too long to post but they end up saying it is a few people with actual brain diseases but different types and many of those this one doctor diagnosed are just psychological problems. The culprit hinted at is pesticides or pollution, but if this was true, why just in this area? I mean it is a trendy claim but doesn't make sense.
The first thing came to my mind was CJD from deer wasting syndrome: A prion disease that there have been cases diagnosed in the USA in those eating deer meat.
The other thing came to my mind is Mad Cow disease in the UK, which had a similar coverup.
Grok says they tested for this and didn't find prion disease. But I thought prion disease was hard to diagnose but never mind:
The mysterious neurological syndrome reported in New Brunswick, Canada, starting around 2019–2021, initially raised concerns because it presented symptoms somewhat similar to prion diseases like Creutzfeldt-Jakob disease (CJD) — a rare, fatal brain disorder caused by misfolded proteins (prions). These symptoms included rapid cognitive decline, muscle spasms, ataxia (loss of coordination), behavioral changes, and dementia-like effects.Health authorities, including the Canadian Creutzfeldt-Jakob Disease Surveillance System (CJDSS), investigated a cluster of cases (initially around 40–48, later reported to grow significantly). Testing explicitly ruled out known human prion diseases, including CJD and any variant linked to animal prions.
Early speculation included the possibility of a novel prion disease potentially related to chronic wasting disease (CWD) — a prion disease affecting deer, elk, moose, and other cervids (sometimes called "zombie deer disease").
CWD is well-established in parts of Canada (mainly Alberta, Saskatchewan, Manitoba, British Columbia, and Quebec) and the U.S., but no cases have been confirmed in wild or farmed deer in New Brunswick. There is also no documented evidence of CWD transmitting to humans, despite ongoing research into potential zoonotic risks.
However, extensive follow-up investigations, including a major 2025 peer-reviewed study published in the Journal of the American Medical Association (JAMA), reassessed cases through independent clinical evaluations and autopsies.
The conclusions were clear: No evidence supported a single new/mystery neurological disease or any prion-related cause (including CWD-like prions).
The cases were attributed to well-known conditions such as Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy, functional neurological disorders, traumatic brain injury, metastatic cancer, and other established neurodegenerative or non-neurodegenerative issues.
Autopsies (including those using specific tests for CWD prions) showed no prion pathology.
Statistical analysis indicated the probability of an undetected novel disease in the broader cluster was extremely low (less than 0.001).
Public Health New Brunswick has largely concluded its investigation into a "neurological syndrome of unknown cause," recommending affected individuals seek care through specialized clinics for their diagnosed conditions.
Some ongoing reviews or debates persisted into late 2025/early 2026, but the scientific consensus points to misdiagnosis rather than a new prion-linked outbreak.
For context on animal prion diseases in the region:CWD in deer (and related cervids) remains a concern across North America, spreading through saliva, urine, feces, and contaminated environments — but it has not been detected in New Brunswick deer.
Bovine spongiform encephalopathy (BSE, or mad cow disease) in cows is extremely rare in Canada due to strict controls (no recent cases), and no links to human cases in New Brunswick.
In summary, the New Brunswick brain disease cluster was not a prion disease in humans, nor connected to prion diseases in deer or cows. It appears to have stemmed from a combination of known neurological conditions, with initial similarities to CJD leading to the prion investigation that was ultimately ruled out.
The results suggest that CHARM can safely suppress prion protein levels in brain cells. It thus could form the basis for potential prion disease treatments. Other neurodegenerative diseases, such as Huntington’s, are also caused by a buildup of toxic misfolded proteins. CHARM might help with treating these diseases as well..
Two of Joy's relaives who live in nearby Bulacan caught it: Originally they thought it was Dengue but the test was negative. The symptoms are similar (everything hurts) but now they are still having pain in large joints.
From Grok:
Chikungunya in the Philippines (as of late 2025)Chikungunya is a mosquito-borne viral disease caused by the chikungunya virus (CHIKV), transmitted primarily by Aedes aegypti and Aedes albopictus mosquitoes—the same vectors that spread dengue and Zika.
It is endemic in the Philippines, with cases often peaking during the rainy season (June–September) due to increased mosquito breeding.
Current Situation (2025)According to the World Health Organization (WHO) Disease Outbreak News update, as of August 16, 2025, the Philippines reported 628 confirmed chikungunya cases — a 78% decrease compared to the same period in 2024 (2,886 cases). This indicates a significant decline in transmission this year, with effective public health responses (e.g., case investigation, vector control, and community engagement) containing small clusters quickly. No deaths were reported in association with these cases.
Chikungunya cases are generally low in number compared to dengue (which saw over 123,000 cases and hundreds of deaths in the first half of 2025).
The virus circulates sporadically, with occasional localized outbreaks, but no nationwide epidemic in recent years.
The Philippines remains at elevated risk for chikungunya, as noted by the U.S. CDC, even without active large outbreaks. Travelers and residents should take precautions.
Symptoms and Treatment
Symptoms typically appear 4–7 days after infection and include:High fever
Severe joint pain (often debilitating and long-lasting)
Muscle pain
Headache
Fatigue
Nausea
Rash
The disease is usually self-limiting, with most recovering fully, though joint pain can persist for months.
that is what they are complaining about now that they are over their acute phase.
There is no specific antiviral treatment; management focuses on symptom relief (painkillers, rest, hydration). Vaccines are approved in some countries but not widely available or used in the Philippines.
PreventionThe Philippine Department of Health (DOH) promotes the 4S strategy (enhanced for dengue, chikungunya, and Zika):Search and destroy mosquito breeding sites (e.g., empty water containers, tires).
Self-protection (use repellents, wear long sleeves/pants).
Seek early medical consultation if symptoms appear.
Support fogging in high-risk areas.
Additional tips: Eliminate standing water around homes, use bed nets, and avoid outdoor activities during peak mosquito hours (dawn and dusk).If you're in the Philippines or planning to travel there, stay vigilant—especially in urban or rural areas with poor drainage during rainy periods. For the latest official updates, check the DOH or WHO websites.
Novel monoclonal antibody targets deadly sepsis by preventing 'cytokine storms'
Scientists at the University of Virginia School of Medicine and the University of Michigan have developed a monoclonal antibody to stop sepsis, a deadly full-body infection. The antibody also has the potential to treat a broad array of other inflammatory conditions, including autoimmune disorders, their research indicates.
,,,,Ma and his collaborators' new antibody, they hope, could become the first treatment that directly targets the underlying immune system dysregulation responsible for sepsis. It seeks to prevent the "cytokine storms" that made headlines in the pandemic, shutting down the body's hyperactive immune response before organ damage can occur.
very early research and now will go into reality i.e. clinical trials.
reading the Tale of Genji has made me curious about that era.
I am working my way through this book because it gives information on disease in Haien period Japan
before the Haien period, there was a lot of trade and immigration from Korea and even China, and this included the introduction of diseases and Buddhism.
Buddhism and an unknown disease that caused an epidemic, probably smallpox arrived at the same time, but it wasn't until 200 years later in 735 that a verified smallpox epidemic depopulated Japan and much of the aristocracy (25 percen mortality).
and I ran into a quote describing the household of a rich guy during the Haien period, whose servants include.... a yogurt maker.
Yogurt? as in milk based yogurt? Yup. Apparently along with small pox and sutras, yogurt and ghee came to Japan with Buddhist monks. After all, Buddhism was originally an Indian religion, and yogurt and ghee were commonly used in India.
the use of milk products died out in Japan, but continued in some parts of China. But milk products continued to be used as medicine.
Dairy was also known to early Chinese civilization. Huang (2002, p. 809) states that “oracle-bone and bronze inscriptions suggest that the collecting of milk from cows and mares was not an unfamiliar art during the Shang Dynasty (ca. 1520–1030 b.c.)”. We might ask the extent to which dairy was consumed not only in China in later centuries—particularly during the first millennium CE—but also whether contemporary Japan had a comparable industry. Buddhism, medicine, astronomy and the Chinese script were transmitted from the mainland to Japan, but what about cattle rearing and the production of dairy products?
The role of dairy in premodern China is slowly becoming recognized today, despite some past preconceived notions that peoples in East Asia seldom enjoyed milk and cheese until the twentieth century. Miranda Brown recently published a study of a text from 1504 that includes a recipe for cheese-stuffed pasta by a certain Mr. Song. The use of cheese in Chinese culture, particularly in premodern periods, is generally not recognized today by historians of food
there are several papers out there about trade between China Korea and Japan, which introduced Buddhism and disease among other things. This one states;
Smallpox was first introduced to the islands of Japan by merchants and Buddhist
missionaries from the Korean kingdom of Paekche in the sixth century CE. Once
it reached the shores of Japan, smallpox did not disappear but emerged in waves
that were sometimes manageable and were at other times catastrophic. In 735, a
second smallpox epidemic afflicted Japan, reducing the population by 30 percent
and resulting in labor shortages and declines in agricultural production and tax
revenue for the court
and periodic epidemics continued: The author of Tale of Genji lost her husband to small pox. But there is not a lot of information about epidemics in either that novel or the diaries and books of other court ladies, nor is there any mention of smallpox scars....
in Genji several deaths are described: Post partum eclampsia death of Genji's wife (such seizures can occur up to six weeks post partum), the lingering death of the seducer of the Third princess that sounds like Beri beri, and the lingering death of Murasaki, probably from tuberculosis.
But no mention of yogurt or ghee/clarified butter.
so how was smallpox treated?
At the height of the epidemic, Emperor Shomu consulted his officials at
the Bureau of Medicine. They recommended various remedies and guidelines,
including a prohibition against drinking water, an encouragement to eat boiled
rhubarb, and a recommendation to apply powdered silkworm cocoons to boils.
When these guidelines did not help to quell the disease, Emperor Shomu ordered
Buddhist monks and nuns to read sutras to the afflicted and prayers to kami, whom
he interpreted to be deities that were part of the Buddhist universe.
In Heian period Japan (794–1185), yogurt and butter were rare and valued mostly for their medicinal uses, mainly among the aristocracy and in Buddhist practices. Dairy was not widely consumed due to Buddhist prohibitions on animal products, but it held a special place in elite and religious contexts.
**Medicinal Yogurt**: A yogurt-like product called *raku* (possibly fermented milk) was documented in texts like the *Ishinpō* (984 CE), a medical treatise. It was considered a health-promoting food, used to aid digestion and treat illnesses, especially among nobles. Its use was influenced by Chinese medicine, where dairy was seen as beneficial for vitality. *Raku* was likely consumed in small amounts by the elite, as dairy production was limited and tied to imperial or aristocratic estates.[](https://www.incrediblediscourse.com/post/dairy-in-japan)[](https://traditional-foods.maff.go.jp/en/bunrui/chikusankakohin)
**Medicinal Butter**: Butter, referred to as *so* or *gyuuraku*, was also a luxury item, primarily supplied to the imperial court, as noted in the *Engi Shiki* (927 CE). It was used medicinally to support health and digestion, often prescribed in Chinese-influenced medical practices. Butter was sometimes processed into forms like *hakugyūraku* (a condensed milk product) for its nutritional value. Its production was overseen by the Bureau of Medicine, showing its link to health rather than everyday diet.[]>
**Buddhist Context**: Dairy, including yogurt and butter, was used in Buddhist rituals, inspired by Indian traditions via China. Texts like the *Vairocanābhisambodhi* mention dairy in offerings, such as yogurt rice or butter in magical rituals. While direct evidence of ritual use in Japan is limited, the influence of Chinese Buddhism suggests dairy was likely part of similar practices, especially in aristocratic temples.[](https://www.incrediblediscourse.com/post/dairy-in-japan)[](https://www.thechinastory.org/dairy-the-deep-historical-link-between-china-and-japan/)
**Limitations**: Dairy was scarce, expensive, and mostly inaccessible to commoners. Its use declined toward the end of the Heian period as aristocratic power waned and Buddhist vegetarianism grew stronger, reducing dairy’s presence until the modern era.[](https://www.incrediblediscourse.com/post/dairy-in-japan)
In summary, yogurt and butter were elite, medicinal products in Heian Japan, tied to Chinese medical traditions and Buddhist rituals, with limited use beyond the aristocracy.
Scientists from the Institut Pasteur, the CNRS, and the University of Colorado (USA), in collaboration with various institutions in America and Europe, reveal that a recently identified second species of bacteria responsible for leprosy, Mycobacterium lepromatosis, has been infecting humans in the Americas for at least 1,000 years, several centuries before the Europeans arrived.
Leprosy is a neglected disease, mainly caused by the bacterium Mycobacterium leprae, affecting thousands of people worldwide: approximately 200,000 new cases of leprosy are reported each year.
Although M. leprae remains the primary cause, this study focused on another species, Mycobacterium lepromatosis, discovered in the United States in 2008 in a Mexican patient, and later in 2016 in red squirrels in the British Isles. Led by scientists from the Laboratory of Microbial Paleogenomics at the Institut Pasteur, also associated with the CNRS, and the University of Colorado, in collaboration with Indigenous communities and over 40 scientists from international institutions including archaeologists, this study analyzed DNA from nearly 800 samples, including ancient human remains (from archaeological excavations) and recent clinical cases presenting symptoms of leprosy. The results confirm that M. lepromatosis was already widespread in North and South America long before European colonization and provide insights into the current genetic diversity of pathogenic Mycobacteria.
Most Americans are vaguely familiar with scurvy in sailors (the citrus used by the Brits to prevent this is why they are called Limeys).
And of course Pellegra from corn was a major health problem in the southern USA.
we saw this in our heavy drinkers in Africa, who ate local corn sazda but not much else.
But BeriBeri? Various epidemics here including in the Philippines where imported polished rice was given out to local during famine after the clueless Yanks took over.
But I am doing an investigation into ancient Japan, the Heian period, and medical articles suggest deaths from that.
So I asked Grok:
In Heian Japan (794–1185), the diet of the aristocracy, heavily reliant on polished white rice, led to beriberi, a disease caused by vitamin B1 (thiamine) deficiency. White rice, stripped of its nutrient-rich husk, was a status symbol, but its lack of thiamine caused symptoms like fatigue, nerve damage, heart failure, and death.
Commoners, who ate less processed grains like barley or millet, were less affected. Historical records, like court diaries, note unexplained illnesses and deaths, especially among elites, likely linked to beriberi. For example, the disease may have contributed to the high mortality rates in the imperial court, though exact figures are scarce due to limited medical understanding.
By the Edo period, beriberi was better documented, but in Heian times, its cause was unknown, and no effective treatments existed. Dietary diversification or unpolished rice could have mitigated it, but social preferences delayed such changes.
one article I read said 20 percent of the deaths back then And at least one death Kashiwagi , in Gengi was probably partly due to beriberi, since his legs got weak.
...................,
modern story of how a Japanese military doc found how to stop beriberi from killing their sailors in the Japanese Russia war in the early 1900s.
I should note at this time that white rice has a longer shelf life than brown or partially polished rice. Our organic brown rice is healthier, but the germ etc. has oil and gets racid after six months.
So what about the Philippines? At least one book on the multiple epidemics of people and animals (Foot and mouth disease killed the waterbuffalo so people couldn't plow), mentioned deaths because the Yanks supplied imported polishe Rice.
So I asked Grok:.....
Beriberi, caused by vitamin B1 (thiamine) deficiency, was a significant health issue in the Philippines, particularly due to the widespread consumption of polished white rice, which lacks the thiamine-rich husk.
Historically, the disease was prevalent in rice-dependent regions like the Philippines, where milling practices removed essential nutrients.
Historical Context and Impact
Early 20th Century: Beriberi was a major public health problem in the Philippines, especially among populations relying on polished rice. Research from the period, such as a 1911 study, highlighted its preventability through dietary changes.
Infantile Beriberi: A critical issue in the Philippines, infantile beriberi affected babies of thiamine-deficient mothers, leading to high mortality rates.
Studies from 1947 estimated 12,000–20,000 deaths annually in the 1920s–1930s, with symptoms like heart failure and cyanosis in infants aged 2–6 months.
Colonial Period:
During the Spanish and American colonial eras, beriberi was noted among soldiers and prisoners. For instance, in 1898, Spanish soldiers in Baler suffered from beriberi due to poor diet during a siege, with 12 deaths reported.
Japanese Occupation (1942): Malnutrition, including beriberi, surged due to food shortages, affecting both civilians and prisoners in camps like Santo Tomas.
Symptoms and Types
Dry Beriberi: Affects the nervous system, causing numbness, weakness, and potential paralysis.
Wet Beriberi: Impacts the cardiovascular system, leading to edema, heart failure, and high mortality if untreated.
Infantile Beriberi: Seen in breastfed infants of deficient mothers, causing rapid heart failure and death if not addressed.
Causes and Risk Factors
Dietary Cause: Polished white rice, stripped of thiamine, was the primary culprit.
The shift to milled rice in the late 19th century, driven by taste and economic factors, increased beriberi cases.
Other Factors: Alcoholism, bariatric surgery, and conditions like hyperemesis gravidarum increased risk. Breastfeeding mothers with low thiamine intake endangered infants.
Interventions and Decline
Early Interventions: By 1910, American researcher Robert R. Williams in Manila identified rice bran extract as a cure, leading to thiamine’s isolation in 1935.
Rice Enrichment: Post-World War II, enriched rice programs in the Philippines significantly reduced beriberi incidence. By the 1950s, death rates dropped in areas using enriched rice, with costs as low as 35 cents per person annually.
Tikitiki Treatment: Filipino physician Proceso Gabriel developed a tikitiki extract (from rice bran) for beriberi treatment, a notable contribution to local medicine.
Modern Status
Beriberi is now rare in the Philippines due to improved diets, food fortification, and awareness of thiamine-rich foods (e.g., whole grains, meat, beans). However, it persists in vulnerable groups, such as alcoholics or those with restrictive diets.
Diagnosis involves blood/urine tests and neurological exams, with treatment using thiamine supplements (oral or intravenous). Early intervention reverses most symptoms, though severe cases may leave permanent damage.
For further details on historical beriberi in the Philippines, see studies like Acta Medica Philippina (1947) on infantile beriberi. For current prevention, consult resources like the Philippine Department of Health or WHO guidelines on nutrition.
By the way: The Dept of Defense funded a grant to Ecohealth to put up labs to investigate germs in wild animals. A sharp eyed leftist in the government saw this was funded by the DoD not the HHS, and got it stopped, but the money was still waiting there on the website as of last week. But the good news is that today it was no longer there, and it said the grand was finished: I presume it reached it's terminal time but maybe it was because it was used?
Even Grok doesn't know:
The EcoHealth Alliance grant from the U.S. Department of Defense (DoD) for work in the Philippines, specifically aimed at "reducing the threat of viral spillover from wildlife," was awarded in December 2022 with a value of $3 million. According to information from USAspending.gov, this grant was set to run through 2025. However, there is no definitive evidence in the provided references confirming whether this specific grant remains active or has been terminated as of May 18, 2025.
Lots of stuff at that site but it's written in legalese and I am too senile to understand... but it looks like the programs are still going on.
Well, anyway, back to the Grok Answer: And they do note that Ecohealth was canceled by HHS/NIH in 2024, but note about the Dept of Defense also funds them.
Separately, the U.S. Department of Health and Human Services (HHS) suspended all federal funding to EcoHealth Alliance in May 2024, citing the organization’s failure to adequately monitor and report on risky virus experiments, particularly related to its work with the Wuhan Institute of Virology.
This suspension includes three active National Institutes of Health (NIH) grants and proposes debarment, which would prevent EcoHealth from receiving future federal funding.
While the HHS suspension primarily references NIH grants, it raises questions about the status of other federal funding, including DoD grants, given the broad scope of the suspension.
well, as I noted above the DoD funding to Ecohealth was still alive and well until last week but is now no longer on line.
Grok continues:
Additionally, a post on X from January 2024 claimed the DoD grant to EcoHealth was active until 2025, but this is not conclusive evidence, as X posts can be unreliable. There is no direct confirmation in the provided sources that the DoD grant for the Philippine biolab was terminated, but the HHS action could potentially affect all federal grants, including those from the DoD.
Conclusion: As of the latest available information, the DoD grant to EcoHealth Alliance for work in the Philippines was active as of early 2024, with an intended duration until 2025. However, the HHS suspension of all EcoHealth federal funding in May 2024 may have impacted this grant’s status. Without specific confirmation of termination or continuation, the status remains unclear. For precise details, checking official records on USAspending.gov or contacting the DoD directly would be necessary.
More importantly, the EcoHealth Alliance has also been receiving funding from the US Department of Defense’s Defense Threat Reduction Agency (DTRA), which raises further questions on the full nature of its operations.
To recall, the US DTRA has funded an Animal Biosecurity Laboratory in Tarlac, including six other Regional Animal Disease Diagnostic Laboratories (RADDLs) in Luzon, Visayas, and Mindanao amounting around $23 million.
Concerns have previously been raised on the real objectives of the biosecurity project itself, as the US DTRA is an agency under the DoD, which may have unstated military objectives in pursuing the biosecurity project to completion.
With the EcoHealth Alliance’s links with parties which may have objectives other than purely scientific research, the PH government should breadth of EcoHealth Alliance activities in the Philippines.
In its website, the NGO lists three projects currently being undertaken in the Philippines. This includes PREDICT, bat conservation and EIDR (Emerging Infectious Disease Repository). The PREDICT project seeks to “identify new emerging infectious diseases that could become a threat to human health” while EIDR seeks to “unravel the origins of Emerging Infectious Disease (EID) events.”
In South Cotabato, the IPHO is closely monitoring two cases of suspected Mpox infection.,,,Serame said one of the two patients was from nearby province but sought consultations in South Cotabato while the other is from the province but had travel history
so I asked Grok, and even they said there was no information on where the infection came from
however, back in Sept 2024
there were two cases in Minadano and 14 cases in Manila.
a>
this is spread via close contact: so did they visit Africa? Was it spread via sex tourism? Or did it enter the Philippines with imported monkeys? This is how Ebola Reston entered the Philippines and later spread to pigs and their human caretakers in a nearby town a couple years ago.
from Thailand suggests
yes there is a spread via sex tourism:
Travel Med Infect Dis. 2023 May 30;54:102597. doi: 10.1016/j.tmaid.2023.102597
The silent, rapidly unfolding threat of mpox spread via international travel to Southeast Asia: Are we ready?
At the time of this writing, over 84,000 laboratory-confirmed cases and 75 deaths have been identified in 110 countries. Additionally, despite the downward trend in the past months, a 7-day increase of 48.7% has been observed in early December 2022 before decreasing in following weeks. Singapore declared the first imported case in Southeast Asia during the present outbreak, with 38 mpox cases detected in the region as of 5 January 2023 (Singapore, Vietnam, Indonesia, Philippines and Thailand) (https://www.cdc.gov/poxvirus/monkeypox/response/2022/world-map.html). Interestingly, the first autochthonous case in Singapore was identified 2 weeks after detection of the first imported case, with no direct epidemiological link between these two cases. This phenomenon reflects the looming threat of a potential outbreak that could easily spill over to the entire Southeast Asia region. Although recent mathematical modelling suggests no direct association of mpox outbreaks with air travel, these models could be used to assess the probability of an indirect association with air travel [9]. The situation throughout Southeast Asia is fluid, which raises public health concerns regarding the possibility of importing mpox via international travel, subsequently leading to community transmission, especially in places where tourism has resumed during the ongoing COVID-19 pandemic.
Some of these kids who got very sick ended up living in our office with one infection after another until they hit three or four years old and then they got over it.
But adults? Likd Dr. C I have not gotten infected from these kids.
and I seem to remember them having an RSV vaccine years ago: LINK
In 1966, the first vaccine for Respiratory Syncytial Virus (RSV), a formalin-inactivated RSV vaccine, was administered to U.S. infants and children participating in four clinical trials. The vaccinated children were subsequently exposed to RSV in the community and those who had no antibodies against RSV infection prior to vaccination experienced more frequent and severe RSV infection, a condition known as enhanced respiratory disease.
As a result of the failed vaccine and harms caused to those who received this experimental vaccine, development of further vaccines to prevent RSV infection stalled for several decades.
Decades of research defined enhanced RSV disease (ERD) as the result of immunization with antigens not processed in the cytoplasm, resulting in a nonprotective antibody response and CD4+ T helper priming in the absence of cytotoxic T lymphocytes. This response to vaccination led to a pathogenic Th2 memory response with eosinophil and immune complex deposition in the lungs after RSV infection....
italics mine.
enhanced T cells, hyper immune response, maybe even made worse because they used formaldahyde to kill the virus?
I will have to read the whole thing, but my problem is that this immune stuff was not known when I studied in medical school
and the problem seems to be similar to the enhanced immunity for the dengue vacccine if given to those who never had dengue:
Two mysterious observations defied our understanding of ERD susceptibility for decades: ERD never occurred in those infants who were seropositive for RSV at the time of FIRSV administration, and no child ever experienced ERD twice (26).
The answer to these two enigmas also explains why FIRSV elicited antibodies that failed to protect against RSV infection (26).
The mechanism responsible for the absence of a protective antibody response against RSV remained unclear for decades, hampering the development of new vaccines against the virus.,,,,
In summary, vaccines eliciting nonneutralizing antibody against RSV in seronegative individuals may prime for ERD and should not be administered to infants (at least until effective nonneutralizing mechanisms of antibody-mediated protection are demonstrated).
which is what we saw with the Dengue vaccine: Enhanced disease if you gave the shot to kids who never had Dengue.
A lot of thoughtful people are suggesting there will be a major epidemic to destroy Trumpieboy, along with violence in the streets, assasination attempts, and the collapse of the stock market, and maybe even terrorist attacks blaming Russia
Well, bird flu has been out there for a decade, and now the blog legal insurrection wonders if it was made more virulent by Gain of function research:
Back in 2022, during the early days of the “bird flu” pandemic, I wondered if the H5N1 strain of bird flu was a gain-of-function creation.
The reason for it was two-fold. One was the high kill ratio. While a new virus might have a high infection fatality rate, 100% fatality would only likely be achieved if the virus genetics were rearranged to target a host species.
The second reason was that the Chinese were reportedly experimenting with the H5N1 strain. Since 2019, we have all enjoyed the novel coronavirus they generated in their Wuhan labs.
While I may have been right about the gain-of-function (GOF), I was wrong about the laboratory. It turns out this frankenvirus might be a joint American and Dutch creation.
And, as with China, poor biosafety practices may have been a contributing factor.
Proximal Origin of Epidemic Highly Pathogenic Avian Influenza H5N1 Clade 2.3.4.4b and Spread by Migratory Waterfowl” by Nicolas Hulscher et al: LINK.
Abstract
We investigate the possible laboratory origins of the Highly Pathogenic Avian Influenza (HPAI) H5N1 clade 2.3.4.4b genotype B3.13, currently affecting various animal species and causing sporadic human infections. The proximal origins may be the USDA Southeast Poultry Research Laboratory (SEPRL) in Athens, Georgia, and the Erasmus medical center in Rotterdam, the Netherlands. The first detection of HPAI H5N1 clade 2.3.4.4b in the Netherlands in 2020 raises concerns about earlier gain-of-function research. Genetic analysis indicates genotype B3.13, emerging in 2024, and links to genotype B1.2, which originated in Georgia in January 2022 after the start of serial passage experiments with H5Nx clade 2.3.4.4 in mallard ducks at SEPRL in Athens, Georgia, in April 2021. Genotype B1.2 was found in a bottlenose dolphin in March 2022 in Florida, indicating sudden new adaptations. The NP gene of H5N1 clade 2.3.4.4b (genotype B3.13) likely originated from avian influenza A virus in mallard ducks. Significant mutations found in recent human cases suggest possible links to serial passage experiments. However, causation has not been established, and further investigation is urgently needed to confirm these findings and to identify all H5N1 laboratory leaks that may have occurred with a focus on mallard ducks and other migratory waterfowl, which have the potential to infect a large number of poultry and livestock facilities around the world. A moratorium on GOF research including serial passage of H5N1 is indicated to prevent a man-made influenza pandemic affecting animals and humans
H5Nx clade 2.3.4.4 serial passage experiments are currently being conducted in mallard ducks at the USDA Southeast Poultry Research Laboratory (SEPRL) in Athens, Georgia since April 2021 [12,13]. A new H5N1 clade 2.3.4.4b genotype (B1) was first detected in Georgia in January 2022, with gene reassortments either in PB2 and NP or in PB2, PB1 and NP. This genotype resulted in a sustained wild bird outbreak in Florida and northern Midwestern states, causing a second major wild bird outbreak in Michigan (Figure 1).
Bayesian
Figure 1: Spatial diffusion of US H5N1 clade 2.3.4.4b genotype B1.1 and B1.2. Arrows indicate the direction of virus transition as estimated by a Bayesian stochastic search variable selection. The thickness of arrows represents the median Markov jump count/s for all the transitions between geographical location states along phylogenetic branches. The size and intensity of the red circles is proportional to the frequency of detections and number of genotypes found. The temporal formation and extinction of the red circles were superimposed during the surveillance time. The LMRCA (yellow dots) or the location (blue dots) represent the first or second highest mean Markov rewards.
"BREAKING Publication: Proximal Origin of Epidemic Highly Pathogenic Avian Influenza H5N1 Clade 2.3.4.4b and Spread by Migratory Waterfowl Published evidence suggests current outbreak came from a laboratory."
update: CDC report of last year's dengue outbreak in PuertoRico.
During 2024, Puerto Rico reported 6,291 dengue cases and surpassed the epidemic threshold, prompting declaration of a local public health emergency. Approximately one half of patients (52.3%) were hospitalized, 264 (4.2%) had severe dengue cases, and 11 (0.2%) persons died. Persons aged 10–19 years accounted for 28.4% of severe cases.
Since most cases have few symptoms or might not be sick enough to see a physician.
the rest is about treatment (supportive,, including fluids) and mosquito control, things that have been used for a century.
So is there any treatment for Dengue? No medicines?
2018 article suggests ivermectin might help but it was a poor study and the errors of the paper corrected here.
(note a recent article reported hundreds of papers were recently removed from publication because of flaws)
this study showed some lab improvements but wasn't conclusive.
Well, that happens. Outdoor cats catch and eat birds, some of whom are infected.
But these were indoor cats. However someone in their household worked with milk transport or in dairy farms. They refused testing but the family members tested were negative.
Highly Pathogenic Avian Influenza A(H5N1) Virus Infection of Indoor Domestic Cats Within Dairy Industry Worker Households — Michigan, May 2024
published February 20, 2025 / 74(5);61–65
Summary
What is already known about this topic?
Outdoor cats on U.S. dairy farms have been infected with highly pathogenic avian influenza (HPAI) A(H5N1) virus; infection has not been reported in indoor cats.HPAI A(H5N1) virus was detected in two indoor domestic cats with respiratory and neurologic illness that lived in homes of dairy workers but had no known direct exposure to HPAI A(H5N1)–affected farms. Both dairy workers declined testing; other household members received negative test results for influenza A.
PhilInquirer notes that the local physicians groups is pushing the government to approve of a European dengue vaccine.
The Philippine Medical Association (PMA) has urged President Marcos to intervene and expedite the approval of new-generation dengue vaccines amid the surge of dengue cases in the country.
The appeal was made by the country’s doctors at the launching of the Empowering Networks to Defeat Dengue or End Dengue Coalition—founded by PMA, in partnership with health-care organizations, the academe, researchers and advocates—on Tuesday in Quezon City, with the collective goal of achieving zero dengue deaths by 2030.
In a letter addressed to Mr. Marcos read during the event by Dr. Erica Tania Davillo, chair of the PMA’s ad hoc committee on dengue advocacy, the organization acknowledged that the safety of dengue vaccines was of “utmost concern” because of the country’s previous experience with Dengvaxia.
The PMA specifically cited Qdenga of Japanese pharmaceutical company Takeda, which is approved in 40 countries and one of the only two dengue vaccines approved by the World Health Organization (WHO) to prevent dengue in highly endemic countries like the Philippines. (The other WHO-approved dengue vaccine is Dengvaxia of French pharmaceutical giant Sanofi Pasteur.)
The WHO in May last year cleared Qdenga for use in children aged 6 to 16 in areas with high infection rates. The prequalification made it eligible for procurement through United Nations agencies like the UN Children’s Fund.
The vaccine, which contains weakened versions of the four dengue virus strains, is recommended as a two-dose schedule with a minimum interval of three months between doses.
Dengue disease is caused by infection with dengue virus, which is transmitted to humans through the bite of mosquitos. This vaccine contains attenuated versions of the 4 virus serotypes. These versions cannot cause the disease, but they ‘teach’ the immune system (the body’s natural defences) to defend the body against the virus.
When a person is given the vaccine, the immune system identifies the attenuated serotypes as foreign and makes antibodies against them. When a person is later exposed to the virus, the immune system recognises it and can quickly make many more antibodies, which then neutralise the virus before it can cause dengue disease.
so it's not an mRNA vaccine but an old fashioned attenuated virus type.
But the complications of dengue happen in folks who have had the disease before, and get a hyperimmune response. That was the problem with Denguevax.
lancet article.
Cumulative vaccine efficacy against virologically confirmed dengue was 64·2% in dengue-exposed participants and 53·5% in dengue-naive participants from first dose up to 4·5 years after the second dose.
Is new dengue vaccine efficacy data a relief or cause for concern?
The exact immunopathogenic mechanisms of sequential heterotypic DENV infections are incompletely understood, but considerable evidence points to humoral and cellular adaptive immune responses occurring in response to the first infection facilitating increased DENV replication during the second infection which, in turn, drives pro-inflammatory cytokine secretion25,26,27,28,29,30,31. The exact number of annual dengue fatalities is not known but the estimates range between 5000 and 40,000 with many deaths occurring in children32,33.
with dengevax, the immune problem includes:>
Dengvaxia®
Sanofi Pasteur licensed the first dengue vaccine (Dengvaxia®) in Mexico in 2015, and more than 20 countries thereafter, based on the safety and efficacy demonstrated in two phase III trials and a single season of disease surveillance. Unfortunately, the optimisim that a dengue vaccine was finally available quickly became disappointment when a safety signal was observed in vaccine recipients who were dengue non-immune at the time of vaccine administration44,45. In the third year of the phase III clinical trial, the youngest, non-immune vaccine recipients experienced increased rates of hospitalized and severe dengue compared to their unvaccinated peers
The next generation of dengue vaccines
As expected, every dengue vaccine candidate following Dengvaxia® is being stringently reviewed for safety and efficacy in dengue immunes and non-immunes, across a broad age range of recipients, and for their ability to protect against the full spectrum of disease outcomes caused by infection with any DENV type. There is also a requirement for demonstrating safety and efficacy across more than one dengue season56,57,58.
Two new live attenuated dengue vaccines have now completed phase III efficacy trials and there is room for cautious optimism once again. Takeda recently received approval from Indonesia, European Commission, and Brazilian regulators for use of their two-dose vaccine (TAK-003) in people 4 years of age and older, regardless of baseline dengue immune status.
(https://www.takeda.com/siteassets/system/newsroom/2022/qdenga/ema-combined-h-5155-en.pdf) (accessed 21 January 2023).
In summary, the three live attenuated dengue vaccines which have generated clinical endpoint efficacy data have all demonstrated; (1) higher efficacy in dengue immune recipients; (2) higher efficacy against more severe clinical phenotypes; (3) variance in DENV type specific efficacy, and (4) the challenge of capturing data for all desired clinical endpoints (any dengue, severe dengue, hospitalized dengue), across all DENV-1–4 types, in both dengue immune and non-immune recipients.
one of the problem with attenuated virus vaccines is that sometimes the virus escapes and causes the disease (a major problem with the Oral Polio vaccine).
How to assess for the potential of vaccine-associated dengue is not straight forward. After two years of surveillance in the Butantan study there were no severe dengue cases nor cases with clinical warning signs. The Takeda experience, however, is more complex, and even though clinical and regulatory review committees for the European Commission and Brazil’s National Health Surveillance Agency (ANVISA) did not believe there was a safety signal in dengue non-immune recipients, this a point of contention
Conclusion
It is clear the perfect dengue vaccine is not on the immediate horizon, but the Sanofi, Takeda, and Butantan/NIH/Merck experiences do inform us that it is possible to effectively immunize some people against disease scenarios that constitute dengue’s burden. I would contend when it comes to dengue countermeasure development, safety is non-negotiable, but all other expectations must be managed and considered in the aggregate. Our challenges with effectively communicating coronavirus disease 2019 vaccine performance characteristics should be a cautionary tale in this regard. Pursuit of the perfect dengue vaccine is a laudable goal, but not at the cost of overlooking imperfect options that could safely deliver tangible, albeit smaller scale, public health benefit.
I post the text and links etc so I can read these articles in detail on my tablet.
QDenga page
hmmm...it says a lot about the politics of this vaccine that it has a long list of places for you to share the article, but X/twitter is not one of them.
the same ones who gave you covid vaccine are now planning a new vaccine for the Plague.
Few docs in the USA have ever seen a case, but there are a couple eases each year on the Navajo or nearby reservations because it is carried by prairie dogs.
the usual infection is a bite and then you develop huge enlarged lymph nodes (bubos hence the name bubonic plague).
usually it is treated with common antibiotics, but this report says the bacteria is becoming resistant to them.
What is worrying is that if it goes to the lung, it can cause a pneumonia that is easily transmitted to those nearby, and can kill you within 24 hours.
The article mentions that there has been a plague vaccine for over a century:
The first plague vaccine was developed in 1897 by bacteriologist Waldemar Mordechai Wolff Haffkine, who tested it on himself. This early vaccine was widely used in British India, with an estimated 26 million doses distributed between 1897 and 1925, reducing plague mortality by 50-85%.
He was hailed as the “the Jewish Jenner” (Jenner having created the smallpox vaccine), as Haffkine also developed a vaccine for cholera.
When the bubonic plague hit Bombay in October 1896 with a mortality rate double that of cholera, the Indian government asked Haffkine to assist, and he commenced work in a crude laboratory and assumed the daunting task of developing the world’s first vaccine against plague.
Amazingly, working almost entirely by himself, he succeeded in developing a vaccine that was ready for testing only three months later and, again, he first tested it on himself on January 10, 1897. Soon after he announced his successful results to the authorities, plague broke out at Bombay’s Byculla House of Correction. He conducted a controlled test there, the results of which were that the majority of deaths were among the unvaccinated.
Only China and Russia have licensed a live bubonic plague vaccine, which is based on an attenuated Y. pestis strain.
However, this type of vaccine is associated with some adverse effects and does not provide long-term immunity.
yup. it needs three shots and then repeated boosters.
The US Military always gave plague vaccine to soldiers being deployed to certain areas (e.g. Viet Nam). So isn't there a vaccine already?
There is no requirement for routine immunization. Plague vaccine is administered to personnel who are likely to be assigned to areas where the risk of endemic transmission or other exposure is high. Vaccine may not be effective in the prevention of airborne infection. The addition of antibiotic prophylaxis is recommended for such situations.
PLAGUE VACCINE
Plague vaccines ** have been used since the late 19th century, but their effectiveness has never been measured precisely. Field experience indicates that vaccination with plague vaccine reduces the incidence and severity of disease resulting from the bite of infected fleas. The degree of protection afforded against primary pneumonic infection is not known. Persons exposed to plague patients who have pneumonia or to Yersinia pestis *** aerosols in the laboratory should be given a 7- to 10-day course of antimicrobic therapy regardless of vaccination history. Recommended antimicrobials include tetracyclines, chloramphenicol, or streptomycin.
The plague vaccine licensed for use in the United States is prepared from Y. pestis organisms grown in artificial media, inactivated with formaldehyde, and preserved in 0.5% phenol. ...
the bad news? It takes a few shots to give you immunity and some people just don't develop antibodies.
Following the primary series of 3 injections, about 7% of individuals do not produce PHA antibody, and a few fail to develop a titer of 128, the level correlated with immunity in experimental animals. PHA titers should be determined for individuals who have an unusually high risk of infection or who have a history of serious reactions to the vaccine in order to govern the frequency of booster doses. Such testing can be arranged through state health departments. Since plague vaccination may only ameliorate illness, whenever a vaccinated person has a definite exposure, prophylactic antibiotics may be indicated whether or not an antibody response has been demonstrated.
I should add: usually it is sporadic cases, so one doubts it would turn into an epidemic nowadays.
or maybe not given the fact that the homeless and failure to remove garbage has led to lots of rats in some US cities.
(ironically, one of the cases was spread by cat fleas. Uh oh).
there have been three epidemics of Black Plague: The first, the Plague of Justinian, the second the medieval Black death, and the third in the last century (something few know about: but a local outbreak inspired Camus book The plague)
the third epidemic started in China. from the above CDC article;
The third (Modern) pandemic began in southwestern China in the mid-19th, struck Hong Kong in 1894, and was soon carried by rat-infested steamships to port cities on all inhabited continents, including several in the United States
By 1930, the third pandemic had caused more than 26 million cases and 12 million deaths.
the name black plague comes from necrotic lymph node abcesses, aka bubos. But it is not the most frightening type.
Plague in these three pandemics was predominantly the bubonic form, emanating from Yersinia pestis-infected rats and fleas, although terrifying outbreaks of the more virulent person-to-person spreading pneumonic form were recorded during the course of each. The explosive contagiousness and severity of pneumonic plague was most completely documented in Manchurian epidemics in the early 20th century, which involved tens of thousands of cases, virtually all of them fatal (Wu, 1926).
Improved sanitation, hygiene, and modern disease control methods have, since the early 20th century, steadily diminished the impact of plague on public health, to the point that an average of 2,500 cases is now reported annually (World Health Organization, 2003). The plague bacillus is, however, entrenched in rodent populations in scattered foci on all inhabited continents except Australia (Gage, 1998; Gratz, 1999b), and eliminating these natural transmission cycles is unfeasible. Furthermore, although treatment with antimicrobials has reduced the case fatality ratio of bubonic plague to 10% or less, the fatality ratio for pneumonic plague remains high
The idea of using plague as a weapon is not new. Anecdotal reports describe catapulting of plague cadavers into enemy fortifications in 14th and 18th century warfare (Derbes, 1996; Gasquet, 1908; Marty, 2001). In World War II, the Japanese military experimented with plague in human subjects at their clandestine biological research facilities in Manchuria, and on several occasions dropped Y. pestis-infested fleas from low-flying planes on Chinese civilian populations, causing limited outbreaks of bubonic plague and initiating cycles of infection in rats (Bellamy and Freedman, 2001; Harris, 1992; Kahn, 2002). Biological warfare research programs begun by the Soviet Union (USSR) and the US during the Second World War intensified during the Cold War, and in the 1960s both nations had active programs to “weaponize” Y. pestis.
how bad could the release of plague germs be? Uh oh:
Models developed by this expert committee predicted that the intentional release of 50 kg of aerosolized Y. pestis over a city of 5 million would, in its primary effects, cause 150,000 cases of pneumonic plague and 36,000 deaths.
I wonder, but since it is in a peer review paper, maybe not.
LINK thread reader has a pdf download for me to read later.
Not sure if this is the one about humans or just the one decimating the US poultry industry, but the claim is that it was a lab leak and gain of function research.
Dr. Peter McCullough: "The current strain of bird flu is a product of gain of function research done in the USDA Poultry Research Laboratory in Athens, Georgia. So it is a man made problem that, our farms are experiencing right now. It's in the peer reviewed literature, and, I… pic.twitter.com/R4avvTtC7r
"The current strain of bird flu is a product of gain of function research done in the USDA Poultry Research Laboratory in Athens, Georgia. So it is a man made problem that, our farms are experiencing right now. It's in the peer reviewed literature, and, I mean, it's really you know, the next steps in this outbreak is, for people to understand, you know, the ramifications of it personally and how to be prepared."
"It's the circulating clade, which is the kind of the original source strain, is clade 2.3.4.4b, and, again, that is a product of what's called serial passage gain of function research done at the USDA Poultry Research Laboratory."
"It was assisted, by University of Wisconsin School of Veterinary Medicine and, Rotterdam University. The gain of function was to get it to spread from chickens into migratory waterfowl or mallard ducks. And so that's how it's spreading across the world now."
"It's been spreading for 4 years. It continually reinfects the farms because the mallard ducks fly around, and they land in in ponds on farms and they, easily infect the other animals, on the farm. So it was able to, in a sense, expand the host range even into cattle and to sea mammals."
"Now the good news is it's much milder than bird flu of decades ago, and then there's the peer reviewed paper by Nick Hulscher on this. And, you know, and this has not been denied by the USDA Poultry Research Center."
"McCullough Foundation attended the bird flu summits in both, University of Arkansas as well as in Washington, DC. So there's no denial of this. Just like COVID 19, the bird flu problem is a man made problem by the US government."...................\
Dr McC has a discussion here and again I am linking it for reading later on my tablet.
in an earlier post in an article for duck hunters it noted that most bird flu is mild, but that there is a new strain going around
According to a 16 May, 2024 advisory issued by the World Health Organization: “The goose/Guangdong-lineage of H5N1 avian influenza viruses first emerged in 1996 and has been causing outbreaks in birds since then. Since 2020, a variant of these viruses has led to an unprecedented number of deaths in wild birds and poultry in many countries. First affecting Africa, Asia and Europe, in 2021, the virus spread to North America, and in 2022, to Central and South America. From 2021 to 2022, Europe and North America observed their largest and most extended epidemic of avian influenza with unusual persistence of the virus in wild bird populations. Since 2022, there have been increasing reports of deadly outbreaks among mammals also caused by influenza A (H5)-including influenza A (H5N1)-viruses. There are likely to be more outbreaks that have not been detected or reported. Both land and sea mammals have been affected, including outbreaks in farmed fur animals, seals, sea lions, and detections in other wild and domestic animals such as foxes, bears, otters, raccoons, cats, dogs, cows, goats and others” [1].
Most people know that Covid was a lab lead from gain of function research funded by Fauci via Ecohealth to the Wuhan lab.
But as I pointed out a few weeks ago, they are continuing to lie about this in this Scientific American article that quotes the Chinese doctor believed to be responsible for the leak claims they didn't have that covid in their refrigerators (which were examined four years after the lab leak by her, not one week after the problem appeared by a neutral authority).
So anyway, the gaslighting continues.
The LATimes has a scare article that bird flu is going to kill us all. (alternative link): I post it here because both sites get turned off by pop up windows telling you to pay for the article, and I posted it here in large print so I can read it later at my leisure. So sue me LATimes. I have no money, but they could shut down my blog. PFFT>
Why scientists say we are fighting H5N1 bird flu with one hand tied behind our backs
The National Animal Disease Center research facility in Ames, Iowa, tests milk samples amid an outbreak of H5N1 bird flu among dairy cattle. (USDA Agricultural Research Service via Associated Press)
By Susanne Rust and Karen Kaplan
Dec. 24, 2024 3 AM PT
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Gain-of-function research became controversial during the COVID-19 pandemic.
But without it, “we’re just flying in the dark” when it comes to H5N1, said Felicia Goodrum, a molecular virologist at the University of Arizona.
actually her CV says she is a leukemia expert, but of course if you have leukemia you easily get all sorts of weird infections.
As the H5N1 bird flu virus steamrolls its way across the globe — killing wild animals, commercial livestock and even some people — scientists and health officials fear we’re on the precipice of another global pandemic.
it has been around for years, and most of the deaths were people in close contact with birds or who ate infected meat of sick birds which usually are killed when they get sick. That is why at one point, Jakarta banned back yard chickens which in SEAsia are not for food but fighting cocks, but VietNam merely ordered fighting cocks to get a vaccine for the chickens (yes there is a vaccine but it's hard to give a shot to 1000 chickens in a chicken house) ... I think I read that the future might be to give chickens an oral mRNA vaccine to stop the epidemic but don't quote me).
But when, where and how that could come to pass is hard to predict — in part, some researchers say, because of guardrails the federal government has placed around gain-of-function research.
it's the government's fault. /sarcasm
The term describes experiments that seek to understand a virus’ potential to adapt to new hosts, spread more easily, survive longer in the environment and cause those infected to become sicker. Though many scientists view the approach as a critical tool for conducting biological research, other experts have long complained that it’s unacceptably risky — a reputation exacerbated by persistent speculation that the virus responsible for the COVID-19 pandemic was created in gain-of-function experiments in a laboratory in Wuhan, China.
That led many virologists to steer clear of the work to avoid its stigma and regulatory red tape. Some in the field say that has deprived officials of valuable information that could have helped them anticipate and prepare for H5N1’s next moves.
“Do I believe if that research was more widely accepted, we’d have a better grip on this virus and what it might do next? Or how quickly it could change? Or what that would take?” asked Richard Webby, director of the World Health Organization’s Collaborating Center for Studies on the Ecology of Influenza in Animals and Birds. “YES.”
Felicia Goodrum, a molecular virologist at the University of Arizona, said gain-of-function research could enable health officials to recognize worrisome H5N1 mutations and identify targets for antivirals and vaccines.
“Without it, we’re just flying in the dark,” she said.
but they already have a bird flu vaccine, and newer ones in the work. and the article hints they already did gain of function research to find the data, although it is unclear about this.
Just one mutation can make H5N1 bird flu a threat to humans, California researchers say
Dec. 5, 2024
but the vaccine could aim at other sites to give immunity, not on the one site that allows transmission.
Critics of this line of research don’t see it that way. They say the work is too dangerous, making it possible for a souped-up pathogen to escape into the environment where people have no natural immunity. Even worse, they argue, it could wind up in the hands of nefarious actors who could use it as a bioweapon.
These risks outweigh the promise of work that may not be as helpful as its supporters suggest, said Marc Lipsitch, professor of epidemiology at the Harvard T.H. Chan School of Public Health.
What scientists and health officials need to know to contain the outbreak, Lipsitch argues, are things like which animals are infected, which people have been exposed, how many of them caught the virus and how sick they became as a result.
“Those are basic epidemiology and veterinary questions,” Lipsitch said. “I can’t think of any route by which gain-of-function studies could have informed — much less answered — those questions.”
well, the Asian cases had a high mortality, but knowing Asia (and knowing chicken farms) one wonders if most people didn't get very sick so didn't go to the hospital: the US studies suggest this happened in the US dairy worker cases. that I discuss below.
The controversy dates to 2011, when two independent research groups said they had conducted gain-of-function experiments that resulted in strains of H5N1 that could be spread via air between ferrets, a species used to model influenza’s behavior in humans.
H5N1 was first identified in wild geese in China in 1996 and soon spread among birds in Asia, jumping to people on hundreds of occasions along the way. More than half of those known infections were fatal.
The high mortality rate and geographical spread of the virus prompted then-President George W. Bush to establish a $7.1-billion program to prepare for its inevitable arrival on U.S. shores. He spearheaded the establishment of a global surveillance and preparedness network via the WHO, as well as a national one. He also directed federal funds into the stockpile of vaccines and antiviral medications, as well as millions of dollars toward laboratory research.
U.S. Geological Survey biologist Dan Ruthrauff watches a mist net for birds in the Anchorage Coastal Wildlife Refuge.
World & Nation
A Killer Takes Wing
Jan. 10, 2006
Amid this flood of support, Yoshihiro Kawaoka‘s team at the University of Wisconsin in Madison and Ron Fouchier‘s at Erasmus University in the Netherlands simultaneously began to experiment with H5N1, introducing genetic mutations into its RNA to see what changes could transform it from a virus that passed easily between birds into one that passed efficiently between people.
yup. They actually did that.
Kawaoka and his colleagues combined the H5 hemagglutinin gene from the bird flu virus with genes from the 2009 H1N1 swine flu virus. Then they coaxed their hybrid to evolve in a way that allowed it to bind with mammalian cells rather than bird cells. They found that four mutations in the H5 gene were enough to create a virus capable of spreading between ferrets in neighboring cages.
Meanwhile, the researchers in Fouchier’s lab tinkered solely with H5N1. They added a handful of mutations that helped fuel previous flu pandemics, then infected their ferrets. The virus didn’t spread on its own at first, so the scientists helped it along by transferring it from the noses of infected animals to healthy ferrets. After 10 such passages, the virus had evolved to the point where it spread on its own from one ferret to another.
The studies offered valuable confirmation that the bird flu virus had the potential to spark a human pandemic, said Dr. Arturo Casadevall, an immunologist and infectious disease physician at Johns Hopkins University.
“Before those experiments were done, we did not know whether H5N1 had the biological capacity to become mammalian-transmissible,” he said.
But they also underscored the risk that scientists could accelerate the threat. “That was the original gain-of-function poster child,” Casadevall said.
yup. It took awhile but the scientists managed to make the bird flu transmissable to humans in their lab.
Concern that information in the studies could be put to ill use prompted Kawaoka and Fouchier to voluntarily pause their work in 2012, and their papers were published only after passing a thorough safety review by the U.S. National Science Advisory Board for Biosecurity.
because they realized that bad guys could read their paper and manufacture a dangerous bioweapon. But anyway, they did manage to publish it.
But the bad news: it's not just bad guys who are the danger:
Gain-of-function research resumed the following year.
Fears were revived in 2014 after federal labs mishandled samples of smallpox, anthrax and H5N1.
italics mine.
Nobody was sickened, but it prompted a three-year freeze on federal funding for gain-of-function experiments involving particularly dangerous pathogens, until stricter oversight rules were put in place.
Plans for such experiments now go through several layers of review at a potential researcher’s institution. If the work is funded by the National Institutes of Health, additional reviews follow.
translation: Lots of paperwork that if followed correctly and no one made any mistakes would stop a leak from happening.
“There are a lot of regulatory hurdles to assure there’s appropriate risk mitigation,” said Seema Lakdawala, a virologist at Emory University who studies influenza viruses. “We’re all being extra careful because nobody wants to be accused of having done something unsafe.”
translation: no one wants to be accused of doing something unsafe, meaning there is a strong motivation to cover up any mistake.
Those hurdles can delay a research project by several months or more, if they are approved at all, she said. The uncertainties have acted as a deterrent, especially for scientists in the early stages of their careers.
“It’s definitely uncomfortable to do gain-of-function research,” Goodrum said. “We’re discouraging people from entering the field.”
To some, the timing couldn’t be worse.
At least 65 people in the U.S. have been infected with H5N1 since it arrived in North America in 2021, according to the Centers for Disease Control and Prevention
65 cases in four years. Got it.
Most of the cases have involved workers on dairy and poultry farms, and their symptoms — including conjunctivitis and upper respiratory irritation — have tended to be mild. But in two cases, people have become severely ill, including a person in Louisiana and a teenager in Canada.
so two very sick people in four years but no deaths. Out of 65 cases in four years. But how many people got the disease and never sought medical care or were diagnosed? In other words, the virus in humans is not very lethal.
There is no evidence that the virus can spread directly from one person to another, the CDC said.
yes. but just wait: in time, that could happen.
Scientists expect that will change sooner or later. With flu season picking up steam, the risk is rising.
“The thing I’m most afraid of today is a recombination event between the stuff going around in cows and the seasonal flu,”
this is one of the unproven theories behind the 1918 flu epidemic: ordinary flu combined with bird flu. But the high mortality might have been because of spread in close contact (army barracks) or due to the malnutrition during World War I due to blockades and poor nutritional status.
Casadevall said. If both viruses infected the same mammal at the same time, their components could mix and match in a way that creates “a strain that is able to infect humans very easily, and for which we don’t have immunity.”
“That is a gain-of-function experiment being done by nature,” he added.
It’s a point that Webby suggested as well, noting that gain-of-function experiments are a whole lot safer in a sealed-off Biosafety Level 3 laboratory equipped with special ventilation systems and other precautions “than on a farm.”
True, except for the danger of a lab accident....but here is the dirty little secret: as these docs note: Gain of function research might produce the strain that will evolve spontaneously: Influenza tends to mutate a lot. So their research might be useless.
But Lipsitch and others say the fact that the virus is constantly mutating and changing calls into question the relevance of gain-of-function research. A viral strain that can be concocted in a laboratory is not necessarily going to match whatever emerges in the environment.
“There’s a big element of randomness in evolution,” Lipsitch said. “The fact that an experiment goes one way in the lab doesn’t mean it will go the same way somewhere else.”
Even if it’s a close match, Lipsitch said, there’s “compelling evidence that what you learn in one strain can be the opposite for a very closely related strain. So the generalizability is very low.”
He cited a paper that took the mutations that made H5N1 “more mammal-friendly” in Kawaoka’s and Fouchier’s experiments and applied them to a slightly different version of the virus. In that case, the researchers found “a completely different effect.”
These shortcomings make the research risks harder to justify, said Nicholas Evans, a bioethicist at the University of Massachusetts Lowell.
“I think what the gain-of-function debate has yet to answer is, ‘What is the social value of these studies?’” he said.
To Evans, there appears to be very little, especially considering the lack of urgency in the government’s response.
“Saying that this particular piece of extremely niche biological research into H5N1 would have made a material difference in an outbreak that has largely been characterized by a lack of interest on behalf of public federal agricultural and public health regulators just is kind of nonsense to me,” he said.
Kawoaka declined to discuss his research, and Fouchier could not be reached.
That is unclear: does he mean that the government has no interest so it's not important?
but hey: The mRNA vaccines are here, and there is money to be made, so things might change.
The bird flu outbreak in U.S. dairy cows is prompting development of new, next-generation mRNA vaccines — akin to COVID-19 shots — that are being tested in both animals and people.
In June 2024, the U.S. Agriculture Department is to begin testing a vaccine developed by University of Pennsylvania researchers by giving it to calves.
Michael Imperiale, a virologist at the University of Michigan in Ann Arbor, said the experiments conducted by Kawaoka and Fouchier are extremely useful as blueprints of what to watch out for as the virus sweeps the globe.
is the bird flu virus sweeping the globe? Yes, in chickens, and chickens and eggs are a cheap source of high level protein for the poor, so this is a problem for poultry farmers and in preventing malnutrition in the urban poor.
And he’s surprised more people aren’t talking about their value.
“No one seems to point out the fact that those gain-of-function experiments ... gave us an important piece of information, which is that that virus can jump,” Imperiale said.
the ability of viruses to jump species has been known for centuries: E.g. the first vaccine for Rabies was because the virus jumped from mad dogs to humans, and that was invented in 1885. And the original cowpox experiment that resulted in doctors learning that small pox could be prevented by a more benign method than giving people mild cases of the disease was discovered by Jenner in 1798, after he noticed that dairy maids had lovely complexions (no small pox scars) but had a history of catching cow pox.
Other gain-of-function experiments conducted on H5N1 years ago have tipped off scientists about potential mutations that could help the real-world virus spread more easily through the air, get better at infecting cells in the mammalian respiratory tract, and become resistant to antiviral medications.
italics mine. Theory that might or might not be true.
“Those experiments 10 years ago were so informative,” Lakdawala said. “It helped us be better prepared.”
Really?
But unless the scientific community stands up for the work and challenges its negative image, that won’t be the case in the future, Goodrum said. “It’s very likely that we will be less prepared for the next pandemic than we were for the last one.”
Translation: give them money and let them do this dangerous research or they will blame Trumpieboy for the next epidemic because he stopped funding research similar to that which gave us the last epidemic of COVID.
With government shutdown looming, what happens to bird flu surveillance?
author Karen Kaplan covers science and medical research for the Los Angeles Times. She has been a member of the science team since 2005, including 13 years as an editor. Her first decade at The Times was spent covering technology in the Business section as both a reporter and editor. She grew up in San Diego and is a graduate of MIT and Columbia University.
so what does the NIH say about bird flu?
I get the weekly reports from the CDC.
well, in the last few weeks they have had articles on how addicts use fentanyl, Dengue fever, Rocky mountain spotted fever etc etc.
Infections with highly pathogenic avian influenza (HPAI) A(H5) viruses have been detected sporadically in dairy farm workers in the United States since April 2024.
and lots of the farm workers got sick, right?
this report is from a sample of workers who were in close contact with sick dairy cattle (not all of the workers were tested and most of them spoke Spanish, suggesting maybe malnutrtion could bias their ability to get sick): italics mine:
In both states, a convenience sample of persons who work in dairies was interviewed, and blood specimens were collected. Among 115 persons, eight (7%; 95% CI = 3.6%–13.1%) had serologic evidence of recent infection with A(H5) virus;
and they got sick from contact with sick cows:
Among persons with serologic evidence of infection, four recalled being ill around the time cows were ill; symptoms began before or within a few days of A(H5) virus detections among cows.
A total of 115 dairy workers (45 in Michigan and 70 in Colorado) were interviewed and had serum specimens collected; the total number of dairies contacted or workers employed across these dairies was not recorded across states (Table 1). Dairy workers typically spoke Spanish, and 72% of interviews were conducted in Spanish.
Specimens were collected at a median of 49 days after first exposure (IQR = 47–59 days) based on the date HPAI A(H5) infection in the herd was confirmed. Among all workers, 21 (18%) reported receipt of the 2023–24 seasonal influenza vaccine.
Workers reported multiple job tasks; those most frequently reported included cleaning manure (62%), milking cows (59%), and moving or hauling cattle (49%).
Now remember: of all those tested only 8 had evidence of a bird flu infection. But 46 workers were sick during that time. Meaning that maybe some of those who tested positive for antibodies to bird flu might not have been sick from bird flu but from another virus going around. Again, italics mine.
Among all 115 dairy workers, 46 (40%) reported feeling ill shortly before or during the period that A(H5) virus infection was confirmed in cows on the farms where they worked (Table 3). Four of these illnesses were among the eight workers with serologic evidence of infection; among these persons, signs and symptoms most frequently reported were red, draining, or itching eyes (three). These signs and symptoms were also frequently reported among workers who were ill but who had negative HPAI A(H5) serology (26 of 42; 62%).
Among the four workers with positive test results, feverishness, sore throat, runny or stuffy nose, sneezing, diarrhea, and headache were each reported by one worker; these signs and symptoms were also reported by persons with negative serology results. Among persons with serologic evidence of infection, illness onset occurred a median of 5 days before the date of detection of HPAI A(H5) virus among cows within the dairy where they worked.
Those testing positive for bird flu got sick before the cattle got sick?
meaning maybe their illness wasn't from bird flu caught from the cattle. (or maybe they gave the bird flu to the cattle?).
here in the summary they note how few of the workers who milked the cows and cleaned up the shit got sick:
In this analysis, 7% of exposed dairy farm workers in Michigan and Colorado had serologic evidence of infection with HPAI A(H5).
and this part suggests most of them simply didn't get very sick
In this analysis, 7% of exposed dairy farm workers in Michigan and Colorado had serologic evidence of infection with HPAI A(H5).
What to know
H5 bird flu is widespread in wild birds worldwide and is causing outbreaks in poultry and U.S. dairy cows with several recent human cases in U.S. dairy and poultry workers.
While the current public health risk is low, CDC is watching the situation carefully and working with states to monitor people with animal exposures.
CDC is using its flu surveillance systems to monitor for H5 bird flu activity in people.
and here is the summary:
H5 Bird Flu Detections in USA
• Dairy cattle: Ongoing multi-state outbreak
• Wild Birds: Widespread
• Poultry Flocks: Sporadic outbreaks
• Mammals: Sporadic infections
• Person-to-person spread: None
• Current public health risk: Low
One more thing: It is hunting season, so did any hunters catch bird flu from migratory birds? There are sporadic news stories of dead birds being found.
Ducks Unlimited article:most wild birds with the low pathogenic (mile variation) of bird flu don't have symptoms.
Avian flu does not pose a food safety risk when wild or domestic poultry products are handled and cooked properly.
The severity of avian flu varies based on the subtype of the circulating virus and is classified as either low pathogenic avian influenza (LPAI) or high pathogenic avian influenza (HPAI).
Most avian flu subtypes are LPAI and cause little or no signs of illness in domestic or wild birds and pose no threat to human health. These subtypes are found every year in waterfowl.
The subtype responsible for the outbreak that began in 2021 is highly pathogenic, and thus is of heightened concern.
I found this part interesting:
Data from a 2022–23, DU-funded study of waterfowl hunting dogs in Washington state found evidence of HPAI antibodies in only 2% of sampled dogs. As of September 2024, there has been only 1 confirmed case of a domestic dog dying from HPAI infection in North America
because dogs eat raw meat.
the real danger is to the Poultry industry:
Domestic poultry have no natural immunity to HPAI, and so experience nearly 100% mortality when infected. High concentrations of domestic birds facilitate transmission throughout poultry barns. These vulnerabilities mean that HPAI can have devastating economic consequences to the poultry industry and protein supply chain.
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they actually were doing gain of function research on bird flu ten years ago:
In a controversial study published 2 years ago Dutch scientists described a lab-modified strain of H5N1 influenza virus that was capable of airborne transmission among ferrets. Now the same researchers say they have identified five specific mutations that gave the virus this ability, a claim that is renewing debate about the risks of conducting and publishing such experiments.
Writing in Cell, the scientists said they identified two combinations of five mutations that affected specific characteristics of the virus and collectively enabled it to spread by air. They assert that the findings will help in the effort to detect early warning signs of flu strains that could cause a pandemic.
But other experts question the scientific value of the findings and argue that they are not worth the risks involved in conducting such experiments and publishing the full details. They assert that the research poses a risk of either accidental or intentional release of dangerous viruses.
World View
Published: 27 March 2013
H5N1 viral-engineering dangers will not go away
Simon Wain-Hobson
Governments, funders and regulatory authorities must urgently address the risks posed by gain-of-function research, says Simon Wain-Hobson.
Barely two months after a small group of influenza virologists lifted a moratorium on work to make the H5N1 avian flu virus as transmissible between humans as seasonal flu, researchers are at it again. Earlier this month, a Dutch scientist proposed similar experiments with other avian flu viruses, as well as the SARS coronavirus. And a fortnight ago, scientists in Germany and Switzerland reported how they had tweaked canine distemper virus to make it grow in human cells.
The logic behind these kinds of experiments, collectively called gain-of-function (GOF) research, is to identify combinations of mutations that could allow an animal virus to jump to unprepared humans. By knowing the mutations, the thinking goes, we can better prepare and marshal our scientific defences against a possible threat.
GOF research on avian flu provoked heated controversy, much of it covered by this journal. That controversy did not go away with the lifting of the moratorium. On the contrary, it continues to fester. Officials in Washington DC are putting the finishing touches to new guidelines for the review, regulation and oversight of this kind of research. The chill winds that we can anticipate blowing from policy-makers as a result could affect all of us who research viruses and their pathology. To avoid this, researchers in this field need to learn lessons from the past.
Rather than use the avian flu moratorium to seek advice, listen and foster debate, many influenza scientists engaged in an academic exercise of self-justification. There was a single large open meeting, at the Royal Society in London, which engaged a wider audience, including bioethicists. The recent calling off of the moratorium by 40 flu researchers alone — not funders, governments or international bodies — says it all. The flu community simply hasn't understood that this is a hot-button issue that will not go away.
There are parallels here to my own field of HIV. In the early days of research, HIV scientists, buoyed by huge research monies, exuded hubris, promised a vaccine within two years, and all sorts of other things. The crunch came when they realized that they had to engage seriously with patient groups. The result is that HIV patients became the most faithful collaborators of HIV clinicians. It is too easy for scientists in a field to dismiss criticism and ideas from outside.
Here are the issues that must be openly addressed about GOF work with avian flu, the SARS coronavirus — or any other virus.
Influenza virologists are going down a blind alley and the powers that be are blindly letting them go down that alley.
First, is the virological basis for the work sound? The outcomes of the H5N1 experiments are dominated by the artificial-selection systems used. If aerosol-transmitted virus is systematically passaged from ferrets with severe respiratory distress, then the research teams will end up with a transmissible and highly virulent strain. Likewise, if animals with mild symptoms are chosen, a transmissible virus of low virulence would ultimately emerge. Whether nature will take any of these courses is unknown. Take dog breeding. Ruthless selection of alleles over a short period has produced phenomenal phenotypic variation — dachshunds, salukis, whippets and setters. Would nature have come up with the dachshund?
Second, infectious-disease researchers are fond of saying that microbes do not respect barriers. So who makes the rules and provides oversight? Barely a sound has emerged at the international level. The World Health Organization has held essentially closed-door meetings and has failed singularly to widen the debate.
Third, what if these groups generate a highly pathogenic and transmissible virus — which I suspect, within two years, they will? Then what? Should the virus be shared? Should research on this novel virus strain of catastrophic potential be highly restricted?
Fourth, what if there were a leak or a small outbreak? Crippling lawsuits would follow. Are the academic institutions sufficiently covered in terms of insurance? Are university regents or chancellors even aware of the power, and dangers, of the modern molecular biology going on in their labs? Again, not a word has emerged.
Fifth, the world has never been more densely populated. Is it appropriate for civilian scientists to make microbes more dangerous? Is creating a novel human virus antisocial? Was there a failure of duty on the part of funders and regulators? What is the ethical position on such work? Here there has been a start, but as yet there is no consensus.
The global ramifications of GOF research have simply not been sufficiently explored and discussed. Influenza virologists are going down a blind alley and the powers that be are blindly letting them go down that alley, which is tantamount to acquiescing. So let's be clear: the end game could be viruses more dangerous than the Spanish flu strain.
H5N1 GOF work — indeed all virological GOF work — should be suspended until virologists open up and engage in public discussion of their work and the issues it raises. Given that the flu community failed utterly to use the year-long hiatus to good effect, it is clear that an independent risk–benefit assessment of GOF work is needed.
A moratorium on research that modifies the potential virulence of avian influenza virus has now been lifted. Credit: JAMES CAVALLINI/SPL
An international group of scientists this week ended a year-long moratorium on controversial work to engineer potentially deadly strains of the H5N1 avian flu virus in the lab.
Researchers agreed to temporarily halt the work in January 2012, after a fierce row erupted over whether it was safe to publish two papers reporting that the introduction of a handful of mutations enabled the H5N1 virus to spread efficiently between ferrets, a model of flu in mammals (see Naturehttp://doi.org/fxv55r;2012). Both papers were eventually published, one in Nature1 and one in Science2.
Now, in a letter simultaneously published on 23 January by Nature3 and Science, the 40 scientists involved say that the moratorium has served its purpose: allowing time for authorities to review the conditions under which the research could be safely conducted and for scientists to explain the public-health benefits of the work. Scientists who now have official approval in their countries to conduct such research “have a public-health responsibility to resume this important work”, the letter states, “because the risk exists in nature that an H5N1 virus capable of transmission in mammals may emerge”.
The move follows a large international workshop convened 17–18 December by the US National Institutes of Health in Bethesda, Maryland, to discuss ‘gain-of-function research’ — that intended to increase the transmissibility, host range or virulence — in H5N1 viruses, and the development of US rules for stricter oversight of research in this area. The proposed rules require an assessment of, for example, whether the scientific aims of such studies could be addressed using alternative, less-risky approaches, and whether biosafety and biosecurity risks can be adequately mitigated. They are expected to enter into force soon, allowing scientists working in the United States or on US-funded grants to restart such research.
there is a danger that in nature, mutations will allow person to person transmission. So they plan to do experiments in how to make the virus transmissiable from person to person so that they will be prepared for when this happens. Except of course the mutations they make in the lab might not be the same mutations that evolve spontaneously (influenza mutates quickly which is why Flu vaccine doesn't always work).
But the scientific community remains divided on whether the practical benefits of the research outweigh the risks of an accidental or deliberate release of a lab-created flu strain. Ian Lipkin, a specialist on emerging infectious diseases at Columbia University in New York, believes that the risks are high and, worse, that such research may end up being done in labs with insufficient biosafety standards.
The debate has drawn attention to, and exposed gaps in, the rules that govern ‘dual-use’ research — work that can bring public benefit but might also be used for harmful purposes.
translation: The gain of function research will help make vaccines in case of a mutation, but can also be used to engineer germ warfare.
The United States is the main funder of such research, and what it decides is key to international thought. The proposed framework for assessing H5N1 gain-of-function research, outlined by the US National Institutes of Health at an international meeting in Bethesda, Maryland, in December, spells out several criteria that such research would need to meet before being funded.
One can quibble with some ambiguities in the wording of those proposals, but overall the framework should serve as an important checklist. The criteria include sensible questions, such as whether safer, alternative approaches exist that could address the same scientific points
Wikipedia list of germ releases from labs: Probably not complete of course. Note that one Chinese lab release of Brucellosis infected 10 thousand people. That release was from a lab making a vaccine.
there are plenty of other lab leaks and not all get publicity.
In 1977, the H1N1 virus was thought to have leaked from a Chinese laboratory.18 During the first outbreak of SARS in 2004, two accidental releases from a Beijing laboratory were reported to have occurred. In 1979, anthrax spores were released accidentally from a Soviet research facility near Sverdlovsk, Russia. These events provide some background for accidental-release theories for SARS-CoV-2. As reported in Nature Medicine, had there been genetic manipulation, it would have been done with a reverse-genetic system used for betacoronaviruses.
and the author lauds the WUHAN lab for knowing the viral sequence so they could make the vaccine faster.
Ironically, vaccine development received a head start from the same laboratory studying coronaviruses in Wuhan that was suspected of leaking the virus. This laboratory had already sequenced the viral genome and shared its code, thus eliminating months of standard vaccine research
If that was true, then how did they find the viral sequence to make the vaccine so fast? Anyone? Anyone?
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this is all about gain of function experiments to protect people and the danger of a lab accident.
But what if someone leaks it deliberately? What stops most countries from doing this is blowback: it will return and kill their own people unless you stop person to person spread (e.g. anthrax is a good weapon because it doesn't spread beyond the initial release).
oh by the way: Remember all that fuss about Iraqi WMD that propaganda first said they had, then the MSM and powers that be said never existed? Well, Israel just bombed a bunch of WMD in Syria, reminding one of those satellite reports of trucks taking stuff to Syria shortly before the US invasion...apparently these sites only had missiles and chemical weapons, but as the CNN article shows, the bombings were highlighted in a way making one think it was just Israel being wicked and bombing stuff to be mean, with paragraph two mentioning strategic weapon sites: You don't know this means WMD until you read to paragraph six that mentions chemical weapons. But it is not about biological weapons.
Very little open source information exists to characterize Syria’s interest and potential activities in biological warfare (BW). Official U.S. government assessments note that Syria’s infrastructure could support the production of biological agents, but make no definitive comment on whether or not a program actually exists. ...
it did mention that dual function use (the lab that uses a germ to make a vaccine also makes the germ as a weapon).
Instead, discussions on this topic have focused on speculative extrapolations of Syrian dual-capable industry and on Syrian political motivations. Such analysis can be neither detailed nor comprehensive. Although the existence of a biotechnology industrial base would suggest that Syria has some indigenous expertise useful for developing a biological weapons capability, it does not imply and cannot confirm the existence of an offensive biological weapons program. Furthermore, from the Syrian perspective, the tactical utility of deploying biological weapons is questionable given that their use against its foremost security concerns, whether foreign or domestic, poses a significant risk of “blowback.”
translation: they probably could make biological weapons but could kill their own people if the disease spread person to person and Assad wouldn't risk that. Uh Isis might, but that's another worry for another time.
explains why Covid was not a biological weapon: it spread too slowly and only killed high risk people, not military age men. And the vaccines did stop the spread (the death rate went down with giving it out: you can argue repeated shots were not needed but initially it did slow the epidemic).And it notes a lot of the conspiracy theories against the US biolabs are China and Russia propaganda trying to divert attention to the more probably lab leak theory from Wuhan and the dirty little secret that both countries have active bioweapon programs.
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So is the hysteria about bird flu just the same ones who shut down the world economy for covid for two years instead of two months, which might have been warranted?
And are the gaslighting articles such as the one I quote at the start of this long essay a way to persuade the public (and Trumpieboy's RFK JR) to let them do this risky research?
Or is the reason twofold: One, allow gain of function research and two: let the WHO treaty that allows them the power to order countries how to response to the next epidemic be passed?
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the fear is that bird flu mixed with either human or pig flu was behind the 1918 epidemic of influenza.
But that epidemic hit a civilian population suffering from malnutrition from World War I (blockades and collapse of the food distribution system especially in Eastern Europe). and in soldiers poorly ventillated barracks.
Van Wijhe et al. (6) returned to the question of the origins of the 1918 virus by exploring the epidemiologic imprint of the 1918 virus on Danish mortality records, echoing recent work on immune imprinting (18–20). They identified several age breakpoints in pandemic mortality that were suggestive of the cycling of different influenza strains between the mid-19th century and the 1918 pandemic. Most notably, they argued for co-circulation of 2 subtypes of influenza virus (carrying type I and II hemagglutinin surface antigens) between 1873 and 1908. As a result, persons born between 1873 and 1908 (aged 10–45 years during the 1918 pandemic) may have been primed by either hemagglutinin type, potentially explaining the intriguing age profile of pandemic mortality in adults.
