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Research Article
SARS-CoV-2: OF SPANISH DESCENT
Taliah Safah Muhammad¹,²,*
¹Divine Ayat, LLC., Henrico, P.O. Box 29004, Henrico, Virginia 23242.
²Halal Natural Products Academy, LLC., Henrico, Virginia.
Author Email: ummnadia@divineayat.com
Publish Date: July 2, 2021
Abstract: SARS-CoV-2 is a genetically engineered SARS-COV vector which has been
embedded into the backbone of bacteriophage HP2 of Nontypeable Haemophilus Influenza
(NTHi). The design of SARS-CoV-2’s spike (S) protein is notable for its ability to facilitate
cellular entry via not only the ACE2 receptors but also ICAM-1 which becomes upregulated in a
NTHI infection. Technologies used in the development of SARS-CoV-2 were patented by the
Spanish National Research Council in 2006 and include methods for creating a SARS-COV
vector for gene editing, particularly “gene silencing”, and vaccine administration via “virus
particles”. This patent calls for the engineering of a SARS-COV vector using a helper virus such
as HP2 for replication and/or transcription. According to this patent, the said system could be
constructed using a genome of SARS-COV containing sequences encoding a heterologous
reporter gene or a gene derived from a different infectious agent and the construction of a full-
length cDNA, which in the case of SARS-CoV-2 was most likely performed using hnRNP Q
CRISPR Activation Plasmid (h) cDNA. Further, NTHI lysates increase exosome release in the
human middle ear epithelial cells. Exosomes can regulate gene expression via their miRNAs.
SARS-CoV-2 shares a 76% homology with SARS-COV which is an engineering requirement
mentioned in the said patent. The patent also sets forth modification principles and sequences
for engineering the ORF of gene 7a. This engineering can be observed as a structural analysis
has revealed that SARS-CoV-2 ORF 7a has structural homology with ICAM-1. ORF 7a plays a
vital role in virus tropism allowing SARS-CoV-2 to be “guided” to gene editing targets via the
hosts inflammatory secretions. Manipulation of ORF 7a to evade the hosts natural defenses
against virus tropism as well as the use of NTHI lysates can cause an excessive inflammatory
response or a “cytokine storm” in high-risk populations who become infected with COVID-19.
This mode of engineering would necessarily classify SARS-CoV-2 a biological weapon.
Keywords: SARS-CoV-2, HP2, viral vectors, CRISPR, cDNA, hnRNP Q, gene silencing, CCR5
Social Science & Medicine
Volume 298, May 2022, 114930
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1. Introduction
The scientific community and the world at large have been misled about the origins of
SARS-CoV-2, its design, and its primary mechanisms of action. This pandemic has killed
roughly 4 million people worldwide and has compromised the health, safety, and livelihood of all
of humanity. Confronting the truths of this matter is both urgent and essential.
It has been encouraging to see calls by the U.S. government to investigate the origins of
SARS-CoV-2, however, I am afraid that the current focus of these efforts is off target. While the
world has turned its focus completely to the Wuhan Lab and the “Bat Lady” in China, the more
culpable country(s) and persons have gone largely unnoticed.
The U.S. National Institutes of Health (NIH) and the National Institutes of Allergies and
Infectious Diseases (NIAID) has provided Luis Enjuanes, a virologist at the National Center for
Biotechnology, in Madrid, Spain, and his colleagues millions of dollars in funding over the past
three decades. Much of Enjuanes work that was funded by the NIH / NIAID involved research
on bacteriophages, influenza, coronaviruses, gain-of-function research, HIV, vaccine
development, and methods for gene therapy using coronavirus vectors (1). Enjuanes, a
longtime colleague of Peter Daszak of EcoHealth Alliance, was also one of the 27 scientists
who signed a statement affirming the natural origin theory of SARS-CoV-2 which was published
in the Lancet on February 18, 2020 (2).
In 2006, Enjuanes’ research on coronavirus derived expression systems led to a patent
for the use of SARS-CoV as a gene editing tool (3). This patent details methods for using an
attenuated SARS-CoV vector, more specifically a defective interfering (DI) genome of SARS-
COV as a mode for gene editing and vaccine delivery. This expression system requires a
helper virus as well as a full-length cDNA clone assembled in a bacterial artificial chromosome
(BAC) plasmid (4). In 2015, Enjuanes’ and colleagues in Spain and Rochester, NY., wrote a
protocol entitled; “Engineering Infectious cDNAs of Coronavirus as Bacterial Artificial
Chromosomes”, which was partially funded by the U.S. National Institutes of Health (5).
The said patent which was issued by the WIPO to the Spanish National Research Council,
details the sequence modification requirements of SARS-CoV coat proteins and S proteins.
Viral tropism is the affinity of a virus for a particular cell type, tissue, or species. It has been well
established that coronaviruses can be modified via manipulation of the spike (S) protein which
enables engineering of the tropism of the vector (6). The expression system detailed in the said
patent requires that the coat proteins of the modified virus have a sequence homology of at
least 60%, preferably at least 75%, and most preferably at least 95% to the wild type of SARS-
CoV proteins. Notably, the S proteins of SARS-CoV-2 share roughly a 76% and 97% of amino
acid sequences with SARS-COV and RaTG13 respectively (7).
The said patent also contains sequencing data for a variety of ORF genes including ORF 3a
and b, ORF 6, ORF 7a and b, ORF 8a and b, and ORF 9b. ORF 7a is significant as it has a
structural homology with ICAM-1 allowing both ORF 7a and ICAM-1 to bind to LFA-1. ORF 7a
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is also a critical factor in viral tropism as it plays a role in immune system modulation and the
inflammatory response. Further, recent research shows the ORF 7a amino acid sequence of
SARS-COV and SARS-CoV-2 are 85% similar (8). The said patent requires that the protein of
gene 7a has a sequence with a homology of at least 70%, preferably at least 85%, or at least
95% to SARS-COV.
2. Background
For the past year and half, I have researched the pathophysiology of COVID-19. To
date, I have published two papers (this one is the third) and one book detailing my research
findings. This paper is the culmination of those findings and points to the origins of SARS-CoV-
2 and helps to shed more light into the pathophysiology of a COVID-19 infection.
My first research paper entitled; “COVID-19, The Plague that Strikes Behind the Ear”,
explored how the bacteria Nontypeable Haemophilus Influenza, a quite common gram-negative
coccobacillus that colonizes the nasopharyngeal region in up to 80% of all humans, might be
involved in the pathophysiology of a COVID-19 infection. I also described how a NTHI and
SARS-CoV-2 coinfection would cause upregulation of ICAM-1, a binding receptor which viruses
like HIV use for cellular entry via CCR5 and CXCR4 co-receptors. During ICAM-1 upregulation,
the adaptive immune system responds via the release of inflammatory secretions which can
lead to excessive inflammation or what is better known as a “cytokine storm”, a phenomenon
seen in many COVID-19 patients with progressed disease (9).
Later, in my book; “Informed Consent: Exposing the Eugenics Cult and Their Latest
Experiment on Mankind: COVID-19”, the NTHI – SARS-CoV-2 connection was further explored,
revealing how a coronavirus might be manipulated to perform a gene editing experiment, in vivo
(10). It has been discovered that genes encoding high molecular weight adhesion proteins of
NTHI are part of important gene clusters, specifically Hmw1 and Hmw2 genes which encode B
ORFs and C ORFs of NTHI (11). As a result, many scientists have developed ways to perform
gene silencing procedures using this opportunistic bacterium including a group of scientists at
Harvard University who identified how NTHI might be exploited and used to cause a “loss-of-
function” to the CCR5 co-receptor via “virus like particles”. The work of these scientists led to
the issuance of a patent on August 18, 2020, entitled; “Editing of CCR5 receptor gene to protect
against HIV infection”. It should be noted that this patent was issued to Harvard University and
the research was partially funded by the U.S. NIH (12).
As an Islamic Medicine Practitioner, I also examined the spiritual aspects of disease which
contribute greatly to the rise of emerging infectious disease (EID). Also discussed in this work
was a 2008 publication in Nature about the global trends in EIDs. This research, performed by
Peter Daszak and his colleagues, included an analysis of a database of 335 EID events which
occurred between 1940-2004. The researchers noted a correlation between the rise in EID
events and the HIV pandemic. They further noted that EIDs place a huge burden on global
economics and public health and that methods should be employed to control EIDs to prevent
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global economic collapse and widespread disease (13). It should be noted that CCR5 has
found to be upregulated in COVID-19 patients. Further, a loss-of-function to the CCR5 co-
receptor is thought to eliminate certain infectious diseases like HIV, Influenza, and other viral
diseases (14).
On June 3, 2021, I wrote an Open Letter to the U.S. Intelligence and Scientific
Communities entitled; “COVID-19 is a Covert CCR5 Gene Silencing Experiment using a
Genetically Engineered Virus Containing Decoy Parts “. This letter was sent to several U.S.
government departments and officials including the Senate Select Committee on Intelligence,
the Office of the Intelligence Community Inspector General, House Representatives Ihan Omar
and Abigail Spanberger and Senators Mitch McConnell and Rand Paul. In this letter, I
summarized my previous research and encouraged an investigation into the origins of SARS-
CoV-2 using said research. I specifically called for an investigation into gain-of-function
research involving bacteriophages of NTHi and coronaviruses done within the U.S. and abroad;
Peter Daszak / EcoHealth Alliance and his research partners / associates, Bill Gates, the
Wuhan Institute of Virology, and the National Institutes of Health concerning research on NTHi,
CCR5 Silencing, CRISPR-Cas9 technologies, HIV/AIDS research, P6, Influenza, and HIV
vaccine development, genetic drug therapies, etc., all experiments involved in the creation of
Harvard University’s patent number # 10745677. Further, I expressed urgency in the
performance of this investigation as COVID-19 is a biological warfare event committed against
all of humanity and is a blatant violation of informed consent (15).
In this paper I will briefly address my most recent research findings on SARS-Cov-2
which points to its genetically engineered design using the Spanish patent and other research
performed by Luis Enjuanes and his colleagues around the world.
3. Embedding SARS-CoV-2 into the Backbone of Bacteriophage HP2: A Pathway to
Gene Manipulation
As previously mentioned, the Spanish patent details methods for using defective
interfering (DI) genomes of coronaviruses might act as a vector for gene therapy with the use of
a helper virus for replication and or translation. In my book; “Informed Consent: Exposing the
Eugenics Cult and Their Latest Experiment on Mankind: COVID-19” (10), I detailed how SARS-
CoV-2 was a genetically engineered coronavirus using bacteriophage HP2 of Hemophilus
influenza, designed to carry out a covert gene editing procedure, specifically, a CCR5 loss-of-
function experiment. It has been long established that genomes of phage P2 and of P2-related
phages can serve as helper viruses especially once they become prophages (16). A study of
bacteriophage HP2 of Haemophilus influenza has demonstrated the ability of prophages to
inhibit gene expression (17). I have already detailed in my book how mRNA vaccines are able
to disguise prophage inducing chemicals as seemingly harmless ingredients (i.e., salts, chloride,
lipids). Recent research has discovered that SARS-CoV-2’s general mode of action is as a co-
receptor dependent phagocyte, a type of cell capable of encompassing and digesting bacteria
(18).
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4. COVID-19 is a Covert Gene Editing Experiment
a. The Experiment Pt. 1: Gene Targeting via Pro-Inflammatory Cytokines
As previously mentioned, viral tropism deals with a virus’s propensity for a specific cell type,
tissue, or species. Viral tropism can be dictated via pro-inflammatory cytokines (19). In my
paper; “COVID-19: The Plague that Strikes Behind the Ear”, I described how viral infections in
patients colonized with high concentrations of NTHI may be at risk as specific viruses like
SARS-CoV-2, on top of a bacterial infection may significantly enhance the risk for excessive
inflammation. Much like Human herpesvirus 8 (HHV-8), HIV, and AIDS, NTHI can inhibit the
hosts epithelial defense proteins. Once compromised, airway epithelial cells respond to the
invasion of NTHI by secreting pro-inflammatory acute phase reactants such as IL-6, IL-8, and
TNF-ą (20-22). NTHI then increases the expression of ICAM-1 by airway epithelial cells which
increases the susceptibility of viruses binding to the cells, a common method used by
rhinoviruses for cellular entry (23).
In a gene editing experiment, viral tropism is essential as a coronavirus vector can be
engineered to a particular genetic sequence/(s) guided by specific pro-inflammatory reactants.
In the Spanish patent, the use of immunostimulant cytokines such as TNF-ą, INF-g, IL-2, IL-12,
or IL-18 is recommended to overcome the host’s barriers designed to restrict viral tropism (3). It
should be noted that such a manipulated virus will ultimately yield a highly dangerous
bioweapon.
In a 2015 study, NTHI lysates were used to identify bacterial proteins and their biological
effects. It was found that the most common and highly concentrated proteins found in NTHI
lysates either contributed to biofilm formation (HMW 2A and HMW 1A), elude the innate immune
system (IgA), or activate epithelial pro-inflammatory pathways such as Toll Like Receptor (TLR-
2) signaling and NF-kB transcription factor which are mediated by outer membrane proteins
(OMP5, OMP1, OMP26, OMP6 and OMP2) (24). It is important to note that OMP6 has long
been studied as a potential vaccine antigen (25).
b. The Experiment Pt. 2: Gene Silencing via NTHI Exosome Release in Middle Ear
Exosomes are small vesicles that are involved in genetic signaling between cells. These
vesicles contain proteins and nucleic acids such as mRNAs, microRNAs (miRNAs) or
noncoding RNAs which can regulate gene function (26). In a 2018 experiment, scientists used
NTHI lysate treatments on human middle ear epithelial cell (HMEEC) lines to analyze protein
secretions. It was found that several heterogenous nuclear ribonucleoproteins (hnRNPs)
including hnRNP A2B1 and hnRNP Q were regulated by the NTHI lysates. These hnRNPs are
both involved in miRNA packing in exosomes. It is important to note that miRNAs are involved
in RNA silencing and post-transcriptional regulation of gene expression (27). According to the
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Spanish patent (3), a coronavirus as a vector for gene therapy would require 1) a coronavirus
genome, 2) the presence of a helper virus (bacteriophage HP2 of NTHI), 3) virus assembly in a
BAC, and 4) the construction of a full-length cDNA clone which could be performed using
hnRPQ CRISPR Activation Plasmid (h) cDNA encoding the human SYNCRIP gene (28-29).
Data has shown that expression levels of hnRNP Q influence HIV-1 replication (30).
c. The Experiment Pt. 3: Delivery of Lysates: CCR5 Loss-of-Function via Harvard
Patent #10745677
This matter has been previously discussed in my book; “Informed Consent: Exposing the
Eugenics Cult and Their Latest Experiment on Mankind: COVID-19” (10), for brevity I will
summarize the main points.
Scientists at Harvard University developed methods and chemical compositions which can
cause a “loss-of-function” to the CCR5 co-receptor in humans. One of these systems suggest
the use of the CRISPR-Cas9 gene editing tool to cause a loss-of-function to CCR5 via mutation.
According to the researchers, this may be accomplished by introducing the CRISPR-Cas9
system via mRNA virus particles. Further, to promote effective gene targeting, they also
suggest combining LtxA, the GAM protein of the bacteriophage Mu, which is the endotoxin of
NTHI along with a mRNA fusion. This combination would effectively become a NTHI lysate,
promoting exosome release thereby initiating the gene editing procedure once a host becomes
infected with SARS-CoV-2. It is important to note that translation can be delayed through
modifying a sequence in the mRNA of the coronavirus vector. Essentially, the mRNA can carry
a message to “delay” translation until certain conditions are met such as the administration of
mRNA vaccines.
In this scenario, LtxA would increase the infectivity of CD4 T-cells which would grant the
coronavirus vector, SARS-CoV-2 more access to CCR5 co-receptors for editing. LxtA is also
secreted as part of the immune response which would act to facilitate effective Homology
Directed Repair (HDR) through its ability to bind to the double strand breaks thereby protecting
against the degradation of the DNA in the places where the edits are made (12).
d. The Experiment Pt. 4: mRNA Vaccines
Current mRNA vaccines facilitate the delivery of sodium, sugars, phosphates, and chloride
which might be necessary components to activate Cas9. Vaccines also deliver mRNA which
causes the process of translation. The PFIZER-BIONTECH Covid-19 vaccine includes “dibasic
sodium phosphate dihydrate” which is the radioactive form of sodium phosphate (31). In a 1952
research paper entitled; “Independent functions of viral protein and nucleic acid in growth of
bacteriophage”, scientists observed that radioactive phosphorus entered the bacterium
increasing the replication rate of the virus giving it more control over the protein making
functions of the cells (32).
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Additionally, the cell wall of Gram-negative bacteria such as NTHI consists mainly of
Lipopolysaccharides (LPS), an endotoxin which is released when the cell wall of dead bacteria
is broken down. LPS consists of polysaccharides and lipid A. Lipid A is responsible for the
toxic properties that make any invasive Gram-negative infection a potentially serious medical
emergency. To circumvent this, some COVID-19 vaccines, might have been intentionally
designed to act as a mechanism to deliver lipids to the bacterium to prevent NTHI from
completely dying so that it can continue to function normally and produce genetic material.
This would allow SARS-CoV-2 genetic material to replicate within NTHIs’ genome giving it the
ability to 1) control gene expression by stimulating the lytic cycle; 2) control transcription; and 3)
control the translation process. The lipid content of certain COVID-19 vaccines might also serve
as part of the density-gradient centrifugation allowing rapid sediment of mRNA as NTHI has an
asymmetric arrangement of phospholipids.
These topics have previously been covered in detail in my book; “Informed Consent: Exposing
the Eugenics Cult and Their Latest Experiment on Mankind: COVID-19” (10).
It is important to note that currently, Luis Enjuanes and his colleagues at the National Centre for
Biotechnology are developing the world’s first intranasal vaccine for COVID-19 set to be
released in 2022 (33). The creation an intranasal vaccine is logical as NTHI colonizes the ear,
nose, and throat areas of almost 80% of the world’s population which would allow for a very
direct mode of delivery. It is also important to note that also in 2006, Spanish National
Research Council was issued another patent entitled; “Vaccine Against Severe Acute
Respiratory Syndrome Causing Coronavirus (SARS-COV). Luis Enjuanes was listed as one of
the inventors (34).
5. Concluding Remarks
The COVID-19 pandemic is biological terrorism event against all of humanity. It is a gene
editing experiment whereby majority of the participants (humans) are involuntary test subjects
due to the intentional release of SARS-CoV-2. SARS-CoV-2 is a genetically engineered SARS-
CoV vector which has been embedded in the backbone of HP2 using methods from Spanish
patent no.: WO 2006/136448 and Harvard University patent no.: 10745677. The purpose of
COVID-19 is to perform a covert CCR5 gene silencing experiment, in vivo.
Further, COVID-19 is a mass genocide attempt targeting persons of African descent, Hispanics,
Native Americans, Asians, and Middle Eastern persons. It is also a population control effort
targeting the world’s poorest residents including those in Africa, India, and South America. The
risk and side effects of this experiment include mild-to-severe reactions to SARS-CoV-2 virus
particles which may result in long term disease, permanent disability, and death. It can also
cause irreversible changes to your DNA and ultimately the DNA of unborn offspring. Further,
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off-target editing might result in unintended chromosomal changes and ultimately birth defects in
the next generation.
To date roughly 4 million people have died from COVID-19. It is time for the perpetrators to
be identified and held accountable for their evil actions towards humanity. Individuals within
world governments, academic institutions, the medical and scientific communities, business
world, who have planned, facilitated, and/or helped in the cover-up of the origin of SARS-CoV-2
and the purpose for COVID-19 should be publicly identified and held accountable for their
crimes which includes blatant violations of informed consent.
References:
1. Luis Enjuanes ORCID https://orcid.org/0000-0002-0854-0226
2. Statement in support of the scientists, public health professionals, and medical professionals of China
combatting COVID-19. Authors: Charles Calisher,Dennis Carroll,Rita Colwell,Ronald B Corley,Peter
Daszak,Christian Drosten,Luis Enjuanes,Jeremy Farrar,Hume Field,Josie Golding,Alexander
Gorbalenya,Bart Haagmans,James M Hughes,William B Karesh,Gerald T Keusch,Sai Kit Lam et al.
Publication: The Lancet. Publisher: Elsevier. Date: 7–13 March 2020. https://doi.org/10.1016/S0140-
6736(20)30418-9
3. Enjuanes, L.S., Lopes, M.D., Alvarez, E.G., and Almazan, F.T. (2006). Attenuated SARS and Use as a
Vaccine. Spain. Patent No: WO 2006/136448, WIPO.
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2006136448
4. Almazán F, Sola I, Zuñiga S, Marquez-Jurado S, Morales L, Becares M, Enjuanes L. Coronavirus reverse
genetic systems: infectious clones and replicons. Virus Res. 2014 Aug 30;189:262-70. doi:
10.1016/j.virusres.2014.05.026. Epub 2014 Jun 12. PMID: 24930446; PMCID: PMC4727449.
5. Almazán F., Márquez-Jurado S., Nogales A., Enjuanes L. (2015) Engineering Infectious cDNAs of
Coronavirus as Bacterial Artificial Chromosomes. In: Maier H., Bickerton E., Britton P. (eds) Coronaviruses.
Methods in Molecular Biology, vol 1282. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-
2438-7_13
6. Enjuanes, L et al. “Coronavirus derived expression systems.” Journal of biotechnology vol. 88,3 (2001): 183-
204. doi:10.1016/s0168-1656(01)00281-4
7. Ou, X., Liu, Y., Lei, X. et al. Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its
immune cross-reactivity with SARS-CoV. Nat Commun 11, 1620 (2020). https://doi.org/10.1038/s41467-
020-15562-9
8. Nizamudeen, Zubair Ahmed et al. “Structural assessment of SARS-CoV2 accessory protein ORF7a predicts
LFA-1 and Mac-1 binding potential.” Bioscience reports vol. 41,1 (2021): BSR20203837.
doi:10.1042/BSR20203837
9. Taliah S. Muhammad. (2021). COVID-19: That Plague that Strikes Behind the Ear.
http://doi.org/10.5281/zenodo.4896389
10. Taliah S. Muhammad. (2021). Informed Consent Exposing the Eugenics Cult & Their Latest Experiment on
Mankind: COVID-19. Zenodo. http://doi.org/10.5281/zenodo.4876338
11. Barenkamp SJ, St Geme JW 3rd. Genes encoding high-molecular-weight adhesion proteins of nontypeable
Haemophilus influenzae are part of gene clusters. Infect Immun. 1994 Aug;62(8):3320-8. doi:
10.1128/iai.62.8.3320-3328.1994. PMID: 8039903; PMCID: PMC302962.
12. “Editing of CCR5 receptor gene to protect against HIV infection”. Juan Pablo Maianti and David R. Lui.
Harvard University (Assignee). Patent No.: 10745677. U.S. Patent and Trademark Office.
https://patents.justia.com/patent/10745677
13. Jones, K., Patel, N., Levy, M. et al. Global trends in emerging infectious diseases. Nature 451, 990–993
(2008). https://doi.org/10.1038/nature06536
9
14. Mehlotra, Rajeev K. “Chemokine receptor gene polymorphisms and COVID-19: Could knowledge gained
from HIV/AIDS be important?.” Infection, genetics and evolution : journal of molecular epidemiology and
evolutionary genetics in infectious diseases vol. 85 (2020): 104512. doi:10.1016/j.meegid.2020.104512
15. Taliah S. Muhammad. (2021, June 3). COVID-19 is a Covert CCR5 Gene Silencing Experiment using a
Genetically Engineered Virus Containing Decoy Parts. Zenodo. http://doi.org/10.5281/zenodo.4897109
16. Erich W. Six, Carol A.Connelly Klug. “Bacteriophage P4: a satellite virus depending on a helper such as
prophage P2”. Virology, Volume 51, Issue 2,1973, Pages 327-344, ISSN 0042-6822,
https://doi.org/10.1016/0042-6822(73)90432-7
17. Williams, Bryan J et al. “Bacteriophage HP2 of Haemophilus influenzae.” Journal of bacteriology vol. 184,24
(2002): 6893-905. doi:10.1128/JB.184.24.6893-6905.2002
18. Birger Sørensen, Angus Dalgleish & Andres Susrud. The Evidence which Suggests that This Is No
Naturally Evolved Virus A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike. (2020)
https://www.minervanett.no/angus-dalgleish-birger-sorensen-coronavirus/the-evidence-which-suggests-that-
this-is-no-naturally-evolved-virus/362529
19. McFadden G, Mohamed MR, Rahman MM, Bartee E. Cytokine determinants of viral tropism. Nat Rev
Immunol. 2009 Sep;9(9):645-55. doi: 10.1038/nri2623. Epub 2009 Aug 21. PMID: 19696766; PMCID:
PMC4373421.
20. Jono, H., and T. Shuto. “Transforming growth factor B-Smad signaling pathway cooperates with NF-kB to
mediate nontypeable Haemophilus influenzae-induced MUC2 mucin transcription.” Journal of Biological
Chemistry,, vol. 277, no. 47, 2002, pp. 44547-45557.
21. Khair, O. A., et al. “Bacterial induced release of inflammatory mediators by bronchial epithelial cells.”
European Respiratory Journal, vol. 9, no. 9, 1996, pp. 1913-1922. 32. Dupin, Nicolas, et al. Distribution of
human herpesvirus-8 latently infected cells in Kaposi’s sarcoma, multicentric Castleman’s disease, and
primary effusion lymphoma. Proceedings of the National Academy of Sciences Apr 1999, 96 (8) 4546-4551;
DOI: 10.1073/pnas.96.8.4546.
22. Mackow ER, Gavrilovskaya IN. Hantavirus regulation of endothelial cell functions. Thromb Haemost. 2009
Dec;102(6):1030-41. doi: 10.1160/TH09-09-0640. PMID: 19967132.
23. Sajjan, U. S., et al. “H. influenzae potentiates airway epithelial cell responses to rhinovirus by increasing
ICAM-1 and TLR3 expression.” FASEB J., vol. 20, 2006, pp. 2121-2123
24. Preciado D, Poley M, Tsai S, Tomney A, Brown K, Val S. A proteomic characterization of NTHi lysates. Int J
Pediatr Otorhinolaryngol. 2016 Jan;80:8-16. doi: 10.1016/j.ijporl.2015.11.016. Epub 2015 Nov 24. PMID:
26746604; PMCID: PMC4706994.
25. Centers for Disease Control. Recommendations for Use of Haemophilus b Conjugate Vaccines and a
Combined Diphtheria, Tetanus, Pertussis, and Haemophilus b Vaccine Recommendations of the Advisory
Committee on Immunization Practices (ACIP). MMRW September 17, 1993 / 42(RR-13).
https://www.cdc.gov/mmwr/preview/mmwrhtml/00023705.htm
26. Edgar, J.R. Q&A: What are exosomes, exactly?. BMC Biol 14, 46 (2016). https://doi.org/10.1186/s12915-
016-0268-z
27. Isabel Sola, Pedro A. Mateos-Gomez, Fernando Almazan, Sonia Zuñiga & Luis Enjuanes (2011) RNA-RNA
and RNA-protein interactions in coronavirus replication and transcription, RNA Biology, 8:2, 237-248, DOI:
10.4161/rna.8.2.14991 https://www.tandfonline.com/doi/full/10.4161/rna.8.2.14991
28. Val, Stéphanie et al. “Nontypeable Haemophilus influenzae lysates increase heterogeneous nuclear
ribonucleoprotein secretion and exosome release in human middle-ear epithelial cells.” FASEB journal :
official publication of the Federation of American Societies for Experimental Biology vol. 32,4 (2018): 1855-
1867. doi:10.1096/fj.201700248RR
29. Example of hnRNP Q CRISPR Activation Plasmid (h) cDNA: https://www.labome.com/product/Santa-Cruz-
Biotechnology/sc-402869-ACT.html
30. Hadian K, Vincendeau M, Mäusbacher N, Nagel D, Hauck SM, Ueffing M, Loyter A, Werner T, Wolff H,
Brack-Werner R. Identification of a heterogeneous nuclear ribonucleoprotein-recognition region in the HIV
Rev protein. J Biol Chem. 2009 Nov 27;284(48):33384-91. doi: 10.1074/jbc.M109.021659. Epub 2009 Oct 5.
PMID: 19808671; PMCID: PMC2785182.
31. “Pfizer-BioNTech COVID-19 Vaccine EUA Fact Sheet for Recipients and Caregivers.” Centers for Disease
Control. Access Date: 30, April, 2021.
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32. HERSHEY, A D, and M CHASE. “Independent functions of viral protein and nucleic acid in growth of
bacteriophage.” The Journal of general physiology vol. 36,1 (1952): 39-56. doi:10.1085/jgp.36.1.39
33. Interview with Luis Enjuanes. Indrastra. Accessed 6/2/21. https://www.indrastra.com/2021/06/interview-
with-virologist-luis-enjuanes.html
34. Enjuanes, L.S., Alvarez, E.G. (2006). Vaccine Against Severe Acute Respiratory Syndrome Causing
Coronavirus (SARS-COV). Spain. Patent No: WO 2006/024543, WIPO.
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2006024543
