Archive for the ‘research’ Category

Tackling Long-Haul Diseases

https://www.technologyreview.com/2024/02/28/1087617/tackling-long-haul-diseases/

Tackling long-haul diseases

Long-haul covid and chronic Lyme disease are surprisingly similar. MIT immunoengineer Mikki Tal is on the case.
February 28, 2024

MIT immunoengineer Michal “Mikki” Tal remembers the exact moment she had an insight that would change the trajectory of her research, getting her hooked on studying a long-neglected disease that leaves millions of Americans suffering without treatment.

It was 2017, and she was a Stanford postdoc exploring connections between her immune regulation research and immuno-oncology, which harnesses the body’s immune system to combat cancer. Her work focused on how healthy cells broadcast “Don’t eat me” messages while cells that are cancerous or infected with a pathogen send self-sacrificing “Eat me” messages. Immune cells, in turn, receive these missives in pocket-like receptors. The receptor that receives the healthy cells’ signal, Tal read as she was poring over the literature that day, is the third most diverse protein in the human population, meaning that it varies a lot from one person to the next. It was a fact that struck her as “very odd.”

Tal, who has been obsessed with infectious disease since losing an uncle to HIV/AIDS and a cousin to meningococcal meningitis, wondered what this striking diversity could reveal about our immune response to infection. According to one hypothesis, the wide array of these receptors is the result of an evolutionary arms race between disease-causing microbes and the immune system. Think of the receptor as a lock, and the “Nothing to see here” message as a key. Pathogens might evolve to produce their own chemical mimics of this key, effectively hiding from the immune system in plain sight. In response, the human population has developed a wide range of locks to frustrate any given impostor key.

Wanting to test this hypothesis, Tal found herself walking the halls of Stanford, asking colleagues, “Who’s got a cool bug?” Someone gave her Borrelia burgdorferi, the bacterium that causes Lyme disease. Previous research from Tal’s collaborator Jenifer Coburn, a microbiologist now at the Medical College of Wisconsin, had established that Lyme bacteria sport a special protein crucial for establishing a lasting infection. Knock this protein out, and the immune system swiftly overwhelms the bugs. The big question, however, was what made this protein so essential. So Tal used what’s known as a high-affinity probe as bait—and caught the Borrelia’s mimic of our “Don’t eat me” signal binding to it. In other words, she confirmed that the bacteria’s sneaky protein was, as predicted, a close match for a healthy cell’s signal.  (See link for article)

“Long covid looks exactly, and I mean exactly, like chronic Lyme.” ~ Michal “Mikki” Tal, MIT immunoengineer

_______________

**Comment**

Yet, despite knowing of this ‘sneaky protein’ that establishes a lasting infection, ‘the powers that be’ deny chronic/persistent illness with Lyme/MSIDS.

 While the article factually states there’s no objective way to diagnose chronic Lyme and no medically ‘accepted’ therapy, it regurgitates the ‘same o, same o’ myth that only 10% suffer chronic symptoms.
It also correctly points out that short-term doxycycline, the widely ‘accepted’ treatment for Lyme, only prevents the bacteria from replicating which relies upon the immune system to kill off invaders which often doesn’t work due to the fact Lyme effectively gives patients immune system dysfunction – rendering it virtually useless. The article states that lengthy antibiotics can “ease” symptoms.  I would disagree with this.  For a subset of patients, it makes them completely well.
Predictably coinfection involvement is entirely missing from the conversation.
The author is far more into gender differences, which is the buzz word of the day, matters little, and won’t matter a tittle in helping patients get better.  This ‘flavor of the day’ approach to research is the new norm and is unfortunately now required to get coveted government grants.  All researchers know this little factoid, but the public remains in the dark.
Complaint aside, I did find the mouse experiment extremely interesting as it showed how Lyme ‘completely disfigured’ the uterus, which would explain why so many infected women have difficulties with pregnancies.  Only ONE other study in the history of Lyme documented uterine infection.
This does show the extremely limited and biased approach to all things Lyme/MSIDS and it always amazes me that researchers literally have to stumble into this knowledge.
Blaming men is not the answer regarding the problems in research. The problem stems from conflicts of interest and corruptionwith females just as culpable as males.
While gender differences might be interesting, even illuminating, there are far bigger fish to fry in the Lyme/MSIDS kitchen.
The article then switches gears into Long COVID, a contested term that has yet to be proven conclusively, yet accepted at face value by many.  The first thing that crosses my mind when I hear that “Long COVID” and Lyme have identical symptoms is, who’s to say it isn’t Lyme?  
Testing for both diseases is abysmal, and seriously comical if lives weren’t at stake.  Yet, testing by ‘the powers that be’ simply is and continues to be accepted and utilized.
The article then gives the hypothesis dichotomy:
  1. persistent pathogens drive ongoing symptoms
  2. the immune system remains in a faulty state – driving symptoms

Tal’s project uses AI which she hopes will allow her to predict who will go on to have persistent symptoms.  She has already learned that current Lyme tests only look at IgG and IgM – not IgE, which she describes as an immune system ‘air strike’ and that those with this type of immune reaction have been ignored in research.  She received $2 million to further test this hypothesis and she expects to publish findings as early as 2025.

And hold the press! – Tal states that at a conference the keynote speaker actually apologized for what he had written in the past about chronic Lyme after he got ‘Long COVID.’

Sadly, right after this, the article predictably blames ‘climate change’ for pushing ticks into new habitats – a notion refuted by independent research, as well as more and more climate scientists, and more and more data proving there is no ‘climate emergency,’ but how the media is using corrupt data to push a narrative pushed by the UN which is bankrolling politics under a ‘climate change’ narrative.  ‘Climate change’ is big, big business, and part of a much larger agenda which utilizes science and technology for ultimate control.

For more:

Long COVID Or Not Long COVID, That is the Question

Hopefully the inaccurate term ‘long covid’ will disappear just like the inaccurately deceptive term PTLDS will disappear.

After the link between the clot shots and ‘long covid’ has been finally gaining some acceptance, American virologist Dr. Robert R. Redfield, who served as the director of the CDC during the ‘pandemic,’ has admitted that reports of ‘so-called Long Covid’ are actually a cover-up for global surges of “mRNA vaccine injury.”

The evidence continues to mount showing the experimental gene therapy injections are maiming and killing people.

Another recent study admonishes against using the term Long COVID as the symptoms are no worse than those after the flu. In fact, PCR testing can’t distinguish between COVID and the flu. So, what in fact is causing lingering symptoms in some people and how severe are they actually?  That is the important question.

The following information is at the heart of the “persistence” war.  A few points:
Corrupt ‘public health’ has been effectively playing us.  While fragments of viral RNA are uniformly blamed for lingering symptoms, those with chronic Lyme/MSIDS are kicked to the curb.

https://www.lymedisease.org/covid-virus-can-stay-in-body/

COVID virus can stay in the body more than a year after infection

3/10/24

The COVID-19 virus can persist in the blood and tissue of patients for more than a year after the acute phase of the illness has ended, according to new research from University of California, San Francisco that offers potential clues to why some people develop long COVID.

The scientists found pieces of SARS-CoV-2, referred to as COVID antigens, lingering in the blood up to 14 months after infection and for more than two years in tissue samples from people who had COVID.

“These two studies provide some of the strongest evidence so far that COVID antigens can persist in some people, even though we think they have normal immune responses,” said Michael Peluso, MD, an infectious disease researcher in the UCSF School of Medicine, who led both studies.

The findings were presented at the Conference on Retroviruses and Opportunistic Infections, held recently in Denver.

Evidence of long-term infection

Early in the pandemic, COVID-19 was thought to be a transient illness. But a growing number of patients, even those who had previously been healthy, continued having symptoms, such as, brain fog, digestive problems and vascular issues, for months or even years.

The researchers looked at blood samples from 171 people who had been infected with COVID. Using an ultra-sensitive test for the COVID “spike” protein, which helps the virus break into human cells, the scientists found the virus was still present up to 14 months later in some people.

Among those who were hospitalized for COVID, the likelihood of detecting the COVID antigens was about twice as high as it was for those who were not. It was also higher for those who reported being sicker, but were not hospitalized.

“As a clinician, these associations convince me that we are on to something, because it makes sense that someone who had been sicker with COVID would have more antigen that can stick around,” Peluso said.

Virus persists up to two years in tissue 

Since the virus is believed to persist in the tissue reservoirs, the scientists turned to UCSF’s Long COVID Tissue Bank, which contains samples donated by patients with and without long COVID.

They detected portions of viral RNA for up to two years after infection, although there was no evidence that the person had become reinfected. They found it in the connective tissue where immune cells are located, suggesting that the viral fragments were causing the immune system to attack. In some of the samples, the researchers found that the virus could be active.

Peluso said more research is needed to determine whether the persistence of these fragments drives long COVID and such associated risks as heart attack and stroke.

But, based on these findings, Peluso’s team at UCSF is involved in multiple clinical trials that are testing whether monoclonal antibodies or antiviral drugs can remove the virus and improve the health of people with long COVID.

“There is a lot more work to be done, but I feel like we are making progress in really understanding the long-term consequences of this infection,” Peluso said.

SOURCE: University of California, San Francisco

Long-COVID Symptoms Mirror Those in Other Viral Illnesses, Study Shows

https://www.theguardian.com/society/2024/mar/15/long-covid-symptoms-flu-cold

Time to stop using term ‘long Covid’ as symptoms are no worse than those after flu, study finds

Researchers compared the symptoms and impairment of Covid and influenza patients a year after they tested positive

Long Covid may be no different from other post-viral syndromes such as those experienced after flu, according to new research from Queensland Health.

The lead author of the study, the state’s chief health officer Dr John Gerrard, said it was “time to stop using terms like ‘long Covid’” because they imply there is something unique about the longer-term symptoms associated with the virus, and in some cases create hypervigilance.

There are different definitions of long Covid but the World Health Organization defines post-Covid or long Covid as occurring in people still experiencing symptoms three months after their initial Covid-19 infection, when those symptoms can’t be explained by an alternative diagnosis. (See link for article)

Important quote:

Gerrard said long Covid may have appeared to be a distinct and severe illness because of the high number of people infected with Covid-19 within a short period of time, rather than the severity of long Covid symptoms.

_______________

**Comment**

The author states that the symptoms patients experience are real but that the incidence of these symptoms is no greater in COVID than it is with other respiratory viruses and that using the term ‘Long COVID’ is misleading and harmful.

He also admitted that the findings are associations and do not represent prevalence as well as the fact there was no laboratory pathophysiological assessment making it impossible to detect if this is indistinguishable from flu-related or any other post-viral syndrome.  But, it’s important to mention here that the PCR test used is utterly useless and can’t detect if a person has COVID or just the flu, and it can’t identify variants.

But to keep the COVID narrative alive and well he states that because 90% of people in Queensland are ‘vaccinated’ with the gene therapy when Omicron emerged, the lower severity of COVID could be due to ‘vaccination’ and the variant.

Research and reality; however, shows just the opposite.

There is actually increased risk of new variant infections which can be severe in the ‘vaccinated’ only, which has been recorded many, many times.

Can Lyme Disease Cause Speech Issues?

https://danielcameronmd.com/can-lyme-disease-cause-speech-issues/

CAN LYME DISEASE CAUSE SPEECH ISSUES?

Can-Lyme-cause-speech-issues

“Lyme can affect the nerves that are responsible for controlling the muscles in the vocal cords,” says Amesh A. Adalja, MD, an infectious disease specialist at Johns Hopkins Center for Health Security. “As a result, someone could technically lose their voice if they had Lyme disease.”

“Lyme disease has been associated with a wide variety of persistent neuropsychological and cognitive symptoms, including: impaired attention, focus, concentration, judgment, and impulse control,” in addition to impaired memory and speech functions, according to an article published by Amen Clinics.¹

Recent studies of patients with post-treatment Lyme disease syndrome (PTLDS) have found “consistent deficits in memory and processing speed,” according to the authors of a new study “Language Fluency Deficits in Post-treatment Lyme Disease Syndrome.”² But are language fluency deficits due to poor performance in these other neurocognitive areas?

The study by Gorlyn et al. evaluated 38 individuals with major depressive disorder (MDD), 59 healthy volunteers, and 31 individuals with Post-treatment Lyme disease Syndrome (PTLDS).

The major depressive disorder group “had a cumulative time since first episode of depression of 13.5 ± 10.9 years, with an average 3.8 ± 3.5 episodes of depression,” wrote Gorlyn et al.

The Post-treatment Lyme Disease Syndrome group “had a duration of illness of 7.7 ± 5.6 years of illness and had gone 13.0 ± 18.5 (median = 7.0) months before being formally diagnosed and treated for Lyme disease.”

Additionally, the PTLDS group “received an average of 2.3 ± 1.7 months of prior intravenous antibiotic treatment and 7.4 ± 9.8 (median = 3) months of prior oral antibiotic treatment.”

The study found that both the PTLDS and MDD groups had deficits in basic verbal abilities, memory, and processing speed.

“…language fluency deficits were evident in PTLDS patients even after controlling for the significant effects of verbal ability, slowed processing speed, and memory difficulties on fluency performance.”

The authors concluded, “Language fluency appears to be an independent area of neurocognitive deficit within the constellation of PTLDS symptoms.”

These deficits in language fluency could not be a function of depressed mood, basic verbal abilities, or other cognitive problems, the authors point out.

“These findings suggest that language problems are a distinct area of cognitive deficit in PTLDS, and not a function of depressed mood, basic verbal abilities, or other cognitive problems frequently observed in PTLDS.”

The findings support those from other studies. “A clearer picture of these patients’ neurocognitive difficulties has emerged incorporating mild slowing, disruptions of learning and information retrieval, and dysfunction in everyday language skills,” wrote the authors.

The study was not designed to determine if the language fluency deficits in Lyme disease were transient or a long-standing effect, although the PTLDS group had been ill for years despite antibiotic treatment. Nor was the study designed to determine the cause of the language fluency deficits in Lyme disease.

References:
  1. Amen Clinics. November 15, 2022. https://rb.gy/ac4geu
  2. Gorlyn M, Keilp JG, Fallon BA. Language Fluency Deficits in Post-treatment Lyme Disease Syndrome. Arch Clin Neuropsychol. Dec 22 2022;doi:10.1093/arclin/acac095

For more:

Lyme-Induced Cardiac Problems Persist Despite Antibiotic Treatment

https://danielcameronmd.com/lyme-cardiac-antibiotic-treatment/

LYME-INDUCED CARDIAC PROBLEMS PERSIST DESPITE ANTIBIOTIC TREATMENT

lyme-cardiac

In their article, “An Unusual Presentation of Lyme Carditis and Adenosine-Sensitive Atrioventricular Block,” Alexandre and colleagues present the case of a 20-year-old female with Lyme disease and cardiac manifestations, who continued to experience cardiac problems despite 4 weeks of antibiotic treatment. [1]

The young woman was admitted to the emergency department with acute pleuritic chest pain and shortness of breath. (Pleuritic chest pain is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling.)

The woman exhibited only mild tachycardia (100/min). However, “Considering the suspicion of acute myocarditis, the patient was admitted to an intensive cardiac care unit,” the authors state.

During hospitalization, cardiac monitoring revealed several asymptomatic episodes of paroxysmal AV block, including second-degree Mobitz I AV block, second degree AV block, and high-grade AV block.

Although there was no evidence of tick exposure or skin lesions, clinicians ordered testing for Lyme disease, which was positive by Western blot. “… an IgM Western-Blot test was performed, confirming positivity and recent Borrelia spp. infection.”

The patient was diagnosed with Lyme disease with cardiac manifestations of high-grade AV block. She was treated with a 4-week course of IV ceftriaxone, which led to a complete resolution of chest pain and shortness of breath.

However, the AV conduction disturbance continued after 4 weeks of antibiotic treatment. And subsequently, the woman was given an alternative diagnosis of extrinsic idiopathic paroxysmal AV block (“adenosine-sensitive AV block”).

This could be an extremely rare course of Lyme carditis, or the patient may have had asymptomatic AV conduction problems that surfaced when she developed Lyme disease, according to the authors.

“The patient was started on theophylline 400 mg twice daily, and after one week of treatment, the Holter monitoring demonstrated a significant reduction in AV conduction disturbances,” the authors state.

At her 18-month follow-up appointment, the woman continued to have fewer AV conduction disturbances, no cardiac complaints, and no need for a permanent pacemaker.

Authors conclude:

“This case illustrates a challenging scenario of [Lyme carditis] with high grade AV block, which persisted after appropriate antibiotic treatment and had key features supporting the diagnosis of extrinsic idiopathic paroxysmal AV block (‘adenosine sensitive AV block’).

References:
  1. Alexandre A, Ribeiro D, Sousa MJ, Reis H, Silveira J, Torres S. An Unusual Presentation of Lyme Carditis and Adenosine-Sensitive Atrioventricular Block. Arq Bras Cardiol. 2024 Jan;121(1):e20230228. Portuguese, English. doi: 10.36660/abc.20230228. PMID: 38324857.

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