August 18, 2022

To begin:

Subacute sclerosing panencephalitis (SSPE) is a slowly progressing fatal human disease of the central nervous system (CNS) that is associated with measles virus persistence. Virus nucleocapsids are present in the brain and the patient is in a state of hyperimmunization towards this agent. However, although all other structural polypeptides are recognized by the immune system, there is a markedly decreased antibody response towards virus matrix or membrane protein M. Matrix protein has not been detected in brain cells and infectious virus is not present.

Defective translation of measles virus matrix protein in a subacute sclerosing panencephalitis cell line

So, what does this mean? In a small percentage of those that are infected with Measles, the virus persists – but in a very interesting way. The Matrix protein (the one that holds the virus together, that gives it its structure as a complete virion) is NOT translated. In other words, proteins of the virus are translated, but the complete virus is not translated and therefore does not bud and is not released. However, the N protein IS translated and it is believed it travels synaptically, inducing SSPE.


Now we need to look at SSPE. What exactly is it?

Subacute sclerosing panencephalitis is a rare neurological disease of childhood or young adulthood. The first signs are usually behavioral changes such as failing schoolwork, memory loss, and/or irritability. Involuntary muscle movements (myoclonic jerks) and generalized seizures follow. Subacute sclerosing panencephalitis is a progressive disease which results in personality changes, outbursts of temper, sleeplessness, disorientation, stupor, spasticity, loss of previously acquired intellectual skills, poor memory and judgment (dementia), and general neurological deterioration. Blindness may develop because of a lesion in the vision center of the brain (cortical blindness) and the nerves of the eyes may waste away (optic atrophy). The late symptoms of subacute sclerosing panencephalitis may include muscle rigidity, elevated body temperature (hyperthermia) and/or abnormalities of respiration, heartbeat, and blood pressure. These disturbances of normal bodily functions (homeostasis) indicate that the hypothalamus gland, which is located deep inside the brain, may be affected.

Subacute Sclerosing Panencephalitis

The parallel we need to evaluate is that the S protein of the SARS-CoV-2 virus also persists without the presence of infectious virus, but it travels via extracellular vesicles.

Persistent Circulation of Soluble/EV-Linked Spike Protein and Viral RNA in Individuals with Post-Acute Sequelae of COVID-19

What concerns me the most here, is that the S1 subunit of the Spike Protein, the one that seems to persist more often, tends to aggregate in the hypothalamus.

This supports a previous report showing that shed spike protein (subunit 1) of SARS-CoV-2 appears more consistently in the hypothalamus than the olfactory bulb after nasal inoculation.

The route of SARS-CoV-2 to brain infection: have we been barking up the wrong tree?


HY is the Hypothalamus

The “icing on the cake” for me, and what definitively drew me to this parallel, is the association of SSPE with neurofibrillary tangles, echoing my findings and the studies confirming the amyloidogenic nature of the Spike Protein.

Histological study disclosed features of inflammatory disease associated with others of a neurodegenerative nature, such as the formation of neurofibrillary tangles, which would relate SSPE with other tauopathies.

Adult-onset subacute sclerosing panencephalitis: Clinico-pathological findings in 2 new cases

There have been inklings of this observed. I believe I have found the mechanism.

For example, the subacute sclerosing panencephalitis and postencephalitic parkinsonism tauopathies have been suggested to be triggered by viral infections. These diseases share the neuropathological hallmarks of hyperphosphorylated tau, neurofibrillary tangles, and neurodegeneration. In post-mortem samples from individuals with subacute sclerosing panencephalitis, measles virus has been detected in neurons and glial cells that contain tau neurofibrillary tangles. Postencephalitic parkinsonism is thought to be a long-term sequela of encephalitis lethargica that occurred during and after the 1918 influenza pandemic. Subacute sclerosing panencephalitis is diagnosed 3–34 years (median 9–10 years) after measles infection, whereas postencephalitic parkinsonism was generally diagnosed 1–5 years after encephalitis lethargica.

Only 0·01–0·1% of measles infections lead to subacute sclerosing panencephalitis.5 If a COVID-19-induced tauopathy develops at a similar rate, there could be 10 000–100 000 cases for every 100 million people infected with SARS-CoV-2.

Could SARS-CoV-2 cause tauopathy?

Why do I sound this alarm?

SSPE usually develops 2 to 10 years after the original Measles viral attack.