The systemic virus myth
Much of the fear of covid is based on the idea that it behaves in a more dangerous way than other respiratory viruses. In particular, the spike protein is blamed for causing an array of pathology.
However the very same pathology ascribed to spike protein has previously been ascribed to influenza.
Influenza causes cardiovascular problems, brain damage, and in severe cases, acute respiratory distress syndrome. Inflammation from infection can lead to conditions such as pulmonary hypertension and heart fibrosis. Some patients mount an exaggerated immune response creating a cytokine storm. The inflammation it causes can destabilise atherosclerotic plaques narrowing the coronary arteries which leads to acute myocardial infarctions i.e. heart attacks.
It can also influence the coagulation cascade, promoting the formation of blood clots. On rare occasions, these clots can travel to the brain, causing strokes by interrupting blood supply. Some studies have linked the virus to an increased likelihood of degenerative disorders such as Parkinson’s and Alzheimer’s disease. For the few with a severe infection, the effects can last more than a year,, with increased risks of both death and disability.
It is well accepted that influenza causes all of this pathology without entering the bloodstream in order to do so. Many of the effects are a result of the immune response, with cytokines reaching high levels in the blood and driving systemic inflammation. Where haemagglutinin protein contributes directly, it does so after the virus is broken down and its components enter the circulation, persisting briefly until cleared by the immune system.
There are no reports of influenza virus being found in tissues outside the respiratory tract at post-mortem.
The same is not true for SARS-CoV-2. There have been reports of viral proteins being expressed in tissues even after mild covid infections. Should we take these reports at face value?
The earliest reports were from severe covid cases, often with multi-organ failure. These studies claimed that virus was present in endothelial cells of the lung, and Matschke et al. even concluded the virus entered cells in the brain. In such cases, where viral load and inflammation are high, viral entry into the bloodstream and dissemination to distant tissues is plausible. However, even in these cases, detection of the virus in distant organs was inconsistent and often weak, as we shall see.
More controversially, some claims come from animal studies in which mice were injected with viral spike protein, leading to detection in the vessels of the skin, brain meninges, and bone marrow. If applicable to human infection, these results would suggest a mechanism unlike that of any common respiratory virus. But closer inspection of the methodology raises questions.
The majority of these findings rely on a common laboratory tissue staining method called immunohistochemistry (IHC) to detect spike protein. The stain works through using animal antibodies to bind to the spike protein specifically. Another animal antibody with stain attached is then bound to the first antibody. While IHC is a standard method in pathology, it is known to suffer from issues of specificity, especially when applied to inflammatory tissues. The second antibody can bind to human antibodies present in inflamed tissue and the inflammation can also trigger the stain independently.
The study by Matschke et al. is often cited to support the idea of SARS-CoV-2 neuroinvasion. However, spike detection relied on a GeneTex antibody clone that has not been validated using non-covid inflammatory brain tissue. There are reports of nonspecific staining with this clone in inflamed tissue (e.g., lung, pigmented areas), including from Roden et al. Moreover, the authors themselves described positive immunohistochemistry in samples where viral RNA could not be detected by qRT-PCR, raising the possibility of false positives.
A multicentre validation study by Krasemann et al. further demonstrated that many widely used anti-spike antibodies performed poorly, producing nonspecific or no signal in infected tissues. The authors recommended against relying on spike antibodies for IHC in autopsy samples, especially in the absence of matched controls and confirmatory methods.
Claims of SARS-CoV-2 in tissues in long covid turn out to involve nucleocapsid protein debris found within macrophages, not active infection of local tissues. A large autopsy and surgical specimen study found IHC positivity for viral proteins, and separately detected viral RNA only in rare macrophages in the liver, heart, and kidney. Skin biopsies from covid patients have been thoroughly examined and consistently shown to reflect inflammatory responses, not direct viral infection.
Recent pathology reviews have shown that anti-spike antibodies and antibodies to other SARS-CoV-2 proteins can produce false-positive staining in tissues from patients with other viral infections such as influenza, or even non-viral lung injury. Granular cytoplasmic staining, which can be interpreted as a spike signal, has also been seen in macrophages and epithelial cells of patients with adult respiratory distress syndrome (seen in ventilated patients) or influenza. Importantly, when the same antibodies are applied to extrapulmonary tissues, such as skin or kidney, in pre-2020 samples, similar staining can sometimes be seen.
Even when viral material is detected, the distinction between whole, replicating virus and residual fragments is crucial. PCR and in situ hybridization can detect viral RNA but cannot prove infectivity. Likewise, IHC can detect proteins but cannot differentiate between spike produced by infected cells and spike contained in viral debris taken up by immune cells.
No large studies have validated spike detection in extrapulmonary tissues after mild infection using parallel different methodologies let alone blinded studies. The few that have attempted to compare IHC with RNA-based methods have found that IHC lacks both the sensitivity and specificity needed to reliably localise viral protein in tissue.
Therefore, the assertion that spike protein travels through the blood and invades distant tissues during mild or asymptomatic covid remains unproven. In the absence of viral replication, systemic effects may still occur – as with influenza – due to circulating cytokines and immune activation. But this is not evidence of viral invasion.
To attribute symptoms such as rashes, fatigue, or neurological changes to lingering spike protein requires more than isolated reports using a single, poorly controlled detection method. It requires rigorous validation, use of appropriate inflammatory controls (such as influenza), and demonstration that the protein is not just present, but functionally active and pathogenic – not just debris.
The same caution applies to interpretation of spike protein detection after vaccination. However, there is likely too much focus on spike as being the cause of pathology after vaccination. The expression of any foreign protein leads to immune targeting and cell death and it is that which causes the pathology. Indeed, mRNA vaccines produced many different foreign proteins thanks to fragmented incomplete spike RNA and “frameshifting” where the sequence is misread.
For the virus, the idea that spike protein uniquely travels through the blood and deposits itself in tissues throughout the body – even after mild illness – remains a hypothesis in search of evidence.
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