Dr. Story and Taylor discuss Covid, mRNA vaccines, and more health information. This is a DEEP DIVE into Covid-19 and why vaccination matters and is safe. We go into the actual mechanics of the virus and the mRNA vaccines so you can be sure you are making the right decision when vaccinating. We take the time and tackle some misinformation coming from anti-vaccine figures as well - just to be sure we cover the bases. After the interview, I go IN-DEPTH on the topics we discussed.
Craig Story is a Professor of Biology at Gordon College, a small non-denominational Christian college located on the North Shore of Massachusetts. There, he teaches a number of cell biology courses including immunology and biochemistry. He serves as the health professions advisor. He studied antibody transport in pregnancy for his doctoral research at Brandeis University, and in his postdoctoral training at MIT and Harvard Medical School he worked on an unusual virus immune evasion process. Since 2013, Dr. Story has worked with church leaders, seminary professors, and the public to foster important conversations about science and the Christian faith. He keeps busy with beekeeping, gardening and observing God’s marvelous creation.
Learn more: https://www.gordon.edu/craigstory
Relevant Citations
———————————————————————————————————————————
The virus can injure the lungs in 3 ways: acute respiratory distress syndrome (ARDS) with diffuse alveolar damage (DAD), diffuse thrombotic alveolar microvascular occlusion, and inflammatory mediator-associated airway inflammation [9,10]. The results of these combined actions include impaired alveolar oxygenation, hypoxemia, and acidosis. In the absence of effective treatment, the consequences of this poor oxygenation are either death of the patient from respiratory failure, or the sequelae of permanent lung injury if the patient recovers [9–11].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
The degree of cell damage may depend not only on the effects of viral replication, but also on the release of pro-inflammatory cytokines, resulting in impaired function of type 2 pneumocytes [4,10]. These 2 effects result in impaired cell function, followed by cell death (necrosis) or apoptosis, exudates, desquamation of pneumocytes, and formation of hyaline membranes, which are characteristic of diffuse alveolar damage (DAD) [10]. Interstitial edema and inflammatory infiltrates of mononuclear and multinucleated syncytial cells also contribute to alveolar dysfunction [10–12]. As a result, the typical pathophysiological feature of COVID-19 pneumonia/ARDS is that alveolar gas exchange and oxygenation are severely impaired [13].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
Effective alveolar gas exchange by diffusion depends on the integrity and normal function of the alveolar epithelium and a normal microcirculation with patent alveolar capillaries [13,14]. SARS-CoV-2 damages the 2 major functional components of alveolar gas exchange: the integrity of the alveolar epithelium, and the patency and function of the alveolar microcirculation [15,16].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
SARS-CoV-2 not only damages alveolar gas diffusion functions, but also induces airway inflammation to reduce the ventilation function of the airway. The common association of bronchopneumonia with COVID-19 pneumonia provides direct evidence that SARS-CoV-2 affects airway ventilation function [8,9].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
With the rapid increase in the numbers of COVID-19 patients and the appearance of different symptoms and signs, reports of neurological damage have gradually attracted attention [28,29]. It was initially thought that SARS-CoV-2 had great difficulty in passing through the dense blood–brain barrier (BBB), but this is not the case. Post-mortem studies on the cerebral pathology of COVID-19 patients and the use of an advanced 3D microfluid model of the human BBB identified 3 important findings [29,30].
First, the SARS-CoV-2 spike (S) protein-binding receptor, ACE2, is widely expressed in brain microvascular endothelial cells [29,30]. Second, the S protein can directly damage the integrity of the BBB to varying degrees [29,30]. Third, the S protein can induce the inflammatory response of microvascular endothelial cells that change the function of the BBB [29,30]. These findings support that SARS-CoV-2 can alter the BBB and enter the brain, and support the appearance of neurological symptoms, the formation of fatal microthrombi, and even the occurrence of encephalitis associated with COVID-19 [29,30]. These neurologic associations of COVID-19 support the clinical reports of early neurological changes, and support the potential basis for the occurrence of long-term neurological sequelae. In addition, to cross the BBB, SARS-CoV-2 may enter the brain by trans-synaptic transfer, optic and olfactory nerve channels, and vascular endothelial cells [29,30].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
This was conjecture, but educated conjecture at least “The SARS-CoV-1 infection epidemic in 2003 was reported to cause various types of neurological damage, including the axonal-variant Guillain-Barré syndrome, ischemic stroke, and seizures [30–32]… These results provide indirect evidence for possible mechanisms of cerebral damage caused by SARS-CoV-2.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
For both SARS-CoV-1 and SARS-CoV-2, these highly pathogenic coronaviruses enter the brain via the viral S protein, which can bind to the ACE2 receptor [4]. The expression of the ACE2 receptor in the cell determines the cell tropism of the virus [4,35–37]. Increasing numbers of studies have supported this molecular pathogenesis in the brain, as the distribution of ACE2 expression at different sites in animal and human brain tissues is widely expressed in neurons, astrocytes, and oligodendrocytes throughout the brain [36]. These findings support a molecular mechanism by which SARS-CoV-2 enters the brain and then causes neuronal damage [36–38].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
The olfactory nerve is now considered to be a potential pathway for entry of the SARS-CoV-2 into the brain [7,36], as sustentacular cells that maintain the integrity of the sense of smell [37] and stem cells in the olfactory epithelium [38] all highly express ACE2 and transmembrane serine protease 2 (TMPRSS2) [37].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
Neurodegenerative disease is an umbrella concept including a range of conditions that primarily affect the neurons in the human brain and is one of the key factors leading to the decline in quality of life. Whether SARS-CoV-2 causes neurodegenerative diseases or accelerates their premature occurrence is still unclear, and it is also difficult to draw conclusions within just a few months. However, the high expression of the ACE2 receptor in a wide range of sites in the brain not only provides an initial target for SARS-CoV-2 to cause acute brain damage, it may also be the basis for later neurodegenerative changes [68]. This possibility is supported by the findings from recent studies that showed the presence of functional inhibition of viral and nicotinic acetylcholine receptor complexes in the pathogenesis of SARS-CoV-2 infection [7].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
The SARS-CoV-2 virus has many unique properties that increase its transmission and pathogenic effects. At such an early stage of the pandemic, the potential long-term sequelae of COVID-19 are just beginning to be realized. This review has highlighted the need for more long-term clinical follow-up data on patients who have had COVID-19, and for attention to the management of long-term sequelae, which will emerge in patient care settings. Finally, the economic impact of this disorder, together with patient care, must be worked out in advance.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7643287/
Different paper, this part is educated conjecture from 2020: “Experience from other coronaviruses, including MERS and SARS-CoV, suggest that fibrotic disease as an outcome of COVID-19 is a concern (reviewed in Ref. 58). A study of MERS noted that 33% of patients with abnormal chest radiographs had lung fibrosis (59). These patients had longer ICU stays, were older, and had higher chest radiographic scores as well as higher peak lactate dehydrogenase levels versus patients without pulmonary fibrosis. Studies from SARS-CoV indicated that 27.8% to 62% of patients infected with SARS-CoV exhibited decreased lung function and increased fibrosis (60–64).”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7900916/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7900916/
You will also see people mention how their infection went and suggest others should see their experience as THE experience. This is not necessarily the case – this VERY brief review article outlines different types of infections.
https://pubmed.ncbi.nlm.nih.gov/34198106/
COVID-IN COVID infection but no disease: these are the people who have tested positive on a screening test but never reported any major symptoms beyond a low-grade fever and myalgia.
COVID -RI COVID infection resulting in respiratory infection URTI or LRTI. These occur in early stage of disease and persists for longer duration only in elderly or immunocompromised people.
https://pubmed.ncbi.nlm.nih.gov/34198106/
COVID-I COVID infection resulting in Immunological condition. This subset consists of relatively young people with a strong immune system who have responded to COVID infection in an unusually strong and atypical fashion much like an autoimmune disease
https://pubmed.ncbi.nlm.nih.gov/34198106/
COVID -S COVID sequalae e No active infection but COVID has resulted in residual damages. These appear between 4 weeks and 3 months of the COVID infection [CITE]. Depending on the primary subtype, it may affect different organs.
https://pubmed.ncbi.nlm.nih.gov/34198106/
Let’s follow that cite, shall we? Oh wait… that’s where we started. Which, by the way, references 93 (NINETY-THREE!!!!) papers. Not bad. Not all on point of course, but still shows academic rigor to compile it down to one article.
If there is ANYTHING you take from this thread, there is more to Covid than death.
VAERS
“VAERS is a passive reporting system, meaning that reports about adverse events are not automatically collected, but require a report to be filed to VAERS. VAERS reports can be submitted voluntarily by anyone, including healthcare providers, patients, or family members. Reports vary in quality and completeness. They often lack details and sometimes can have information that contains errors.” https://vaers.hhs.gov/data/dataguide.html
“Healthcare providers are required to report to VAERS the following adverse events after COVID-19 vaccination….” https://vaers.hhs.gov/faq.html
*MY COMMENTARY: DOES NOT MEAN VAX CAUSED IT.*
VAERS DEATH 4710 All vaccines
VAERS DEEP VEIN THROMBOSIS 1584
VAERS occurrences 443201 events as of AUG 6
VACCINES up to AUG 6th – 193764457 at least one dose, 165918256 fully vaxxed
About 13674107 JandJ by aug 8th
MECHANISM OF COVID 19
I started in this research as in answer the question that is derived from whether or not COVID has long term side effects. My research then, started with this article: https://content.iospress.com/articles/journal-of-alzheimers-disease/jad200581 Which states that a spike protein facilitated entry into a cell. This article eventually led me to this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167588/ Stating the mechanisms of the spike protein attaching an entering the cell. This article then led me to ask the question, what happens after the spike protein attaches to a cell? “Once the virus enters the cell, the viral RNA is released, polyproteins are translated from the RNA genome, and replication and transcription of the viral RNA genome occur via protein cleavage and assembly of the replicase–transcriptase complex. Viral RNA is replicated, and structural proteins are synthesized, assembled, and packaged in the host cell, after which viral particles are released (Fig. 1d) [9].” https://www.nature.com/articles/s41401-020-0485-4
That quote begs the question, what does the viral RNA do?
“SARS-CoV-2 is an enveloped, positive-sense, single-stranded RNA virus that, upon infection of a host cell, deploys a ‘translation-ready’ RNA molecule, which uses the protein synthesis machinery of the host to express a set of viral proteins crucial for replication2.” https://www.nature.com/articles/s41564-020-00846-z.
Where does that site go?
“Cytopathic viruses, including SARS-CoV-2 (ref.51), induce death and injury of virus-infected cells and tissues as part of the virus replicative cycle.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187672/
“Viral infection and replication in airway epithelial cells52 could cause high levels of virus-linked pyroptosis with associated vascular leakage, as seen in patients with SARS-CoV53. Pyroptosis is a highly inflammatory form of programmed cell death that is commonly seen with cytopathic viruses54. This is a likely trigger for the subsequent inflammatory response55. IL-1β, an important cytokine released during pyroptosis, is elevated during SARS-CoV-2 infection11.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187672/#CR51 presumably, without the viral RNA, this cell death would not occur and thus would make the vaccines that only create spike protein safer?
Other Notes I find:
SARS-CoV-2 infection and the destruction of lung cells triggers a local immune response, recruiting macrophages and monocytes that respond to the infection, release cytokines and prime adaptive T and B cell immune responses. In most cases, this process is capable of resolving the infection. However, in some cases, a dysfunctional immune response occurs, which can cause severe lung and even systemic pathology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187672/
HOW VACCINE WORKS
mRNA wouldn’t survive in its natural state, so we modify it. This also helps control inflammation:
“In an effort to improve half-life as well as translatability and safety, Karikó et al. tested a variety of naturally occurring modifications to nucleosides in mRNA molecules, including pseudouridine, 5-methylcytidine, N6-methyladenosine, 5-methyluridine, and 2-thiouridine [5]. Of these variants, they found that the incorporation of N1-methyl-pseudouridine (m1Ψ) in place of uridine led to a 10-fold increase in translation over unmodified mRNA. Furthermore, they were able to show that mRNA molecules possessing this modification did not trigger pathogen-associated molecular pattern sensing mechanisms such as toll-like receptors (TLRs) or retinoic acid-inducible gene I (RIG-I) [4,5]. This is crucial to avoid excessive inflammation, which could result in undesired vaccine side-effects. For these reasons, many candidates, including the two recently licensed mRNA vaccines mRNA-1273 and BNT162b2, adopted this m1Ψ mRNA modification in their vaccine design [6,7,8,9,10,11,12,13,14,15,16].” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
Vaccine changes two amino acids to prevent spike protein subunits from separating.
To stabilize the S protein, a few different strategies have been adopted (Figure S1). A mutation where amino acids 986 and 987 are replaced with prolines (S-2P), stabilizing the transmembrane-anchored S glycoprotein in the prefusion conformation but still allowing for cleavage of the S1 and S2 subunits [17,21], is the approach used in the licensed vaccines mRNA-1273 and BNT162b2 [6,7,8,9,10,11,12,15,16]. Another approach consisted of designing an mRNA construct where the full-length S protein lacks the furin cleavage site (Δfurin) and cannot be cleaved after translation [23,24].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
The mRNA is surrounded by lipid nano particles and this prevents damage prior to introduction to the cell. Neat.
“The advent of lipid nanoparticle (LNP) encapsulation was a turning point in the development of mRNA vaccines, as LNPs are able to efficiently deliver mRNA in vivo [30,31]. When injected intramuscularly, mRNA-LNPs can be internalized and quickly translated by antigen-presenting cells at both the injection site and in draining lymph nodes, thus promoting the initiation of adaptive immune responses [32]. Additionally, LNPs can protect mRNA from degradation by nucleases. Although the precise composition of the LNPs used by many vaccine developers is proprietary information, it is known that LNPs contain a combination of ionizable cationic lipids, cholesterol, phospholipid and PEGs that self-assemble into ~100 nm nanoparticles encapsulating the mRNA [33,34,35]. Of the vaccine candidates in clinical trials, LNPs are the standard method being used to introduce mRNA vaccines to participants. “
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
“While mRNA vaccine uptake/biodistribution and the innate immune response to mRNA vaccines are critical for the initiation of adaptive immunity, these processes are thoroughly reviewed elsewhere [36] and will not be covered in this article due to a lack of available data generated in the context of SARS-CoV-2 mRNA vaccines.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
Either mRNA-LNPs or locally produced antigen are taken up by antigen-presenting cells (APCs) (2), such as dendritic cells (DCs). These APCs then traffic to the lymph nodes (3) where they are able to prime CD4 and CD8 T lymphocytes (4). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
mRNA-based vaccines have become an increasingly attractive platform to fight the ongoing SARS-CoV-2 pandemic for a multitude of reasons. Firstly, the need for only a DNA template of the desired antigen to produce a vaccine candidate, resulting in an exceedingly fast manufacturing timeline [4]. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
Secondly, mRNA vaccines elicited a very potent immune response in both animal studies and human clinical trials, as extensively discussed in Section 3 and Section 4. Importantly, these potent immune responses are substantiated by an impressive protection from COVID-19 in phase 2/3 studies [10,16]. While the FDA has initially stated that SARS-CoV-2 vaccines will require a minimum of 50% efficacy to qualify for approval [78], both of the current mRNA vaccines currently approved for emergency use authorization (mRNA-1273 and BNT162b2) reported a greater than 94% efficacy [10,16]. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
mRNA vaccines also possess additional desirable features. Compared to other vaccine platforms, mRNA vaccines are appealing because of their minimalist nature. mRNA vaccines do not need a vector for their delivery/expression, thus removing the possible complication of pre-existing and/or de novo anti-vector immunity [80]. Differently from inactivated or attenuated vaccines, less important antigenic targets that do not lead to nAb generation are not included. Since there is no need for the involvement of any viral growth, the possibility of other contaminating viruses from the cell lines is removed. mRNA vaccines that are encapsulated in LNPs also do not require complex delivery methods involving electroporation, as required by DNA vaccines, nor do they need the addition of an adjuvant, which is required with protein vaccines. Moreover, as described earlier, all available data suggest that the mRNA-LNP platform polarizes T cells towards a Th1 bias, suggesting that the likelihood of these vaccines causing adverse events, such as VAERD (discussed in Section 3.2.2), seems quite remote. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
Finally, mRNA vaccines can be readily modified based on need. Target immunogenic epitopes can be easily switched in and out of candidates, as all that is needed is the DNA sequence of the antigen to serve as a template. A SARS-CoV-2 vaccine construct can be quickly adjusted to target a newly emerged coronavirus strain [8]. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918810/
__________________________________________________________________________________________
Additional Reading
This material was not expressly “cited” in the podcast but was provided by the host and guest for those of you with rabid curiosity on the topic. I stuck to scientific articles ONLY for the podcast, that is not the case in this section, which was NEVER directly cited. There are some scientific articles, some pre-prints, and even MSM sources.
From Dr. Story:
Another Overview of Covid/Vaccines from NIH: https://directorsblog.nih.gov/2021/06/22/how-immunity-generated-from-covid-19-vaccines-differs-from-an-infection/
“Lots of YouTubers are promoting “natural” immunity. That approach is just not as effective at ending the pandemic, and as we discussed, has lots more negative consequences health-wise” See: https://www.sciencemag.org/news/2021/07/when-will-covid-19-vaccines-be-fully-approved-and-does-it-matter-if-they-are
Evidence grows IVM is not effective: https://elemental.medium.com/ivermectin-for-covid-19-an-update-5e913bb49483
From Taylor Ealand
https://youtu.be/lXfEK8G8CUI How the immune system works.
https://quillette.com/2021/08/14/vexed-by-the-un-vaxxed/
Durability of mRNA-1273 vaccine–induced antibodies against SARS-CoV-2 variants https://science.sciencemag.org/content/early/2021/08/11/science.abj4176?utm_campaign=SciMag&utm_source=Social&utm_medium=Twitter
On Vaccine Safety, Ivermectin and the Dark Horse Podcast: An Investigation https://medium.com/rebel-wisdom/on-vaccine-safety-ivermectin-and-the-dark-horse-podcast-an-investigation-f32491d4c970
On Bret Weinstein, Alternative Media, Ivermectin and Vaccine-Related Controversies https://areomagazine.com/2021/08/12/on-bret-weinstein-alternative-media-ivermectin-and-vaccine-related-controversies/
Moderna Announces Positive Initial Booster Data Against SARS-CoV-2 Variants of Concern https://investors.modernatx.com/news-releases/news-release-details/moderna-announces-positive-initial-booster-data-against-sars-cov
Column: Major study of Ivermectin, the anti-vaccine crowd’s latest COVID drug, finds ‘no effect whatsoever’ https://www.latimes.com/business/story/2021-08-11/ivermectin-no-effect-covid
(Citing myself. Bite me!) 44: Yuri Deigin - Vaccines, IVM, Misinformation, and Pickles https://youtu.be/GBw0mIxn3iI
‘Joe Rogan Is Getting This Completely Wrong,’ Says The Scientist Who Conducted The Vaccine Study https://www.forbes.com/sites/andreamorris/2021/08/08/joe-rogan-is-getting-this-completely-wrong-says-the-scientist-who-conducted-the-vaccine-study/?sh=5ded59707bd1
NYC's vaccine mandate will test the authority of a 1905 Supreme Court case https://finance.yahoo.com/news/new-york-city-vaccine-mandate-will-test-the-authority-of-a-1905-supreme-court-case-113833108.html
(That Supreme Court Case) Jacobson v. Massachusetts, 197 U.S. 11 (1905) https://supreme.justia.com/cases/federal/us/197/11/
COVID-19 Vaccine Breakthrough Cases: Data from the States https://www.kff.org/policy-watch/covid-19-vaccine-breakthrough-cases-data-from-the-states/
Rates of SARS-CoV-2 transmission and vaccination impact the fate of vaccine-resistant strains https://www.nature.com/articles/s41598-021-95025-3
Get vaccinated! It could help you, like, not die… https://yurideigin.medium.com/get-vaccinated-it-could-help-you-like-not-die-71ebf63555f4
PREPRINT - Antibody Evolution after SARS-CoV-2 mRNA Vaccination “bioRxiv posts many COVID19-related papers. A reminder: they have not been formally peer-reviewed and should not guide health-related behavior or be reported in the press as conclusive.” https://www.biorxiv.org/content/10.1101/2021.07.29.454333v1
Is the Delta Variant Making Younger Adults ‘Sicker, Quicker’? https://www.nytimes.com/2021/08/03/health/covid-young-adults-sicker.html
(This article is a preprint and has not been peer-reviewed. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.) Virological and serological kinetics of SARS-CoV-2 Delta variant vaccine-breakthrough infections: a multi-center cohort study https://www.medrxiv.org/content/10.1101/2021.07.28.21261295v1
'The sky is not falling': Provincetown outbreak shows vaccines work, even against Delta https://www.yahoo.com/news/eight-hundred-cases-seven-hospitalizations-and-no-deaths-the-provincetown-outbreak-shows-vaccines-work-125324207.html
If you get this far and have read everything… A. WOW and B. God help you. If you have further questions, ask away. I’ll dig more.
__________________________________________________________________________________________
Share the show!
Where to find us:
Taylor: @contrarix on everything.
Kyle: @VoteKyleHermann on Instagram and Facebook
Guest: @ydeigin on Twitter
Music By: Garrett Vandenburg