the sudden/hasty step-up in gain-of-function r and d

February 26, 2023 - S.D. Wells From LAB to LUNGS: The real COVID timeline in a nutshell (Natural News) . Here’s where it all began, and how we got to where we are today. December, 2004: Liver damage from SARS vaccine documented. Lab animals (ferrets) vaccinated with rMVA-S and then exposed to SARS-CoV suffered liver damage from elevated levels of a specific enzyme, as discovered by researchers in Canada 16 years before the Wuhan virus was released from labs in China. Canadian researchers were developing a vaccine for SARS and started testing it on ferrets in laboratories, as reported in the Journal of Virology, when they found hepatitis in the ferrets and began urging extreme caution for other investigators working on SARS vaccines. Virus Mania: How the Medical Industry Continually Invents Epidemics, Making Billion-Dollar Profits At Our Expense Paperback – September 19, 2007 by Torsten Engelbrecht (Author), Claus Köhnlein (Contributor) A daily scan through the news gives the impression that the world is constantly invaded by virus epidemics. The latest headlines feature the human papillomavirus (HPV) alleged to cause cervical cancer and the avian flu virus, H5N1. The public is also continually terrorized by reports about SARS, BSE, hepatitis C, AIDS, Ebola and polio. However, this virus mayhem ignores very basic scientific facts: the existence, the pathogenicity and deadly effects of these agents have never been proven. The authors of Virus Mania, journalist Torsten Engelbrecht and doctor of internal medicine Claus Köhnlein, show that these alleged contagious agents are, in fact, particles produced by the cells themselves as a consequence of certain stress factors such as drugs, malnutrition, pesticides and heavy metals. The central aim of this book is to steer the discussion back to a real scientific debate and put medicine back on the path of an impartial analysis of the facts. It will put medical experiments, clinical trials, statistics and government policies under the microscope, revealing that the people charged with protecting our health and safety have deviated from this path. To substantiate these statements the authors cite dozens of highly renowned scientists and present approximately 1,100 pertinent scientific references. The topic of this book is of pivotal significance. The pharmaceutical companies and top scientists rake in enormous sums of money by attacking germs and the media boosts its audience ratings and circulations with sensationalized reporting (the coverage of the New York Times and Der Spiegel are specifically analyzed). "The primary purpose of commercially-funded clinical research is to maximize financial return on investment, not health," says John Abramson of Harvard Medical School. Virus Mania will inform you on how such an environment took root-and how to empower yourself for a healthy life. https://www.amazon.com/Virus-Mania-Continually-Epidemics-Billion-Dollar/dp/1425114679 ………………… September 2010: The year was 2010, and Bill Gates said the quiet part out loud, at a TED conference, explaining how the world population could be reduced by several billion people if we … “do a really great job on new vaccines, healthcare, and reproductive services…” and by healthcare and reproductive services, he meant abortions, and by vaccines he meant instead of just causing extreme allergies, asthma, and autism, that NEW vaccines literally exterminate people, as the Covid clot shots do now by sending millions of spike proteins into vital organs, while clogging up the vascular system, causing turbo cancer and heart attacks. Bill Gates planned it all: How to depopulate the planet with abortions and “new vaccines” – listen to him speak on planned genocide at TED talks. November 2015: • Viruses that are related to SARS and that are found in some species of bats could become a source of future human outbreaks, ]according to a new study (some of which is shown below) released Monday. And it appears that there are fewer barriers to that spillover than scientists initially thought…. The UNC scientists wanted to see if cousin viruses — coronaviruses that are carried by Chinese horseshoe bats — also posed a threat to people. They used one, SHC014, as a representative of the group. They inserted a key part of the virus, its spike protein, into a SARS virus and then ran experiments to see if the hybrid virus could infect human respiratory tract cells (in a dish) and mice that were vulnerable to the SARS virus. It did. “I think the existence of viruses that can jump directly is the important part, that was unanticipated,” lead author Vineet Menachery, who researches viral immunology, told STAT in an interview. “Based on what was known in the literature, we would have expected that viruses coming out of bats would have needed that one-in-million mutation.” Another coronavirus expert, Dr. Stanley Perlman at the University of Iowa, suggested the paper was a useful investigation. But he noted the hybrid virus was attenuated — weakened — and said the virus would probably need to adapt more in people before it could spread widely. SARS wasn’t a highly transmissible virus. Many patients didn’t infect anyone else during the 2003 outbreak. Once hospitals learned how to recognize the disease and put stringent infection control measures in place — isolating patients and requiring staff treating them to wear the right protective equipment — the outbreak was contained. The SHC014 virus is part of a cluster of related coronaviruses, explained senior author Ralph Baric, a professor of epidemiology at UNC. Some are quite similar to the SARS virus while others are more distant relatives, varying in terms of their genetic structures by between 5 percent and 60 percent. SHC014 was about 12 percent different from SARS. A coronavirus expert, Baric said if the viruses were too distantly related to SARS — more than 25 percent different — they would not be able to make a hybrid that would infect human cells. “Not all SARS-like coronaviruses have the inherent potential to replicate in mammalian cells and replicate in human cells.” And being able to do something in the artificial confines of a laboratory does not guarantee it will happen in nature. For a bat virus to start infecting people, the bat would have to come into contact with people in a way that would allow transmission. Even if a single person became infected, the virus would have to work efficiently in human cells, producing lots of copies of itself that could be coughed or sneezed out toward the airways of other people. “There are a lot of steps down this road,” Menachery said. “SHC014 has taken a step ahead. But there’s still a lot of other factors that are involved.” -Helen Branswell Senior Writer, Infectious Diseases] ………………………….. January, 2018: Fauci steers massive funding to Wuhan lab’s “gain of function” coronavirus research so a bat disease can spread to humans (and it works) …https://www.naturalnews.com/2023-02-26-lab-to-lungs-real-covid-timeline-in-a-nutshell.html …………………………. • Download PDF Published: 09 November 2015 A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence Vineet D Menachery, Boyd L Yount Jr, Kari Debbink, Sudhakar Agnihothram, Lisa E Gralinski, Jessica A Plante, Rachel L Graham, Trevor Scobey, Xing-Yi Ge, Eric F Donaldson, Scott H Randell, Antonio Lanzavecchia, Wayne A Marasco, Zhengli-Li Shi & Ralph S Baric  Nature Medicine volume 21, pages 1508–1513 (2015) 2.78m Accesses Abstract The emergence of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome (MERS)-CoV underscores the threat of cross-species transmission events leading to outbreaks in humans. Here we examine the disease potential of a SARS-like virus, SHC014-CoV, which is currently circulating in Chinese horseshoe bat populations1. Using the SARS-CoV reverse genetics system2, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone. The results indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV. Additionally in vivo experiments demonstrate replication of the chimeric virus in mouse lung with notable pathogenesis. Evaluation of available SARS-based immune-therapeutic and prophylactic modalities revealed poor efficacy; both monoclonal antibody and vaccine approaches failed to neutralize and protect from infection with CoVs using the novel spike protein. On the basis of these findings we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo. Our work suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating in bat populations. Main The emergence of SARS-CoV heralded a new era in the cross-species transmission of severe respiratory illness with globalization leading to rapid spread around the world and massive economic impact3,4. Since then, several strains—including influenza A strains H5N1, H1N1 and H7N9 and MERS-CoV—have emerged from animal populations, causing considerable disease, mortality and economic hardship for the afflicted regions5. Although public health measures were able to stop the SARS-CoV outbreak4, recent metagenomics studies have identified sequences of closely related SARS-like viruses circulating in Chinese bat populations that may pose a future threat1,6. However, sequence data alone provides minimal insights to identify and prepare for future prepandemic viruses. Therefore, to examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs, we built a chimeric virus encoding a novel, zoonotic CoV spike protein—from the RsSHC014-CoV sequence that was isolated from Chinese horseshoe bats1—in the context of the SARS-CoV mouse-adapted backbone. The hybrid virus allowed us to evaluate the ability of the novel spike protein to cause disease independently of other necessary adaptive mutations in its natural backbone. Using this approach, we characterized CoV infection mediated by the SHC014 spike protein in primary human airway cells and in vivo, and tested the efficacy of available immune therapeutics against SHC014-CoV. Together the strategy translates metagenomics data to help predict and prepare for future emergent viruses. The sequences of SHC014 and the related RsWIV1-CoV show that these CoVs are the closest relatives to the epidemic SARS-CoV strains (Fig. 1a,b); however, there are important differences in the 14 residues that bind human ACE2, the receptor for SARS-CoV, including the five that are critical for host range: Y442, L472, N479, T487 and Y491 (ref. 7). In WIV1, three of these residues vary from the epidemic SARS-CoV Urbani strain, but they were not expected to alter binding to ACE2 (Supplementary Fig. 1a,b and Supplementary Table 1). This fact is confirmed by both pseudotyping experiments that measured the ability of lentiviruses encoding WIV1 spike proteins to enter cells expressing human ACE2 (Supplementary Fig. 1) and by in vitro replication assays of WIV1-CoV (ref. 1). In contrast, 7 of 14 ACE2-interaction residues in SHC014 are different from those in SARS-CoV, including all five residues critical for host range (Supplementary Fig. 1c and Supplementary Table 1). These changes, coupled with the failure of pseudotyped lentiviruses expressing the SHC014 spike to enter cells (Supplementary Fig. 1d), suggested that the SHC014 spike is unable to bind human ACE2. However, similar changes in related SARS-CoV strains had been reported to allow ACE2 binding7,8, suggesting that additional functional testing was required for verification. Therefore, we synthesized the SHC014 spike in the context of the replication-competent, mouse-adapted SARS-CoV backbone (we hereafter refer to the chimeric CoV as SHC014-MA15) to maximize the opportunity for pathogenesis and vaccine studies in mice (Supplementary Fig. 2a). Despite predictions from both structure-based modeling and pseudotyping experiments, SHC014-MA15 was viable and replicated to high titers in Vero cells (Supplementary Fig. 2b). Similarly to SARS, SHC014-MA15 also required a functional ACE2 molecule for entry and could use human, civet and bat ACE2 orthologs (Supplementary Fig. 2c,d). To test the ability of the SHC014 spike to mediate infection of the human airway we examined the sensitivity of the human epithelial airway cell line Calu-3 2B4 (ref. 9) to infection and found robust SHC014-MA15 replication, comparable to that of SARS-CoV Urbani (Fig. 1c). To extend these findings, primary human airway epithelial (HAE) cultures were infected and showed robust replication of both viruses (Fig. 1d). Together the data confirm the ability of viruses with the SHC014 spike to infect human airway cells and underscore the potential threat of cross-species transmission of SHC014-CoV. Figure 1: SARS-like viruses replicate in human airway cells and produce in vivo pathogenesis.  (a) The full-length genome sequences of representative CoVs were aligned and phylogenetically mapped as described in the Online Methods. The scale bar represents nucleotide substitutions, with only bootstrap support above 70% being labeled. The tree shows CoVs divided into three distinct phylogenetic groups, defined as α-CoVs, β-CoVs and γ-CoVs. Classical subgroup clusters are marked as 2a, 2b, 2c and 2d for the β-CoVs and as 1a and 1b for the α-CoVs. (b) Amino acid sequences of the S1 domains of the spikes of representative β-CoVs of the 2b group, including SARS-CoV, were aligned and phylogenetically mapped. The scale bar represents amino acid substitutions. (c,d) Viral replication of SARS-CoV Urbani (black) and SHC014-MA15 (green) after infection of Calu-3 2B4 cells (c) or well-differentiated, primary air-liquid interface HAE cell cultures (d) at a multiplicity of infection (MOI) of 0.01 for both cell types. Samples were collected at individual time points with biological replicates (n = 3) for both Calu-3 and HAE experiments. (e,f) Weight loss (n = 9 for SARS-CoV MA15; n = 16 for SHC014-MA15) (e) and viral replication in the lungs (n = 3 for SARS-CoV MA15; n = 4 for SHC014-MA15) (f) of 10-week-old BALB/c mice infected with 1 × 104 p.f.u. of mouse-adapted SARS-CoV MA15 (black) or SHC014-MA15 (green) via the intranasal (i.n.) route. (g,h) Representative images of lung sections stained for SARS-CoV N antigen from mice infected with SARS-CoV MA15 (n = 3 mice) (g) or SHC014-MA15 (n = 4 mice) (h) are shown. For each graph, the center value represents the group mean, and the error bars define the s.e.m. Scale bars, 1 mm. Full size image To evaluate the role of the SHC014 spike in mediating infection in vivo, we infected 10-week-old BALB/c mice with 104 plaque-forming units (p.f.u.) of either SARS-MA15 or SHC014-MA15 (Fig. 1e–h). Animals infected with SARS-MA15 experienced rapid weight loss and lethality by 4 d post infection (d.p.i.); in contrast, SHC014-MA15 infection produced substantial weight loss (10%) but no lethality in mice (Fig. 1e). Examination of viral replication revealed nearly equivalent viral titers from the lungs of mice infected with SARS-MA15 or SHC014-MA15 (Fig. 1f). Whereas lungs from the SARS-MA15–infected mice showed robust staining in both the terminal bronchioles and the lung parenchyma 2 d.p.i. (Fig. 1g), those of SHC014-MA15–infected mice showed reduced airway antigen staining (Fig. 1h); in contrast, no deficit in antigen staining was observed in the parenchyma or in the overall histology scoring, suggesting differential infection of lung tissue for SHC014-MA15 (Supplementary Table 2). We next analyzed infection in more susceptible, aged (12-month-old) animals. SARS-MA15–infected animals rapidly lost weight and succumbed to infection (Supplementary Fig. 3a,b). SHC014-MA15 infection induced robust and sustained weight loss, but had minimal lethality. Trends in the histology and antigen staining patterns that we observed in young mice were conserved in the older animals (Supplementary Table 3). We excluded the possibility that SHC014-MA15 was mediating infection through an alternative receptor on the basis of experiments using Ace2−/− mice, which did not show weight loss or antigen staining after SHC014-MA15 infection (Supplementary Fig. 4a,b and Supplementary Table 2). Together, the data indicate that viruses with the SHC014 spike are capable of inducing weight loss in mice in the context of a virulent CoV backbone. Given the preclinical efficacy of Ebola monoclonal antibody therapies, such as ZMApp10, we next sought to determine the efficacy of SARS-CoV monoclonal antibodies against infection with SHC014-MA15. Four broadly neutralizing human monoclonal antibodies targeting SARS-CoV spike protein had been previously reported and are probable reagents for immunotherapy11,12,13. We examined the effect of these antibodies on viral replication (expressed as percentage inhibition of viral replication) and found that whereas wild-type SARS-CoV Urbani was strongly neutralized by all four antibodies at relatively low antibody concentrations (Fig. 2a–d), neutralization varied for SHC014-MA15. Fm6, an antibody generated by phage display and escape mutants11,12, achieved only background levels of inhibition of SHC014-MA15 replication (Fig. 2a). Similarly, antibodies 230.15 and 227.14, which were derived from memory B cells of SARS-CoV–infected patients13, also failed to block SHC014-MA15 replication (Fig. 2b,c). For all three antibodies, differences between the SARS and SHC014 spike amino acid sequences corresponded to direct or adjacent residue changes found in SARS-CoV escape mutants (fm6 N479R; 230.15 L443V; 227.14 K390Q/E), which probably explains the absence of the antibodies' neutralizing activity against SHC014. Finally, monoclonal antibody 109.8 was able to achieve 50% neutralization of SHC014-MA15, but only at high concentrations (10 μg/ml) (Fig. 2d). Together, the results demonstrate that broadly neutralizing antibodies against SARS-CoV may only have marginal efficacy against emergent SARS-like CoV strains such as SHC014. Figure 2: SARS-CoV monoclonal antibodies have marginal efficacy against SARS-like CoVs.  (a–d) Neutralization assays evaluating efficacy (measured as reduction in the number of plaques) of a panel of monoclonal antibodies, which were all originally generated against epidemic SARS-CoV, against infection of Vero cells with SARS-CoV Urbani (black) or SHC014-MA15 (green). The antibodies tested were fm6 (n = 3 for Urbani; n = 5 for SHC014-MA15)11,12 (a), 230.15 (n = 3 for Urbani; n = 2 for SHC014-MA15) (b), 227.15 (n = 3 for Urbani; n = 5 for SHC014-MA15) (c) and 109.8 (n = 3 for Urbani; n = 2 for SHC014-MA15)13 (d). Each data point represents the group mean and error bars define the s.e.m. Note that the error bars in SARS-CoV Urbani–infected Vero cells in b,c are overlapped by the symbols and are not visible. Full size image To evaluate the efficacy of existing vaccines against infection with SHC014-MA15, we vaccinated aged mice with double-inactivated whole SARS-CoV (DIV). Previous work showed that DIV could neutralize and protect young mice from challenge with a homologous virus14; however, the vaccine failed to protect aged animals in which augmented immune pathology was also observed, indicating the possibility of the animals being harmed because of the vaccination15. Here we found that DIV did not provide protection from challenge with SHC014-MA15 with regards to weight loss or viral titer (Supplementary Fig. 5a,b). Consistent with a previous report with other heterologous group 2b CoVs15, serum from DIV-vaccinated, aged mice also failed to neutralize SHC014-MA15 (Supplementary Fig. 5c). Notably, DIV vaccination resulted in robust immune pathology (Supplementary Table 4) and eosinophilia (Supplementary Fig. 5d–f). Together these results confirm that the DIV vaccine would not be protective against infection with SHC014 and could possibly augment disease in the aged vaccinated group. In contrast to vaccination of mice with DIV, the use of SHC014-MA15 as a live, attenuated vaccine showed potential cross-protection against challenge with SARS-CoV, but the results have important caveats. We infected young mice with 104 p.f.u. of SHC014-MA15 and observed them for 28 d. We then challenged the mice with SARS-MA15 at day 29 (Supplementary Fig. 6a). The prior infection of the mice with the high dose of SHC014-MA15 conferred protection against challenge with a lethal dose of SARS-MA15, although there was only a minimal SARS-CoV neutralization response from the antisera elicited 28 d after SHC014-MA15 infection (Supplementary Fig. 6b, 1:200). In the absence of a secondary antigen boost, 28 d.p.i. represents the expected peak of antibody titers and implies that there will be diminished protection against SARS-CoV over time16,17. Similar results showing protection against challenge with a lethal dose of SARS-CoV were observed in aged BALB/c mice with respect to weight loss and viral replication (Supplementary Fig. 6c,d). However, the SHC014-MA15 infection dose of 104 p.f.u. induced >10% weight loss and lethality in some aged animals (Fig. 1 and Supplementary Fig. 3). We found that vaccination with a lower dose of SHC014-MA15 (100 p.f.u.), did not induce weight loss, but it also failed to protect aged animals from a SARS-MA15 lethal dose challenge (Supplementary Fig. 6e,f). Together the data suggest that SHC014-MA15 challenge may confer cross-protection against SARS-CoV through conserved epitopes, but the required dose induces pathogenesis and precludes use as an attenuated vaccine. Having established that the SHC014 spike has the ability to mediate infection of human cells and cause disease in mice, we next synthesized a full-length SHC014-CoV infectious clone based on the approach used for SARS-CoV (Fig. 3a)2. Replication in Vero cells revealed no deficit for SHC014-CoV relative to that for SARS-CoV (Fig. 3b); however, SHC014-CoV was significantly (P < 0.01) attenuated in primary HAE cultures at both 24 and 48 h after infection (Fig. 3c). In vivo infection of mice demonstrated no significant weight loss but showed reduced viral replication in lungs of full-length SHC014-CoV infection, as compared to SARS-CoV Urbani (Fig. 3d,e). Together the results establish the viability of full-length SHC014-CoV but suggest that further adaptation is required for its replication to be equivalent to that of epidemic SARS-CoV in human respiratory cells and in mice. Figure 3: Full-length SHC014-CoV replicates in human airways but lacks the virulence of epidemic SARS-CoV.  (a) Schematic of the SHC014-CoV molecular clone, which was synthesized as six contiguous cDNAs (designated SHC014A, SHC014B, SHC014C, SHC014D, SHC014E and SHC014F) flanked by unique BglI sites that allowed for directed assembly of the full-length cDNA expressing open reading frames (for 1a, 1b, spike, 3, envelope, matrix, 6–8 and nucleocapsid). Underlined nucleotides represent the overhang sequences formed after restriction enzyme cleavage. (b,c) Viral replication of SARS-CoV Urbani (black) or SHC014-CoV (green) after infection of Vero cells (b) or well-differentiated, primary air-liquid interface HAE cell cultures (c) at an MOI of 0.01. Samples were collected at individual time points with biological replicates (n = 3) for each group. Data represent one experiment for both Vero and HAE cells. (d,e) Weight loss (n = 3 for SARS-CoV MA15, n = 7 for SHC014-CoV; n = 6 for SARS-Urbani) (d) and viral replication in the lungs (n = 3 for SARS-Urbani and SHC014-CoV) (e) of 10-week-old BALB/c mice infected with 1 × 105 p.f.u. of SARS-CoV MA15 (gray), SHC014-CoV (green) or SARS-CoV Urbani (black) via the i.n. route…. Overall our approach has used metagenomics data to identify a potential threat posed by the circulating bat SARS-like CoV SHC014. Because of the ability of chimeric SHC014 viruses to replicate in human airway cultures, cause pathogenesis in vivo and escape current therapeutics, there is a need for both surveillance and improved therapeutics against circulating SARS-like viruses. Our approach also unlocks the use of metagenomics data to predict viral emergence and to apply this knowledge in preparing to treat future emerging virus infections…. This paper has been reviewed by the funding agency, the NIH. Continuation of these studies was requested, and this has been approved by the NIH. SARS-CoV is a select agent. All work for these studies was performed with approved standard operating procedures (SOPs) and safety conditions for SARS-CoV, MERs-CoV and other related CoVs. Our institutional CoV BSL3 facilities have been designed to conform to the safety requirements that are recommended in the Biosafety in Microbiological and Biomedical Laboratories (BMBL), the US Department of Health and Human Services, the Public Health Service, the Centers for Disease Control (CDC) and the NIH. Laboratory safety plans were submitted to, and the facility has been approved for use by, the UNC Department of Environmental Health and Safety (EHS) and the CDC. Electronic card access is required for entry into the facility. All workers have been trained by EHS to safely use powered air purifying respirators (PAPRs), and appropriate work habits in a BSL3 facility and active medical surveillance plans are in place. Our CoV BSL3 facilities contain redundant fans, emergency power to fans and biological safety cabinets and freezers, and our facilities can accommodate SealSafe mouse racks. Materials classified as BSL3 agents consist of SARS-CoV, bat CoV precursor strains, MERS-CoV and mutants derived from these pathogens. Within the BSL3 facilities, experimentation with infectious virus is performed in a certified Class II Biosafety Cabinet (BSC). All members of the staff wear scrubs, Tyvek suits and aprons, PAPRs and shoe covers, and their hands are double-gloved. BSL3 users are subject to a medical surveillance plan monitored by the University Employee Occupational Health Clinic (UEOHC), which includes a yearly physical, annual influenza vaccination and mandatory reporting of any symptoms associated with CoV infection during periods when working in the BSL3. All BSL3 users are trained in exposure management and reporting protocols, are prepared to self-quarantine and have been trained for safe delivery to a local infectious disease management department in an emergency situation. All potential exposure events are reported and investigated by EHS and UEOHC, with reports filed to both the CDC and the NIH…. Experiments with the full-length and chimeric SHC014 recombinant viruses were initiated and performed before the GOF research funding pause and have since been reviewed and approved for continued study by the NIH. https://www.nature.com/articles/nm.3985 ……………………….. SHC014-CoV is a SARS-like coronavirus (SL-COV) which infects horseshoe bats (family Rhinolophidae). It was discovered in Kunming in Yunnan Province, China. It was discovered along with SL-CoV Rs3367, which was the first bat SARS-like coronavirus shown to directly infect a human cell line. The line of Rs3367 that infected human cells was named Bat SARS-like coronavirus WIV1.[2] Discovery From April 2011 to September 2012, researchers from the Wuhan Institute of Virology collected 117 anal swabs and fecal samples of bats from a Chinese rufous horseshoe bats (Rhinolophus sinicus) colony in Kunming City (Yunnan Province in south-western China). 27 out of 117 samples (23%) contained seven different isolates of SARS-like coronaviruses, among which were two previously unknown, called RsSHC014 and Rs3367.[2] Virology In 2013 bat SARS-like coronavirus Rs3367 was shown to be able to directly infect the human HeLa cell line. It was the first time that human cells had been infected with a bat SARS-like coronavirus in the lab. The strain of Rs3367 that infected the human cells was named “Bat SARS-like coronavirus WIV”.[2] In 2015 the University of North Carolina at Chapel Hill and the Wuhan Institute of Virology conducted research showing that SHC014 could be made to infect the human HeLa cell line, through the use of reverse genetics to create a chimeric virus consisting of a surface protein of SHC014 and the backbone of a SARS coronavirus.[3][4] The SL-SHC014-MA15 version of the virus, primarily engineered to infect mice, has been shown to differ by over 5,000 nucleotides from SARS-CoV-2, the cause of the COVID-19 pandemic.[5] … See also Bat coronavirus RaTG13 https://en.wikipedia.org/wiki/SHC014-CoV …………………