University of North Carolina at Chapel Hill — On November 10, 2015 researchers funded by the NIH, the National Natural Science Foundation of China, and EcoHealth Alliance at the University of North Carolina at Chapell Hill discovered a new bat SARS-like virus that can jump directly from it’s bat host to a human without any mutation.
(1) *White Paper: New SARS-like virus can jump directly from bats to humans, no treatment available (2015)
(2) White paper: A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence. (2015)
(3) White paper: SARS-like WIV1-CoV poised for human emergence (2015)
(4) White Paper: Synthetic recombinant bat SARS-like coronavirusis infectious in cultured cells and in mice (2008)
(5) White Paper: Novel SARS-like Betacoronaviruses in Bats, China, 2011 (2011)
(6) White Paper: SARS-like cluster of circulating bat coronavirus pose threat for human emergence (2015)
(7) White paper: Detection of a novel human coronavirus by real-time reverse-transcription polymerase chain reaction. (2012)
(8) White paper: Coronavirus diversity, phylogeny and interspecies jumping. (2009)
(9) White paper: The SARS-like coronaviruses: the role of bats and evolutionary relationships with SARS coronavirus. (2012)
(10) White paper: Molecular diversity of coronaviruses in bats. (2006)
(11) White paper: Bats are natural reservoirs of SARS-like coronaviruses. (2005)
(12) White paper: Complete genome sequence of bat coronavirus HKU2 from Chinese horseshoe bats revealed a much smaller spike gene with a different evolutionary lineage from the rest of the genome. (2007)
(13) White paper: Recent transmission of a novel alphacoronavirus, bat coronavirus HKU10, from Leschenault’s rousettes to pomona leaf-nosed bats: first evidence of interspecies transmission of coronavirus between bats of different suborders. (2012)
(14) White paper: Virome analysis for identification of novel mammalian viruses in bat species from Chinese provinces. (2012)
(15) White paper: ProMEDmail. Novel coronavirus—Saudi Arabia: new case. ProMED-mail 2012. Nov 04 [cited 2012 Nov 4]. http://www.promedmail.org/, article no. 20121104.1391285.
(16) White paper: Human Coronavirus EMC Does Not Require the SARS-Coronavirus Receptor and Maintains Broad Replicative Capability in Mammalian Cell Lines (2012)
(17) White paper: Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia. (2012)
(18) White paper: Identification of a novel coronavirus in patients with severe acute respiratory syndrome. (2003)
(19) White paper: The severe acute respiratory syndrome. (2003)
In case you missed it… Biological warfare expert and international law professor Dr. Frances Boyle, creator of the Biological Weapons Anti-Terrorism Act of 1989, interviews with Alex Jones of Infowars (2-21-2020): Full Transcript of “Smoking Gun” Bombshell Interview: Prof. Frances Boyle Exposes the Bioweapons Origins of the CoVid-19 Coronavirus. “The smoking gun is that the Wuhan coronavirus came out of that BSL-4 facility.. And the smoking gun here is on page 11, near the bottom, the last full paragraph from the bottom where it says, “may provide a gain of function to coronavirus for efficient spreading in the human population.” This is clearly an offensive biological warfare agent and it has no legitimate medical or other– “
Publisher’s note: Government’s around the world would not be in a state of panic as they are if they did not have foreknowledge of the fact that CoVid—19 is a government-sponsored biological weapon which was covertly and intentionally spread to world leaders throughout the civilized world. The incompetence of government is only surpassed by it’s competence for stopping the defense of our civil liberties and attacking the very foundations of our liberty by illegally constructing, and faithfully releasing, narrowly indefensible weapons-systems designed to kill us all. Why is anyone allowed to experiment with biological warfare? None of these dangerous and unconstitutional pursuits have anything at all to do with our American Republic and the civil liberty which all individuals of the world deserve to have defended.
Researchers specifically thanked C.T. Tseng, PhD Professor, Department of Microbiology & Immunology Centers for Biodefense and Emerging Diseases at The University of Texas Medical Branch, with degrees from Taiwan (1976) and the U.S. (1981, 1997); and, M.T. Ferris (Department of Genetics, University of North Carolina).
Is it really any surprise, the nature of the work, considering the personalities U.T. collects as faculty? Consider Professor Eric Pianka and His receiving a standing ovation for calling for a mass-murder of the human population from The Texas Academy of Science. The futurity of our world is in a war for it’s life against the devices of sick people.
Have a gander at C.T. Tseng’s UTMB Health profile for amplified clarity.
Chien-Te (Kent) Tseng, PhD
Department of Microbiology & Immunology
Centers for Biodefense and Emerging Diseases
Phone: (409) 747-0789
Fax: (409) 747-0762
Education: PhD, 1997, University of Arkansas for Medical Sciences
MS, 1981, Mississippi State University
BS, 1976, National Chung-Hsing University, Tai-chung, Taiwan
Overview: Host innate immunity to and the pathogenesis of emerging and reemerging RNA viral infections (SARS, RVF, and Avian Influenza), Virology and viral immunology – Ebola virus; Rift Valley Fever; Hantavirus; Nipah virus; Hepatitis C
1. Pathogenesis of emerging and reemerging RNA viruses
2. Innate antiviral signaling pathways against viral infections
3. Immune evasion of RNA viruses
4. Cytokines and inflammation
5. Antivirals and vaccine strategies against RNA virusses of host innate immunity
My primary research is focused on understanding how RNA viruses trigger the host immune responses and how animals defend against emerging and reemerging viruses. Specifically, we study the molecular and cellular interplays whereby the innate immune responses are initiated and regulated and how an unregulated innate immunity leads to diseases and mortality. We are particularly interested in dissecting the antiviral signaling pathways by which pathologically relevant host cells mount innate immune responses to invading viruses. We are also interested in how viruses evade the host defense system. The ultimate goal of our studies is to understand and identify novel molecules of the innate immune system as targets for preventive and therapeutic intervention against RNA viral infections.
RNA virus infection is detected by the host cells through either toll-like receptor (TLR)-3 and -7/8, which are located primarily on the endosomal membrane, or, the cytosolic, RNA helicase proteins RIG-I (retinoic acid-inducible gene I) and MDA-5 (melanoma differentiation antigen 5), which transmitting activation signals to the cytosolic adaptor TRIF, MyD88, and MAVS/IPS, respectively, that ultimately leads the activation of an array of antiviral genes, including type I interferons (IFNs), inflammatory cytokines and chemokines, and many interferon-stimulated genes (ISGs), via at least three overlapping antiviral pathways mediated by transcription factors NFÎºB, interferon regulatory factor-3 (IRF-3), and ATF2/cJUN intermediate signaling molecules. Among various RNA viruses, we are currently focusing on dissecting the antiviral signaling pathways induced by severe acute respiratory syndrome coronavirus (SARS-CoV, a BSL-3 pathogen), Rift Valley Fever virus (RVFV, a BSL-3+ pathogen), Junin virus (JV, a BSL-4 pathogen), Dhori virus, a tick-born Orthomyxovirus, which is a BSL-2 pathogen sharing a strikingly similar pathogenetic mechanism with avian influenza H5N1 virus in mice. To ensure the success of our studies, we adopt a two-stage strategy for the proposed studies. Specifically, we first perform in vitro studies using virally permissive and pathologically relevant human cells, including lung epithelial cells (SARS, Dhori virus), human umbilical vascular endothelial cells (HUVEC) and hepatocytes (RVF, Dhori), along with two of the most implicated classic innate immune cells, e.g., primary human macrophages and dendritic cells (RVFV and JV). Once specific signaling pathway(s) and cellular targets are identified, we will use suitable animal models for the verification purpose. In this regard, experimental infection of mice has been used successfully as animal models. Particularly, we have been using transgenic mice expressing hACE2 (human angiotensin-converting enzyme 2), the receptor for SARS-CoV, as the animal model for SARS-CoV. We also use mouse-adapted SARS-CoV, designated MA-15, to infect wild type and various strains of selected gene knockout (KO) mice, aiming at dissecting the mechanism of host innate immunity against SARS-CoV and/or immune-mediated diseases. Various state-of-art approaches involving virology, immunology, biochemistry, molecular biology, and genetics are used to establish and characterize cell lines/clones with specific gene KO or knock down (KD) (i.e., loss-of-function) or constitutive expression (i.e., gain-of-function) phenotypes, and identify the role(s) of selected genes in the host antiviral defense. We are also interested in evaluating the impact of the cellular interplays on the pathogenesis of viruses in vitro, via using two- and/or three-dimensional culture systems. Our research is currently supported in part by grants and contracts from the National Institutes of Health, and other Pharmaceutical industries.
Martin Ferris, PhD
Assistant Professor, Genetics
(919) 966-4026 (Office Phone)
5081 Genetic Medicine Building
Chapel Hill, NC
Martin Ferris, PhD states about one of His published works: “These papers really complement each other. We were able to discover sets of genes driving severe disease following either SARS or West Nile virus..” (https://www.med.unc.edu/genetics/taking-stock-of-the-collaborative-cross/)
Original findings allowed the researchers to express uncertainty toward the ability of the virus to jump from human to human though common sense tells me that a virus jumping from host to host without any mutation will experience no interruption of it’s viability as it moves and replicates from and within one human host and into another; and, with China now censoring CoronaVirus critics in the U.S. it is more important than ever to discuss the origins of what is absolutely not a natural occurrence and is unabashedly a conserted effort, by whom is right now a mystery though investigations are active, to (1) spread a lab-made biological weapon, (2) militarization and global martial law by consent or force (3) quell pro-independence protestors in Honk Kong (near-perfect prediction), (4) use sophisticated algorithms, data centers, and unconstitutional law to control narratives and suppress debate, (5) forcing a cashless society, and (6) causing total economic collapse.
Twitter took action against David A .Clarke, the former sheriff of Milwaukee County, after he encouraged Americans to defy restrictions being imposed due to the ongoing coronavirus pandemic.
“TAKE…TO …THE…STREETS,” Mr. Clarke wrote in another tweet no longer available on Twitter. “I will no longer sit back and watch the destruction of this great republic
An Iranian General, Brigadier General Gholam Reza Jalali, is openly stating CoronaVirus is a manmade bio-weapon.
Iran’s Supreme Leader is also stating CoronaVirus is a biological weapon:
Even the creator of the Biological Weapons Anti-Terrorism Act of 1989 stated the CoronaVirus is a Biological Warfare Weapon. A man with these type of credentials ought to have His words finely examined and magnified by academics and the media. What reasons specifically does He think this to be the case? The full transcript of His interview with Infowars: full Dr. Frances Boyle interview transcript.
As Mike Adams of Natural News points out:
That paper describes the CoVid-19 novel coronavirus as possessing unique “gain-of-function” properties that make it the perfect bioweapon, while confirming these new properties were from artificial origins, not natural viral evolution. (In other words, it was engineered.)Mike Adams, 2020, https://www.naturalnews.com/2020-02-19-covid-19-coronavirus-found-to-contain-gain-of-function-for-efficient-spreading-human-population.html
Follow https://www.infowars.com for developing information.