SARS-CoV-2, fungal infections and "Immune Amnesia"

Another way to cancer ?

I seldom refer to recent substacks, or for that matter to most substaks unless they are pertinent to the subject being discussed, but this recent substack bears quite a bit of weight, significant towards many of our current and future problems.

SARS-CoV-2, biofilms and co-evolution

SAR-CoV-2 borderline incestuous relationship with many pathogens is well-known, but SARS-CoV-2 (and the mRNA Spike Protein) effects and changes in fungal diseases are a light mystery, not a complete unknown but there are many unknowns in the road.

Defective antifungal immunity in patients with COVID-19

The relationship between viral infections and fungal co-infection has been observed for decades, respiratory viral infection can disrupt both the normal function of the immune system and damage the epithelial surfaces, creating favorable conditions for fungal infections, especially of the invasive, opportunistic type. Such is the case when someone suffers from Cytomegalovirus infection, or another respiratory infection when a virus and fungi, or bacteria for that matter infect a host at the same time, it is often referred to as a superinfection. Each specific chronic pathology has a particular opportunistic infection, people living with HIV often suffer from pneumonia, or long-term problems with many types of Candida, the dominant geographical fungi will also affect these invasive infections, such as mucormycosis in India.

One of the most known respiratory infections associated with Invasive Aspergillosis (IA) in ICU is Influenza, extensively researched to the point it was given its own name Influenza-associated Pulmonary Aspergillosis (IAPA), with a mortality rate in critical care reaching 51% (this is higher than sepsis, one of the leading causes of deaths in the entire planet). The use of corticosteroids, which are commonly given to reduce inflammation and alleviate influenza symptoms, has been linked to an increased risk of developing IAPA.

When a person is infected with influenza, the virus can suppress the immune system's ability to fight off microbial pathogens, including fungi like Aspergillus. Influenza infection also causes significant damage to the respiratory system, making it easier for secondary fungal infections to occur. Medications specifically designed to treat influenza, such as neuraminidase inhibitors like oseltamivir, have been shown to affect the body's defense against Aspergillus. These inhibitors can impair the ability of certain immune cells to kill Aspergillus, making it harder for the body to fight off the fungal infection.

Other invasive diseases associated with Covid:

• Candidiasis

• Mucormycosis

• Pneumocystis jirovecii

• Cryptococcus spp

• Rhodotorula spp.

• Fusasrium spp.

The authors go on to highlight the possible pathways of immune dysregulation during a SARS-CoV-2 infection. The highlights of these are the following.

• increased inflammatory markers including IFN-α, Interleukin (IL)-1Ra and several type 1 (IFN-γ, IL-12p70), type 2 (IL-4, IL-5) and type 3 cytokines (IL-17A, IL-22) and chemokines that direct leukocyte trafficking (C-C Motif Chemokine Ligand 2 (CCL2), C-X-C Motif Chemokine Ligand 9 (CXCL9))

• The rapid stimulation of T helper 1 (Th1) cells leads to an imbalanced pro-inflammatory response, with particularly high levels of expression of IL-6 and tumor necrosis factor (TNF), leading to impaired acquired immunity (lymphopenia) and an uncontrolled innate response, further propagated by the release of pro-inflammatory cytokines by alveolar macrophages

• Among a few other dynamics

The first two are important because they are the hallmark, even advertised response of the mRNA vaccines. You do need these responses, but balance, and within specific timeframes and periods after exposure to a pathogen, sustained levels (the precise lauded “success” of the mRNA platform) are the exact opposite. More fuel to an already strongly burning fire. The authors last point is one I will write about next, tying quite a few topics together.

Immune exhaustion

Here lies our quandary. Secondary infections, superinfections, invasive and opportunistic pathogens and all the subsequent dysfunction and damage these do are among the most complex dynamics to be researched in science. But even taking into account all that, two things never made sense to me. The “one pathogen leads to immune exhaustion (which I will write about next), and the second non-linear dynamics also don’t properly explain the sudden, sustained increase in certain opportunistic infections.

So in May 2022, I started exploring avenues, and with the help of the same friend I sometimes refer to in this Substack, we found one potential mechanism (that I won’t make public for reasons). The second mechanism came a few months later when I just tweeted “Could SARS-CoV-2 be messing or wiping out a specific protein from the body and affecting immune “memory”, or making us unable to fight diseases for whatever reason ?

Seems my second proposition wasn’t as insane as I thought at the moment.

• Emerging globally recognized issues of deadly fungal infections have been highlightedby the identification of virus-associated fungal infections.

• Neutrophils play essential roles in providing host resistance against fungi; alterationsin their function or recruitment underlie most acquired fungal infections.

• B cells and specialized subsets, including innate B1 cells, provide baseline amounts of systemic antibodies that link humoral and neutrophil responses.

• Viral pneumonia and corticosteroids used to treat inflammatory conditions and COVID-19 disrupt an antifungal host defense axis that couples natural IgG antifungal antibodies, B1a cells, and neutrophil-dependent fungal elimination.

Source

The following news article summarizes the find of the paper above quite well, with this quote being pertinent to our discussion.

"We discovered that influenza and COVID-19 destroy a previously unknown natural immunity that we need to resist invasive fungal infections," says Nicole Sarden, a PhD candidate at the University of Calgary and first author on the study.

Influenza, SARS-CoV-2 infection and the (indiscriminate) use of corticosteroids use both disrupt an important primary axis of immune response that deals with fungal infections. To make matters worse SARS-CoV-2 (all Omicron variants) displace the microbe responsible for creating and maintaining a proper influenza immune response (Akkermansia), this creates a somewhat incestuous relationship opening up the body to many opportunistic loops of infection.

This isn’t a well-elaborated “I was right”, but rather bringing more attention to this section of a highly complex puzzle.

Source

Source

Researchers have found a possible reason for a spike in the rate of colorectal cancer cases among patients under 50: a fungus that usually blamed for nail and skin infections.

The Washington, D.C. university looked at microbial DNA samples from the tumors of colorectal cancer patients who were either under 45 or over 65 when diagnosed.

They found that tumors from younger patients were more likely to contain the fungus Cladosporium sp., which is typically rarely found in the gut, and causes skin and nail infections. It’s still not clear how the pathogen could lead to the cancer, but one theory is it could be responsible for damaging cell DNA.

When profiling the mycobiome of the nasopharyngeal region of SARS-CoV-2 infected individuals, researchers found something quite remarkable. “The infection significantly (p < 0.05) influenced the alpha diversity. Interestingly, a higher abundance of Cladosporium and Alternaria was noted in the infected individuals and inter-individual variation in mycobiome composition was well supported by beta dispersion analysis”

Autoreactive T Cells and Chronic Fungal Infection Drive Esophageal Carcinogenesis

Extensive review of the role of fungi in the development and progression of cancer, a second one can be found here, also really good

While I vehemently stick to everything I wrote so far in regards to SARS-CoV-2, its Spike Protein, its almost endless use of important receptors, all the dysfunction it causes, and how nocive and toxic the current mRNA platform currently finds itself, my point here is as follow, there is a lot more going under the hood than most of us are comfortable saying or accepting.


As my closing remark, and as a hint for you, the curious reader to dig, do you know what causes both immune dysfunction, and immune paralysis, causes latent pathogens to awake, leads your body to tolerate bacterial infections, and opens you up to both secondary infections, often fungi and given all this intricated dynamic can lead to cancer, besides the mRNA ?

Sepsis, and its most proeminent hallmark. Endotoxins.

This is how I view the N-Terminal Domain and the Receptor Binding Domain of SARS-CoV-2.

The 20-minute-long fight can be viewed here

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