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How could Spike Protein Accelerate Brain Threat?

A study revealed that fragments of the SARS-CoV-2 virus remain in the brain’s protective layers, including the skull’s marrow, for up to four years after infection.

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How could Spike Protein Accelerate Brain Threat? | Credits: Shutterstock

SARS-CoV-2, the notorious pathogen responsible for the global COVID-19 upheaval, persists within the cranial cavity and its protective layers for years following initial infection, leaving indelible imprints on cerebral health. A groundbreaking investigation spearheaded by Helmholtz Munich in collaboration with Ludwig-Maximilians-Universität (LMU) reveals that fragments of the virus, specifically its spike protein, linger in the skull’s marrow and the meninges—a vital brain barrier—for an alarming duration of up to four years.

The study uncovers the spike protein’s role as an inflammatory instigator, perpetuating chronic neuroinflammation that elevates the likelihood of neurodegenerative diseases. According to Prof. Ali Ertürk, the eminent director of the Institute for Intelligent Biotechnologies at Helmholtz Munich, these lingering effects hasten cerebral aging, effectively curtailing five to ten years of healthy cognitive functionality in affected individuals according to reports.

Published in the esteemed journal Cell Host & Microbe, this investigation sheds light on neurological anomalies linked to long Covid, including persistent headaches, disrupted sleep cycles, and cognitive impairment often referred to as “brain fog.” Alarmingly, an estimated 5–10 percent of those who contract COVID-19—translating to roughly 400 million individuals globally—might harbor substantial quantities of this spike protein.

Vaccination’s Mitigating Role: A Partial Solution

The researchers emphasize that vaccination markedly diminishes the deposition of spike proteins within the brain, underscoring its pivotal role in curbing long-term consequences. However, even with immunization, the reduction in spike protein retention reached only about 50 percent in murine models, leaving a residual presence that continues to pose a toxic threat to neural integrity.

Advanced Imaging Breakthroughs Reveal Hidden Spike Protein Reservoirs

Visual Representation | Credits: Shutterstock

To decipher the enigmatic mechanisms underpinning these neurological impacts, the research team developed a pioneering AI-enhanced imaging methodology. This cutting-edge technique, offering intricate three-dimensional renderings of viral protein distribution, uncovered previously undetected spike protein reservoirs in both post-mortem human tissue and animal models, as per reports.

Their findings illuminate an unsettling reality: elevated spike protein concentrations persist in the skull’s bone marrow and meninges, even years after the acute phase of infection subsides. The viral spike protein’s affinity for ACE2 receptors—particularly abundant in these regions—further elucidates its enduring presence and its detrimental neurotoxic influence.

This landmark study underscores the necessity of continued vigilance in understanding and mitigating the protracted neurological sequelae of SARS-CoV-2, advocating for ongoing innovation in diagnostic and therapeutic strategies.

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Chronic Fatigue and Long COVID: What Aren’t We Being Told?

Myalgic encephalomyelitis has gained renewed attention as many long COVID patients exhibit similar symptoms or receive ME/CFS diagnoses.

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Chronic Fatigue and Long COVID: What Aren’t We Being Told?

In contemporary society, lamenting exhaustion has become almost ritualistic. Yet, for a subset of individuals, profound fatigue is merely one harrowing symptom of a malady whose prominence surged in the shadow of the COVID-19 pandemic.

This disease, known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), profoundly disrupts daily existence. While ME/CFS is not a novel disorder, its emergence in the aftermath of COVID-19 infections—often under the umbrella of long COVID—has shed light on its debilitating nature. Long COVID describes lingering symptoms persisting for months, if not years, post-infection, according to salon.com.

A significant proportion of long COVID sufferers exhibit symptoms mirroring those of ME/CFS or receive formal diagnoses of the condition. However, akin to the enigmatic character of long COVID, ME/CFS remains an enigma in medical research. This perplexity is compounded by the disease’s longstanding neglect within scientific circles—a neglect attributed to biases both societal and systemic. Historically, the condition has been marginalized, partly due to its predominance among women and its misleading association with unrelenting fatigue—a symptom that belies the illness’s multifaceted complexity.

Misconceptions and Misnomers

The nomenclature “chronic fatigue syndrome” trivializes the reality of the condition. “Chronic fatigue” inadequately encapsulates the lived experience of sufferers, diminishing the gravity of their struggles, as elucidated by Professor Chris Ponting of the University of Edinburgh. Co-leader of the DecodeME study—the world’s most extensive ME/CFS research initiative—Ponting emphasizes the disease’s gendered prevalence. “The majority of those afflicted are women, with a ratio of five to one when compared to men,” he explained. “Moreover, ME/CFS is more likely to strike individuals of advanced age,” as per salon.com.

According to the Centers for Disease Control and Prevention (CDC), ME/CFS severely impairs both physical and cognitive function. Patients endure incapacitating exhaustion, cognitive fog, and an inability to perform basic tasks, such as bathing or preparing meals. There is neither a definitive cure nor a standardized diagnostic protocol for the condition.

Systemic Neglect and Societal Oversight

Ponting highlights a troubling disconnect between policymakers—often young, healthy males—and the predominantly older female demographic afflicted by ME/CFS. This dissonance perpetuates ignorance about the disease’s devastating impact despite its prevalence, affecting approximately one in every 200 people.

A particularly confounding aspect of ME/CFS lies in its counterintuitive relationship with physical activity. Unlike the conventional wisdom extolling exercise as universally beneficial, exertion can exacerbate symptoms for ME/CFS patients. This phenomenon, known as post-exertional disease, undermines health, diminishes quality of life, and further restricts mobility, according to salon.com.

The Search for Answers

The precise biological mechanisms underpinning ME/CFS remain elusive. The prevailing hypothesis suggests an interplay between immune dysfunction and genetic predisposition, often triggered by viral infections. Ponting noted, “Many patients develop the condition following an illness, which may indicate mitochondrial dysfunction—the cellular ‘batteries’ may be compromised.”

DecodeME, an ambitious genetic study, seeks to unravel these mysteries by examining DNA variations among ME/CFS sufferers. Researchers hope such insights will illuminate the disease’s roots and guide future investigations.

Personal Accounts and Coping Strategies

Dr. Charles Shepherd, a UK-based medical advisor to the ME Association, recounts his journey with ME/CFS following a severe bout of chickenpox. Despite being a physician, Shepherd was mystified by his persistent symptoms, which included profound exhaustion and post-exertional malaise. His struggle to obtain a diagnosis, spanning two years, underscores the medical community’s limited understanding of the disorder, as claimed by salon.com.

Shepherd describes his experience as paradoxically fortunate, as he has managed to mitigate symptoms through energy pacing—a strategy involving meticulous management of physical and mental exertion. While this approach offers some relief, the prognosis remains grim; fewer than 10 percent of patients achieve full recovery.

Looking Ahead

Ponting remains cautiously optimistic about the potential breakthroughs emerging from the DecodeME initiative. “Our research will illuminate the path forward, identifying avenues for further study,” he stated. “However, the development of effective treatments remains a distant prospect.”

For the countless individuals grappling with ME/CFS, the quest for answers continues—a testament to resilience amidst adversity. Through rigorous research and heightened awareness, hope endures that this debilitating condition will one day be met with understanding, compassion, and, ultimately, effective remedies.

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The H5N1 Virus Is Now More Dangerous Than Ever – Know More!

H5N1 virus requires only a single genetic mutation to bind effectively to human respiratory cells, potentially enabling human-to-human transmission.

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The H5N1 Virus Is Now More Dangerous Than Ever – Know More!

United States: Researchers have uncovered a disconcerting revelation about the H5N1 strain of avian influenza currently afflicting US dairy herds. The virus requires only one genetic adjustment to effectively bind to human upper respiratory cells. This pivotal discovery, unveiled in Science, delineates a streamlined pathway for the virus to enhance human transmissibility, heightening the specter of a potential pandemic if such a mutation proliferates in the wild. 

Avian flu viruses rely on surface proteins to adhere to specific cell receptors, enabling cellular infiltration. While bird and human receptors differ, this disparity is nuanced, according to James Paulson, a co-author of the study and biochemist at Scripps Research. “For H5N1 to spark a human pandemic, it must alter its receptor specificity from avian to human,” he explained. Remarkably, researchers found that this transformation demands only a solitary mutation, according to scientificamerican.com.

The H5N1 clade fueling the current outbreak first emerged in North America in 2021, affecting a spectrum of species, from wild birds and marine mammals to terrestrial animals like bears and foxes. Its recent leap to dairy cows has intensified scrutiny. 

Though human infections linked to these outbreaks remain infrequent and predominantly mild, they occur chiefly among individuals with high exposure, such as farm workers. Crucially, the virus has yet to display the ability to spread between humans—a barrier rooted in its receptor-binding preferences. 

Jenna Guthmiller, an immunologist at the University of Colorado Anschutz Medical Campus, who was not part of the research, noted, “If the virus enhances its affinity for human receptors, it could pave the way for human-to-human transmission, which poses significant risks.” 

The study focused on hemagglutinin, a surface protein integral to the virus’s ability to attach to host cell receptors and initiate infection. Employing genetic sequences from a Texas case is remarkably subtle, according to James Paulson, a biochemist at Scripps Research and co-author of the study. “For a new pandemic H5N1 virus, we know it has to switch receptor specificity from avian-type to human-type. So what will it take?” Paulson and his team found that this transition required just a single mutation, a surprising and troubling finding, as per scientificamerican.com.

The Mutation at Position 226

The researchers focused on hemagglutinin, a surface protein of H5N1 that facilitates receptor binding. By introducing mutations into the genetic sequence of hemagglutinin, they identified a single change at the 226th amino acid that enabled the virus to switch its binding preference from bird receptors to human upper respiratory tract receptors.

Previous pandemics, such as the 1918 and 2009 influenza outbreaks, typically required multiple mutations for this adaptation. The H5N1 virus could achieve this shift with a single mutation, which signals its potential for rapid evolution, according to Ian Wilson, a structural biologist at Scripps.

Implications for Human Transmission

H5N1 has been circulating in North America since 2021, impacting a wide range of animal species and recently emerging in US dairy herds. While human cases remain rare and primarily linked to direct contact with infected animals, this mutation could increase the risk of human-to-human transmission. Jenna Guthmiller, an immunologist at the University of Colorado, warned, “The better the virus becomes at binding to human receptors, the more likely it is to spread between people,” according to scientificamerican.com.

Viruses that bind more effectively to the upper respiratory tract, such as this mutated H5N1, can spread more easily through coughing or sneezing, posing a greater public health risk. However, receptor binding is just one piece of the puzzle. The virus must also replicate efficiently in human cells to become truly transmissible.

Lessons from a Recent Case

The study’s findings resonate with recent events. In Canada, a teenager hospitalized with severe bird flu symptoms was infected with an H5N1 strain carrying two mutations, including one at position 226. While it’s unclear if these mutations directly contributed to the severity of the illness, they underscore the virus’s potential to adapt to human hosts.

Preparing for a Pandemic Threat

While the current risk of widespread H5N1 transmission remains low, the study highlights critical areas for surveillance and research. By identifying key mutations, scientists can better monitor the virus’s evolution and anticipate its pandemic potential, according to scientificamerican.com.

As Paulson cautioned, “The magic that we hope doesn’t happen is that all the right factors come together to enable the first human-to-human transmission. That’s when we face the risk of a pandemic.”

This research serves as a call to remain vigilant, ensuring preparedness in the face of an ever-evolving threat.

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BEWARE: Walking Pneumonia Is Striking Younger Population Harder

Colorado has seen a significant rise in walking pneumonia cases this autumn, particularly among younger children aged 2 to 4, a group usually less affected by the illness.

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BEWARE: Walking Pneumonia Is Striking Younger Population Harder

United States: Colorado has witnessed a notable upswing in walking pneumonia cases this autumn, with an unexpected rise among very young children who are typically less vulnerable to this ailment, as health authorities have reported. 

The bacterial culprit responsible for this mild lung infection, Mycoplasma pneumoniae, reemerged across the nation for the first time since the onset of the pandemic. Cases reached their zenith in August following a significant escalation in spring, per the Centers for Disease Control and Prevention (CDC), as per denverpost.com.

In Colorado, the apex of cases materialized slightly later, around September. However, Dr. Kevin Messacar, an infectious disease expert at Children’s Hospital Colorado, cautions that the illness is poised to persist at elevated levels well into the forthcoming year. 

“Presently, we’re observing an exponential increase compared to usual figures,” Messacar elaborated. 

Younger Children Hit Harder Than Usual 

Surprisingly, clinicians are encountering infections more frequently in children aged 2 to 4, a demographic traditionally less impacted by walking pneumonia, which typically afflicts school-aged kids. 

Visual Representation

Walking pneumonia spreads insidiously through respiratory droplets expelled during sneezing or coughing. Unlike more aggressive illnesses such as influenza, its transmission is gradual, sometimes taking weeks to traverse an entire household, according to Dr. Messacar. 

Prevention and Symptoms 

Proper hygiene practices, like thorough handwashing and shielding one’s mouth and nose during coughs or sneezes, are effective measures to curtail the bacteria’s spread, as advised by the CDC, according to denverpost.com.

Although walking pneumonia is generally less severe than other forms of pneumonia, its symptoms include fever, chills, sore throat, and skin rashes. The defining characteristic is a persistent, bothersome cough that lingers in the lungs for as long as four weeks, Dr. Messacar noted. 

The term “walking pneumonia” arises from its relatively mild nature, allowing those afflicted to carry on with their routines instead of remaining bedridden. Nonetheless, severe cases may necessitate hospitalization, Messacar added. 

Limited Data on Case Numbers 

While the prevalence of walking pneumonia in Colorado remains uncertain due to infrequent testing, isolated instances such as the recent hospitalization of a 3-year-old child have been reported, according to CBS Colorado. 

Although the Colorado Department of Public Health and Environment has not recorded any specific outbreaks, there has been a discernible increase in emergency department visits for such infections, stated spokesperson Kayla Glad. 

A Cyclical Pattern 

Nationally, the CDC estimates that walking pneumonia affects 2 million individuals annually. Historically, outbreaks tend to occur in cycles ranging from three to seven years. However, the pandemic disrupted this pattern, with cases plummeting as people adhered to masking and social distancing protocols. Unlike the flu or respiratory syncytial virus (RSV), walking pneumonia only resurfaced in 2023, Messacar explained, according to denverpost.com.

Visual Representation

Infections among children aged 2 to 4 have shown a striking rise, climbing from 1 percent of all cases in late March to 7.2 percent by early October, which deviates from established norms. The CDC notes that Mycoplasma pneumoniae rarely leads to pneumonia in very young children. 

“I don’t believe we fully understand why this is happening,” Messacar admitted, proposing that the extended absence of outbreaks may have increased susceptibility within the population due to diminished immunity, as reported by denverpost.com.

“This phenomenon mirrors what we observed with RSV and influenza,” he concluded, referencing their dramatic resurgence following suppression during the pandemic’s early stages.

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