.4 [95% CI, 1.2 to 1.7], respectively). In contrast, patients with RSV and rhinovirus were at lower risk of death (HR, 0.57 [95% CI, 0.51 to 0.65] and HR, 0.79 [95% CI, 0.69 to 0.94], respectively).
Researchers from the Amsterdam University Medical Center have discovered an important mechanism responsible for fatigue in people with Long COVID. They show that essentially it is an energy availability problem within the muscles, rather than hypoxia due to clots blocking tiny blood vessels as previously thought. The results were published in Nature Communications on January 4, 2024.
Monotreme's Blog 
“Living through a mass disabling event”: Will Congress finally take long COVID patients seriously?
https://www.salon.com/2024/01/20/living-through-a-mass-disabling-event-will-congress-finally-take-long-patients-seriously/‘
Nicole Karlis January 20, 2024
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Microstructural brain abnormalities, fatigue, and cognitive dysfunction after mild COVID-19
https://www.nature.com/articles/s41598-024-52005-7
Scardua-Silva et al. 19 January 2024
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Comment: Mild symptoms had subtle, but significant changes in both brain structure and cognitive performance. This is consistent with an erosion of mental functioning after even a mild infection. Someone who had been quite intelligent is reduced to the low-average level. How many mistakes will they make in their job? What will the consequences be if their job is mission critical? Their bosses didn’t hire a low-average employee to do their important job, but now, that’s what they have. What happens after repeated infections with SARS-CoV-2? A continued erosion of intelligence? What does the world look like in a few years?
Persistent complement dysregulation with signs of thromboinflammation in active Long Covid
https://www.science.org/doi/10.1126/science.adg7942
Cervia-Hasler et al. 19 Jan 2024
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Looks like avian flu wiped out the entire Patagonian elephant seal whelping this year, some 17,000 young animals, and some of the adults, too. Described as “apocalyptic.”
Seal pup die-off from avian flu in Argentina looks ‘apocalyptic’
https://www.popsci.com/environment/bird-flu-seals/
Jan 17, 2024
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Comment: The question is: how is the virus spreading? Fecal-oral or respiratory? I wouldn’t be swimming in any public pools for a while.
US scientists proposed to make viruses with unique features of SARS-CoV-2 in Wuhan
https://usrtk.org/covid-19-origins/scientists-proposed-making-viruses-with-unique-features-of-sars-cov-2-in-wuhan/
January 18, 2024 by Emily Kopp
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Comment: The entire article is well worth reading. Chilling. Now, I understand the hysterical attempt to shout down the lab leak hypothesis. But this came out anyway. I don’t know what happens next.
SARS-CoV-2 infection causes dopaminergic neuron senescence
https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(23)00442-3
January 17, 2024 Yang et al.
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Comment: Dopamine is a neurotransmitter. It is a chemical that cells in one part of the brain, the substantia nigra, use to communicate with another part of the brain, the basal ganglia. The death of these neurons causes Parkinson Disease. Senescence of cells puts them in zombie-like state; they are not dead but no longer function normally. This study adds to previous indicators that there may be a wave of patients with degeneration of their brains in the future as a result of even mild SARS-CoV-2 infections.
China Develops New Covid Strain with 100% Mortality in Humanised Mice: Know All About This New Virus Variant
https://www.thehealthsite.com/news/china-develops-new-covid-strain-with-100-mortality-in-humanised-mice-know-all-about-this-new-virus-variant-1055459/
Satata Karmakar |January 18, 2024
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Genetic sequence of coronavirus was submitted to US database two weeks before China’s official disclosure, documents show
https://www.cnn.com/2024/01/17/health/coronavirus-sequence-database/index.html
Katherine Dillinger January 17, 2024
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Comment: Why was it necessary to threaten NIH with a subpoena to get this information? Are NIH leaders loyal to the US or … China?
Xi Jinping lied, people died.
Lethal Infection of Human ACE2-Transgenic Mice Caused by SARS-CoV-2-related Pangolin Coronavirus GX_P2V(short_3UTR)
Wei et al. 2024
https://www.biorxiv.org/content/10.1101/2024.01.03.574008v1
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Comment: Translation: a naturally occurring coronavirus that was not lethal to animals was cultured in the lab. As a result of adaptation to cell culture, the viral sequence changed in such a way that it is now 100% lethal to mice which have been genetically modified to better mimic the effects of infection in humans. This is exactly what has been suggested to cause the SARS-CoV-2 pandemic. So, they’ve done it again, only this time with a virus that may kill everyone on the planet. Get it?
China experimenting with 100% deadly new Covid strain: Report
https://www.firstpost.com/world/china-experimenting-with-100-per-cent-deadly-new-covid-strain-report-13616272.html
January 15, 2024
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Comment: In much more important news, according to the MSM, a movie about a plastic doll won some awards.
Risk of death 3 times higher in Brazilian kids with COVID-19 than with other respiratory viruses, study finds
https://www.cidrap.umn.edu/covid-19/risk-death-3-times-higher-brazilian-kids-covid-19-other-respiratory-viruses-study-finds
Mary Van Beusekom, January 12, 2024
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More evidence vaccination reduces risk of long COVID
https://www.cidrap.umn.edu/covid-19/more-evidence-vaccination-reduces-risk-long-covid
Stephanie Soucheray, January 12, 2024
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Muscle energy depletion linked to Long COVID: study
https://www.thehindu.com/sci-tech/science/muscle-energy-depletion-linked-to-long-covid-study/article67734842.ece
Rajeev Jayadevan January 13, 2024
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One-two punch of COVID and flu is hitting L.A. County hard
https://www.latimes.com/california/story/2024-01-14/covid-19-widely-circulating-in-l-a-county-with-hospitalizations-elevated
Rong-Gong Lin Jan. 14, 2024