Introduction
Whether one has been infected with SARS-CoV-2 or had the Covid-19
vaccine, a robust innate and adaptive immune response is elicited.
Recent studies provide evidence that the adaptive immune response can
persist at high levels for over 6 months after vaccination as measured
by sera antibody titers (Doria-Rose et al, 2021). Sera antibody titers
against the SARS-CoV-2 virus are significantly higher in the vaccinated
compared to those who are infected (Assis et al, 2021; Bartsch et al,
2021). For an unknown number of people, either of these events may lead
to autoimmune disease (Guimarães et al, 2015); here called SARS-CoV-2
induced autoimmune disease (Ehrenfeld et al, 2020), and Covid-19 vaccine
induced autoimmune disease (Toussirot and Bereau, 2015; Segal and
Shoenfeld, 2018). While the two conditions may share similar mechanisms
of an impaired, hyper immune response, long Covid may have additional
mechanisms such as viral persistence (Wang et al 2020; Neurath et al,
2021). Viral persistence, even at low levels, can lead to a number of
consequences, including the release of miRNA packaged into exosomes that
induces a pro-inflammatory, Warburg-like effect in surrounding cells
(Yoshikawa et al, 2019; Proal and VanElzakker, 2021). Common to both
conditions, i.e vaccine induced and Covid-19 induced autoimmunity,
susceptibility to infection or severe outcomes may include the effects
of previous infections or vaccinations. For example,
superantigen-mediated T cell activation can trigger broad B cell
activation, and production of autoantibodies against a range of tissues
has been shown in multi-inflammatory syndrome (Consiglio et al, 2020),
and in patients with acute COVID-19. The spike protein, whether a part
of the virion or of the Covid-19 vaccine, contains a superantigenic
motif known to elicit a hyperinflammatory adaptive immune response
(Cheng et al, 2020). Evidence also finds that the spike protein drives
NLRP3 inflammasome activation in human microglia (Albornoz et al, 2022),
a possible mechanism in developing neurological symptoms following
Covid-19 infection or vaccination. One explanation for this happening is
that the virus, or vaccine related proteins, can now target vascular
endothelial cells and disseminate to the CNS through a hematogenous
mechanism. Once at the blood-brain-barrier (BBB), SARS-CoV-2 or vaccine
related protein, binds the zonulin receptor and promotes zonulin
release. Then zonulin, via PAR2, induces blood-brain-barrier (BBB)
disruption allowing the virus or protein to enter. Disruption of barrier
function in epithelial and endothelial cells has been found by UC
Berkeley scientists to be mediated by the spike protein alone (Biering
et al, 2022), meaning that the spike protein made by mRNA vaccines can
mediate this disruption of barrier function. Further, PEG has never been
used in an approved vaccine until the mRNA vaccines, and its presence in
Pfizer-BioNTech and Moderna-1273 vaccines has raised concerns about
possible anaphylactic and fusogenic adverse effects (Sfera et al, 2022).
Another concern is that PEG promotes temporary permeabilization of the
BBB, a property used by the pharmaceutical industry for drug delivery to
the CNS (Rabenel et al, 2020). This may account, in part, for the
VAERS-reported neuropsychiatric symptoms, including neurodegenerative
disorders (Frontera et al, 2022). Many excipients other than PEG are
also used in the mRNA vaccines, and they too may be causative for
adverse events (Borgsteede et al, 2021). “Hyper accelerated reviews”
of these vaccines by the FDA has been questioned by many scientists,
including Dr. Marion Gruber, Ph.D., director of the FDA’s Office of
Vaccines Research and Review (Brennan, 2023). In other words, safety and
efficacy analysis of mRNA vaccines for Covid-19 have been substandard.
Also, chronic activation of the immune system by viral persistence (or
vaccine persistence, depending on how long the spike protein is made)
can induce autoimmune responses, and molecular mimicry between
components of a pathogen and host tissue can lead to specific
post-infectious autoimmunity. Structural similarity between human
neuronal antigens and SARS-CoV-2 proteins exists. A particular form of
autoimmunity described in long COVID is postural orthostatic tachycardia
syndrome, a form of autonomic dysregulation that is possibly induced by
functional autoantibodies that target G protein–coupled receptors on
neurons (Brodin et al, 2022). Another type of autoimmunity relevant to
SARS-CoV-2 infection is the production of neutralizing autoantibodies to
type I interferons, explaining a sizeable fraction of cases of hypoxemic
COVID-19 pneumonia (Bastard et al, 2021). If such neutralizing
autoantibodies are present before SARS-CoV-2 infection, due to prior
infections or vaccinations, then a patient is clearly at risk of
developing severe acute COVID-19 or vaccine induced autoimmune disease.
Neutralizing autoantibodies may also appear after SARS-CoV-2 infection,
in which case they might instead enable viral persistence, the formation
of a viral reservoir and long COVID. That Covid-19 induced autoimmune
disease and Covid-19 vaccine induced autoimmune disease share common
mechanisms is further evidenced by a recent report that a healthcare
professional had her vaccine induced autoimmune disease exacerbated by a
breakthrough Covid-19 infection (Staahl, 2022).