Page 19 - Dr Stephanie Seneff - Reviewing Some Possible Unintended Consequences of the mRNA Vaccines Against COVID - 19

Autophagy is essential for clearing damaged proteins, organelles, and bacterial and viral pathogens.
Alterations in autophagy pathways are emerging as a hallmark of the pathogenesis of many
respiratory viruses, including influenza virus, MERS-CoV, SARS-CoV and, importantly, SARS-CoV-
2 (Limanaqi et al., 2020). Autophagy is surely critical in the clearance of spike protein produced by
immune cells programmed to produce it through the mRNA vaccines.

One can speculate that impaired autophagy prevents clearance of the spike protein produced by
macrophages from the vaccine mRNA. As we will show later, platelets possess autophagic proteins
and use autophagy to clear viruses. Impaired autophagy is a characteristic feature of ITP, and it may
be key to the autoimmune attack on the platelets (Wang et al., 2019).

3. A Critical Role for the Spleen

The spleen is the largest secondary lymphoid organ in humans and it contains as much as 1/3 of the
body’s platelet supplies. The spleen is the primary site for platelet destruction during ITP, as it
controls the antibody response against platelets. The two main autoantibodies associated with ITP
are against immunoglobulin G (IgG) and the glycoprotein (GP) IIb/IIIa complex on platelets
(Aslam et al., 2016).

The spleen plays a central role in the clearance of foreign antigens and the synthesis of IgG by B
cells. Upon exposure to an antigen, such as the spike protein, neutrophils in the marginal zone of the
spleen acquire the ability to interact with B cells, inducing antibody production (Puga et al., 2011).
This is likely crucial for successful vaccination outcome. The pseudouridine modification of mRNA
is important for assuring RNA survival long enough for it to reach the spleen. In an experiment on
injection of mRNA nanoparticles into mice, both the delivered mRNA and the encoded protein
could be detected in the spleen at 1, 4, and 24 hours after injection, at significantly higher levels than
when non-modified RNA was used (Karikó et al., 2008).
A sophisticated platelet-neutrophil cross-communication mechanism in the spleen can lead to
thrombocytopenia, mediated by a pathological response called NETosis. Platelet-TLR7 (toll-like
receptor 7) recognizes influenza particles in circulation and leads to their engulfment and
endocytosis by the platelets. After engulfing the viruses, the platelets stimulate neutrophils to release
their DNA within Neutrophil Extracellular Traps (NETs) (Koupenova et al., 2019), and the DNA,
in excessive amounts, launches a prothrombotic cascade.

4. Lessons from Influenza

The influenza virus, like the corona virus, is a single-strand RNA virus. Thrombocytopenia is a
common complication of influenza infection, and its severity predicts clinical outcomes in critically
ill patients (Jansen et al., 2020). Platelets contain abundant glycoproteins in their membranes which
act as receptors and support adhesion to the endothelial wall. Autoantibodies against platelet
glycoproteins are found in the majority of patients with autoimmune thrombocytopenia (Lipp et al.,
1998). The influenza virus binds to cells via glycoproteins, and it releases an enzyme called
neuraminidase that can break down the glycosaminoglycans bound to the glycoproteins and release
them. This action likely exposes the platelet glycoproteins to B cells, inducing autoantibody
production. Neuraminidase expressed by the pathogen Streptococcus pneumoniae has been shown
to desialylate platelets, leading to platelet hyperactivity (Kullaya et al., 2018).
International Journal of Vaccine Theory, Practice, and Research 2(1), May 10, 2021 Page | 407