Employers no longer need to pay for AIDS and HIV drugs
The fungal connection
Earlier this morning a piece of news made the rounds, achieving viral status rather quickly.
Employers will no longer have to provide employees with health plans that pay for certain preventive health-care services, including drugs to treat AIDS and HIV.
Obamacare Preventive Care Mandate Limited by Federal Judge (1)
Judge previously found task force not properly appointed
Employer, government disagreed on vacating recommendations
Employers throughout the country will no longer have to provide employees with health plans that pay in full for certain preventive health-care services, including drugs to treat AIDS and HIV.
Services affected include breast and cervical cancer screenings, diabetes screening, and vision tests for preschool-aged children.
A federal judge in Texas Thursday vacated actions taken by the US Health and Human Services Department to implement or enforce certain Affordable Care Act preventive services coverage requirements recommended by a task force that he determined wasn’t constitutionally appointed.
Because of people with debatable levels of intelligence and competence, and the grifters all around, the Spike-centric vaccines like mRNA and the adenovirus ones were all correlated with “VAIDS”, which is not a thing, when you don’t do the research, you wouldn’t know that there is more than one form of primary immune deficiency.
Yet this is important because drugs to treat AIDS and HIV are not merely drugs to treat AIDS and HIV, many drugs have multiple uses in many different diseases, and one of these is a “promising” treatment against many diseases. An anti-CD20 monoclonal antibody. Commercially known as Rituximab.
The list of treatments goes beyond the ones listed here, but the list of pathologies here is already quite intriguing ain’t it ? Many of these are often byproducts of the mRNA vaccine, this is where it gets intriguing. When you go through the literature on IgG4-Related Diseases and their possible treatments, among a few interesting therapeutics, among the most mentioned is… Rituximab.
When I first proposed our hypothesis (PAID - Paradoxical Acquired Immune Dysfunction), at the time I stated this immune state is pretty similar to CVID (Common Variable Immune Dysfunction), CVID is a primary immune deficiency which could be simplified as the opposite of AIDS. Its primary hallmark is dysfunctional CD8 cells. Once again, one of the treatments is Rituximab.
Health insurers, knowing that the demand for specific, patented, highly expensive treatments might skyrocket in the next few years, found a way to circumvent bearing the brunt of the costs. Similar decisions will be made with even more unique treatments.
Now with a better grasp of the complex dynamics interconnecting many of these immune states, I know it isn’t exactly that simplistic, and many other variables apply, metabolic health, microbiome, latent and chronic infections, and inflammatory status, a caleidoscope of pathways leading to these dysfunctional states. Or as I said a year ago, All roads lead to Rome.
Leading to the second, and more complex part of this substack. This news was making the rounds in certain circles, the more “scientific” ones.
Killer plant fungus Chondrostereum purpureum infects man in India in 'world-first case'
A killer plant fungus infected a human and caused flu-like symptoms in what researchers say is a world-first case.
Chondrostereum purpureum causes silver leaf disease in flora, most commonly in species of rose.
Spread by airborne spores, it is named such because it gradually turns leaves silver - and is often fatal.
It was not known to infect humans, but medics in India have reported what they believe is the first ever case.
The patient was a 61-year-old man who received treatment at Consultant Apollo Multispecialty Hospitals in Kolkata, having experienced symptoms including a cough, fatigue, difficulty swallowing and a hoarse voice for three months.
Unlike people deemed most at risk of fungal infections known to jump species, such as those with cancer, HIV, respiratory diseases, and organ transplants, the man had no history of any illnesses.
He was a plant mycologist, which included working with mushrooms and various plant fungi.
On Substack, I superficially touched on the subject of fungal infections, but you can go back 2 years in my tweet history and you will find me forecasting the (possible, most likely probably) mass increase number in fungal infections. Yet this one surprised me.
Species jump is really uncommon unless something is really “wrong” in the infected individual, most often than not they will have a level of immune depression or outright deficiency.
The reasons for the increase in fungal infections are many, in which all the different immune states I covered so far will influence the changes of a person developing a fungal infection, and the type of fungal infection too, and this is why the severity of infection or reaction plays such a heavy role in the long-term effects of this. Our physiology is a compensatory machine, and its goal is reaching balance, so when something tilts an important part of your cellular responses, the body will compensate, something heavily (an effect in regards to the Spike Protein which I named Homeostasis Weaponization). Another aspect is the common side-effect of immunomodulatory therapies, such as Rituximab is secondary fungal infections.
This isn’t unheard of, and a long-term trend, this 2021 paper COVID-19 Impairs Immune Response to Candida albicans , in 2022 this very good article was published.
High prevalence of fungal secondary infections among COVID-19 patients
Some commonly reported secondary fungal infections that are associated with an increased rate of mortality and morbidity include COVID-19-associated pulmonary aspergillosis (CAPA), mucormycosis (CAM), and invasive candidiasis. These infections are caused by pathogens belonging to Rhizopus, Aspergillus, and Candida species, respectively.
Many European, Chinese, and Australian studies have reported that the most commonly diagnosed fungal infection in COVID-19 patients is CAPA, followed by CAC and CAM. Aspergillus fumigatus was identified as the most commonly occurring causal organism.
CAPA patients receive voriconazole as the first line of AFT and amphotericin B as the second line of treatment. The total duration of AFTs was between two and 90 days.
CAC mostly prevailed among the Chinese population, with these patients predominantly treated with echinocandins, azoles, and amphotericin B. Candida albicans was found to be the causal organism of CAC, with the duration of antifungal treatment ranging from four to 21 days.
Fungal infections can also lead to sepsis, with invasive candidiasis, a fairly common invasive fungal infection being among the top ones in causes of sepsis and aiding mortality in many (critically ill) patients. Of course, as I usually do, I tend to attempt to connect with other topics I have written since almost 90% of my science post are one big (SARS-CoV-2) hypothesis.
Given the role of sepsis and endotoxin in regards to SARS-CoV-2 (and the Spike Protein, mRNA vaccines) there is a unspoken role between the complex effects of sepsis in the long-term immune function and response and progression to fungal infections.
And the unspoken aspect, and arguably as important (or even more) than the Endotoxin one. Galectin-3 in response to fungal infections. If, for whatever reason, your body is “forced” to produce large amounts of Galectin-3 in response to cellular signaling, infection, or damage, it will produce much less of it soon after in an attempt to reach equilibrium. (In case you missed it, here is my Galectin-3 substack, which is one of the very few I consider a “must read” and “must understand”.
Inhibition of Galectin-3 Impairs Antifungal Immune Response in Fungal Keratitis
Galectin-3 knockout deteriorated the condition for the inhibition of galectin-3 was benefecial for fungi to survive and thrive in corneal lesions.
Galectin-3 impacts Cryptococcus neoformans infection through direct antifungal effects
Gal-3-deficient mice are more susceptible to cryptococcosis than WT animals, as demonstrated by the higher fungal burden and lower animal survival.
The finding that Gal-3 has effects against P. brasiliensis together with previously reported effects against Cryptococcus neoformans suggests that molecule has a general antifungal role in innate defenses against fungal pathogens.
Galectin-3 plays an important role in protection against disseminated candidiasis
I already know the question or argument going inside the head of many, especially the medically or scientifically inclined, “Doesn’t a major part of your argument hinges on the upregulation and massive presence of Galectin-3 in many ?”.
Yes, it does, but again, the body will attempt to bring this imbalance into harmony, one way or another, and if all else doesn’t work, the body failsafe will be changing your inflammatory responses and creating autoantibodies. (The following substack is open about the shift towards IgG4 subclass in the mRNA vaccinated)
Identification of galectin-3 as an autoantigen in patients with IgG4-related disease
Anti-galectin-3 autoantibody responses were predominantly of the IgG4 isotype (28% of the IgG4-RD cohort, P = .0001) and IgE isotype (11% of the IgG4-RD cohort, P = .009). No significant responses were seen from the IgG1, IgG2, or IgG3 isotypes. IgG4 anti-galectin-3 autoantibodies correlated with increased plasma galectin-3 levels (P = .001), lymphadenopathy (P = .04), total IgG level increase (P = .05), and IgG4 level increase (P = .03).
Conclusion:
Affinity chromatography using patient-derived mAbs identifies relevant autoantigens in patients with IgG4-RD. IgG4 galectin-3 autoantibodies are present in a subset of patients with IgG4-RD and correlate with galectin-3 plasma levels. The marked increases in levels of circulating IgG4 and IgE observed clinically are, at least in part, caused by the development of IgG4- and IgE-specific autoantibody responses.
High Expression of Galectin-3 in Patients with IgG4-Related Disease: A Proteomic Approach
Do you care to guess which type of experimental treatment may be used to treat Galectin-3 antibodies in IgG4-Related Diseases ? Anti-CD20 treatment. This is why I am so invested in understanding Galectins, and the ways and therapeutics to modulate its response, because they play a very significant role in many pathologies, autoimmunity, and disease progression.
To be fair, there are other complex ways the viral infection affects your immune response towards certain fungal infections, which I will cover, but longer-term, at a large scale, the dynamics described above will play a larger role and a heavy hand in the evolution of many of these pathogens.
Grateful for the support of my subscribers, for people who use Kofi as a one-time thing, and for the subscribers who share what they like.
Oh John I wish I had the time to really get into all this microbiology . Like not just reading about a protein or pathway , but understanding it in context of a system better
Great article, thank you.
Let's hope no-one gets infected with Cordyceps and starts a global "The Last of Us" pandemic.