James Odell, OMD, ND, L.Ac.
The development of antibodies has long been the basis or rationale for vaccine efficacy against a large range of infective agents such as viruses and bacteria. However, it is well known that antibodies, which the immune system develops from natural infections, differ from those that are created from vaccines. (Bear this important difference in mind when reading this article.) Additionally, when vaccines do elicit antibodies, most are only temporary and thus require boosters, unlike lifelong immunity gained from an infectious disease, such as childhood measles. Anthony Fauci and others developing or promoting COVID-19 vaccination are talking about the likelihood that the new coronavirus vaccine will have to be administered in multiple doses, perhaps even annually like the influenza vaccine. This article explores COVID-19 vaccine development and safety concerns around “fast tracking” the manufacturing and testing process.
Antibody-Dependent Enhancement (ADE)
In the 1960s, immunologists discovered the phenomenon of what is now commonly referred to as antibody-dependent enhancement (ADE). Virus ADE is a mechanism in which virus specific antibodies (from an infection or from a vaccine) promote the entry and/or the replication of another virus into white cells such as monocytes/macrophages and granulocytic cells. ADE modulates the immune response and may induce chronic inflammation, lymphopenia, and/or a ‘cytokine storm’, one or more of which have been reported to cause severe illness and even death. Essentially, ADE is a disease dissemination cycle causing individuals with secondary infection to be more immunologically upregulated than during their first infection (or prior vaccination) by a different strain.
A more technical explanation of ADE is that when patients are infected by one stereotype of a virus (whether due to a vaccine or by nature) they produce neutralizing antibodies targeting that particular viral serotype (or distinct variation within a virus species). However, if they are later infected with another viral serotype (i.e., from a secondary infection or vaccine), the preexisting antibodies cannot completely neutralize the virus. Instead, the antibodies first bind to the virus and then bind to the immune cell IgG Fc receptors and mediate viral entry into these cells. For certain cases, however, the ADE of these viruses is responsible for non-neutralizing or binding antibodies.
Early stages of the viral infection cycle requires attachment and entry of viruses into the host cell. Virus attachment is typically mediated by the specific binding of viral surface proteins to host cell receptor molecules, concentrating the virus at the cell plasma membrane. Viruses are often studded with one or more surface proteins, each potentially containing multiple subdomains, to facilitate interaction with cellular receptors and induce the entry of the virus into the cell. However, the surface of the virus is also a highly antigenic structure that can trigger cellular and humoral immune responses that eradicate or neutralize the virus in the host. Antibodies contribute to several levels of antiviral defense to efficiently neutralize the virus and reduce its infectivity. In simple terms, antibody neutralization is good, whereas antibody binding is bad.
After the 1960s, studies on vaccine candidates for diseases such as dengue, respiratory syncytial virus and severe acute respiratory syndrome (SARS) have demonstrated a paradoxical trend. Many animals and humans who received the vaccine and were subsequently exposed to the virus developed a more serious disease than those who had not been vaccinated.1, 2, 3 ADE’s have been observed for a variety of viruses, such as dengue virus, Ross River virus, other alpha and flaviviruses, HIV and influenza viruses.4, 5, 6, 7, 8, 9
Developing the COVID 19 Vaccine
Importantly, during the production of new vaccines for a variety of infectious agents, the ADE effects must be carefully examined to ensure that the vaccines do not harm the recipients. ADE is a clear concern about coronavirus vaccines that are soon to be tested on millions – if not billions – from the healthy to the ill and young to old. As a result of ‘fast-tracking,’dozens of coronavirus manufacturers have been given the green light by the FDA to bypass critical manufacturing safety rules, such as pre-human animal trials and the use of ‘inert’ placebo controls. Most significantly the concept of ‘fast track’ means that the length of the trials will be short; not more than 6 weeks. It can take two to three years to learn if there are negative health effects resulting from a vaccine. Many autoimmune and neurological side effects will not manifest within a few short weeks. Several companies are now cutting corners by conducting phase 1, 2 and 3 human trials simultaneously. Global pharmaceutical and biotech companies are now developing over 100 experimental COVID-19 vaccines, with a few leading the race after securing billions of dollars in funding from the U.S. government, the Gates Foundation, and other organizations.10, 11
At the time of this writing, at least 10 of these vaccine-development programs have reached the clinical stage of evaluation, either phase 1 or phase 2. These include programs led by Western pharmaceutical companies such as AstraZeneca plc (in partnership with the University of Oxford); BioNTech SE partnered with Pfizer, Inc.; Inovio Pharmaceuticals, Inc.; Moderna, Inc. (in partnership with NIAID) and Novavax, Inc. 123 other programs to develop a COVID-19 vaccine remain in preclinical evaluation.
Astonishingly, the University of Oxford’s Jenner Institute and Oxford Vaccine Group in the United Kingdom have announced that their researchers are beginning to recruit children aged 5 to 12 years for phase II and phase III clinical trials of the experimental COVID-19 vaccine developed by the university in collaboration with AstraZeneca plc. Researchers at The University of Oxford and AstraZeneca researchers are proceeding with testing the experimental ChAdOx1 nCov-19 vaccine in children, although a report published on May 13, 2020 indicated that small vaccine trials in mice and monkeys were not successful in proving effectiveness against infection. While the animal studies presented evidence that the experimental vaccine induced a “robust humoral and cell-mediated response” in mice and appeared to protect against development of viral pneumonia in monkeys, it did not prevent infection with COVID-19.12, 13 In other words, the animal studies failed, but the developers intend to continue with human trials.
Some of these coronavirus vaccines being developed will use unlicensed DNA, messenger RNA and nanoparticle technology, oil-based adjuvants and even electricity, to genetically manipulate and hyper-stimulate strong inflammatory immune responses in the body.14 Messenger RNA vaccines, which have never been licensed for use in humans, inject cells with mRNA, usually within lipid nanoparticles, to stimulate cells in the body to become manufacturers of viral proteins. mRNA vaccines like all vaccines stimulate cells in the body to become manufacturers of viral proteins. mRNA vaccines have potential safety issues, including local and systemic inflammation and stimulation of auto-reactive antibodies and autoimmunity, as well as the development of edema (swelling) and blood clots.
Conventional vaccines usually contain inactivated disease-causing organisms or proteins made by the pathogen (antigens) that mimic the infectious agent. These activate the body’s immune response, so it is primed to respond more quickly and efficiently if exposed to the infectious agent in the future. RNA vaccines use a different approach that takes advantage of the process that cells use to make proteins: cells use DNA as the template to make messenger RNA (mRNA) molecules, which are then translated to build proteins. An RNA vaccine consists of an mRNA strand that codes for a disease-specific antigen. Once the mRNA strand in the vaccine is inside the cells of the body, the cells use the genetic information to produce the antigen. This antigen is then displayed on the cell surface, where it is recognized by the immune system.
Safety Issues Bypassed
Vaccine safety experts generally agree that animal studies should always be conducted prior to any human clinical trial with any vaccine; COVID-19 (SARS-CoV-2) vaccines are no exception. Clinical trials should always be double-blind placebo-controlled (with an inert placebo and not with another vaccine or adjuvant as a placebo).Careful assessment of possible immune complications should then be made prior to release of the vaccine to the public. In the case of vaccines, this ‘careful assessment’ is a time of waiting and should be no less than two to three years. Importantly, over the last two decades vaccines manufactures have never been able to develop an effective and safe coronavirus vaccine. Previous coronavirus vaccine animal studies with ferrets and mice have demonstrated significant and serious side-effects. After two decades of failed trials, the question is posed as to why a fast-tracking coronavirus vaccine will now result in a different outcome? Given that many of these fast-track trials have bypassed animal studies, are only performed on healthy volunteers and children (not the elderly or those with pre-morbidities), and that trials are conducted without an inert double-blind placebo-controlled environment, and are not given sufficient time to observe effects on the human trials, there is serious safety concern. Many epidemiologists feel this fast track policy is a recipe for mass disaster. According to Marc Lipsitch, an epidemiologist at the Harvard Chan School of Public Health in Boston, MA, “You really have to test a vaccine carefully and not just roll it out because people are clamoring for it with an epidemic underway.”
National Childhood Vaccine Injury Act and Immunity from Liability for Vaccine Harms
By the early 1980s, pharmaceutical companies faced crippling liability for injuries to children caused by their vaccines. Instead of allowing such market forces to push them to develop safer vaccines, Congress passed the National Childhood Vaccine Injury Act (the 1986 Act) which eliminated the liability of pharmaceutical companies for injuries caused by their vaccine products. After eliminating liability for pharmaceutical companies, the 1986 Act established the Vaccine Injury Compensation Program (Vaccine Court), part of the U.S. Court of Federal Claims, to compensate people injured by vaccines. Under the 1986 Act, the U.S. Department of Health and Human Services (HHS) is the defendant in Vaccine Court and is legally obligated to defend against any claim that a vaccine causes injury. HHS is represented by the formidable resources of the U.S. Department of Justice (DOJ). In nearly every case the injured person must prove the vaccine caused the injury. Notwithstanding these hurdles, since 1986, HHS has paid over $4 billion for vaccine injuries with taxpayers’ money, not with pharmaceutical manufacturers’ dollars. Safety is regulated, not only by comprehensive and thorough manufacturing and testing procedures, but also with liability laws. Without any liability consequences, pharmaceutical vaccine manufacturers are less likely to pay due diligence regarding the safety of the vaccine.
Upon removing the market mechanisms that assured vaccine safety, Congress made HHS exclusively responsible for vaccine safety under the ‘Mandate for Safer Childhood Vaccine’ provision of the 1986 Act. HHS recently conceded in federal court, that it did not comply with the essential provisions of this act, such as submitting reports to Congress on how HHS has improved vaccine safety. Such government neglect of vaccine safety also casts a doubt on the future development of coronavirus vaccines.
Vaccine-Associated Enhanced Respiratory Disease (VAERD)
Similar to ADE, another immune enhancement phenomena came to the foreground in the 1960s during clinical trials in which young children were immunized with whole-inactivated respiratory syncytial virus (RSV) vaccines.15 When the children contracted RSV naturally a few months after the vaccinations, those who were immunized became significantly sicker than those who had not been vaccinated. In fact, in one trial, 80 percent of children in the youngest cohort had to be hospitalized, and two died.16 The syndrome the hospitalized children developed is sometimes called vaccine-associated enhanced respiratory disease (VAERD). VAERD is like ADE in that a high concentration of binding antibodies do not fully neutralize the virus and results in the formation of binding antibody-virus complexes that elicit a cytokine storm. As a consequence, elevated pro-inflammatory cytokines associated with the innate immune system have been associated with the VAERD phenomenon.17 In these children, the binding-antibody complexes affected the small airways of the lungs, obstructing these spaces and increasing inflammation.
In another noteworthy study, “Abstract: a formalin-inactivated monkey kidney culture propagated 100-fold concentrated respiratory syncytial (RS) virus vaccine was administered intramuscularly to residents of Harrison and Arthur Cottages in Junior Village, a District of Columbia Welfare Institution for homeless infants and children. No significant local or systemic vaccine reactions were (initially) observed. A sharp outbreak of RS virus infection occurred approximately 9 months after the vaccine study was initiated. Recovery of RS virus was found to be significantly associated not only with the onset of febrile illness but also with the onset of febrile pneumonia illness. The vaccine not only failed to offer protection, but also induced an exaggerated altered clinical response to naturally occurring RS virus infection in the younger vaccines as 9 (69%) of 13 vaccinated and only 4 (9%) of 47 nonvaccinated Harrison Cottage residents, 6–23 months of age developed pneumonia.” The authors concluded, “The paradoxical effect of vaccination suggests that serum antibody may play an active role in the pathogenesis of RS virus disease.”18
Institutions for the homeless and ‘wards of the state’, orphanages, prisons, and developing countries (Uganda, Kenya, Latin America, Caribbean, Thailand) have historically been targeted for experimental vaccine trials. Some larger trials (rarely reported by the media) in Africa have resulted in mass sterility and even death.
The ever-changing mutation terrain of viruses results in ‘vaccine mismatch’ due to the lack of relatedness between the vaccine and the numerous circulating strains. This can potentially create vaccine reactions such as VAERD. Influenza vaccines contain inactivated virus formulated with adjuvants (aluminum, squalene, and several immunological toxins), and this formulation could certainly contribute to the pathology observed in VAERD.19
Another example of VAERD occurred with “Abstract: Field evaluation of two formalin-inactivated respiratory virus vaccines in a selected pediatric population in California during the 1966—1967 respiratory disease season. A total of 441 children ranging in age from four months to nine years were vaccinated: 219 with a respiratory syncytial (RS) virus vaccine and 222 with a trivalent parainfluenza virus (types 1, 2, and 3) vaccine. Very high attack rates of parainfluenza virus types 1 and 3 and RS virus was observed during the study period in infants and children in both vaccine groups. A protective effect was not demonstrable for either vaccine. Infants who received the RS virus vaccine and who subsequently became infected with RS virus tended to have a more severe clinical illness than infants who did not receive this vaccine.”20
There have been numerous studies on VAERD, particularly in children. Unfortunately, mainstream media report little information on this important issue.
COVID-19 Occurrence and Prior Vaccination
One of the more perplexing concerns regarding the current COVID-19 epidemic is the discrepancy between the severity of cases observed in Wuhan, Northern Italy, New York, and those occurring elsewhere in the world. Among the several reasons, such as air pollution, age, and pre-morbidities, another plausible justification is the antibody-dependent enhancement of SARS-CoV-2 due to previous exposure to coronaviruses and widespread influenza vaccine campaigns. Prior to the COVID-19 outbreak, both China and Italy implemented mass influenza vaccination campaigns.21, 22, 23 In one study, ADE was suggested to account for the severity of COVID-19 cases initially observed in China (and elsewhere) relative to other regions of the world.24 The previous infection with other coronaviruses, and/or influenza vaccines may have primed COVID 19 patients, predisposing them to the development of severe disease once infected with SARS-CoV-2.
ADE and VAERD require prior exposure to viral antigenic epitopes, such as those contained in flu and pneumonia vaccines, making it a possible explanation for the observed geographic limitation of severe cases and deaths, as well as the age discrepancy – affecting primarily the elderly people who have received mandated flu and pneumonia vaccines, particularly in nursing homes.
Studies have shown that vaccines developed against another coronavirus, feline infectious peritonitis virus, increased the risk for cats to develop disease caused by the virus.25 Similar effects have been seen in animal studies for other viruses, including the coronavirus, which causes SARS.26, 27
Research suggests that prior infection with other coronaviruses, from the agents of the common cold, as well as certain vaccines may have ‘primed’ COVID-19 patients, predisposing them to the development of severe disease once they have been infected with SARS-CoV-2. While severe cases of COVID-19 were reported later from all over the world, this has occurred mainly in the elderly population with pre-morbidities. Thus, the above hypothesis cannot be completey dismissed. Cross-reactivity of antibodies against to SARS-CoV-2 and SARS-CoV spike proteins is common and some preliminary data claim that they seem to be rarely cross-neutralising.28.
Safety Conclusion
Normally, vaccine development is a lengthy and complicated process, often lasting 10-15 years and involving a combination of public and private involvement. Unfortunately, the rapid worldwide competition between pharmaceutical companies to develop a COVID-19 vaccine has bypassed multiple safety controls, rendering the result both dubious and potentially dangerous for the public. Financial interests have taken precedence over the health and safety of the public. Hasty development of vaccines is always risky, and only thorough research employing all the safety precautions will lead to a safe and effective vaccine.
There are other concerns related to the safety of vaccines not discussed here due to space limitations, in particular adjuvants. Adjuvants are used to induce a stronger immune response from vaccines. These chemicals can have a wide range of compositions, including lipids, proteins, nucleic acids, and even inorganic material, such as aluminum salts. What they all have in common is that they hyper stimulate receptors in immune cells and most do this through their cellular toxicity. Animal studies reveal that aluminum adjuvant particles in vaccines deposit in the brain and bones and are neurologically (brain) toxic. Aluminum ingested in the diet has low oral absorption (about 0.3%), is rapidly excreted by the kidneys, is (mostly) excluded from the brain by the blood-brain barrier, and is in a solubilized, ionic (not particulate)Al3+ form. These defenses are adequate for protecting the brain from natural levels of aluminum exposure. These protective mechanisms are unable to protect the brain from injected aluminum adjuvant particles. Aluminum adjuvant particles are too large to be removed by the kidneys and are transmitted across the blood-brain barrier by macrophages.
Regulators (the Center for Biologics Evaluation and Testing of the U.S. Food and Drug Administration are reckless and unethical not to require that vaccine developers check for potentially adverse reactions in animal studies first, and should insist on double-blind, inert placebo controls with human trials that extend at least two to three years, if not longer. The National Institute of Allergy and Infectious Diseases (NIAID), led by Anthony Fauci argue that the risk of delaying vaccine advancement is far greater than the risk of causing illness in healthy volunteers (children remember). Testing vaccines without proper safety precautions or taking the time required to thoroughly analyze the effects of research volunteers could bring untold disastrous consequences on millions of lives well into the future.
References:
Tirado, Sol M. Cancel, and Kyoung-Jin Yoon. "Antibody-dependent enhancement of virus infection and disease." Viral immunology 16, no. 1 (2003): 69-86. https://www.liebertpub.com/doi/abs/10.1089/088282403763635465
Takada, Ayato, and Yoshihiro Kawaoka. "Antibody‐dependent enhancement of viral infection: molecular mechanisms and in vivo implications." Reviews in medical virology 13, no. 6 (2003): 387-398. https://onlinelibrary.wiley.com/doi/abs/10.1002/rmv.405
Wang, SZ-S., K. E. Rushlow, C. J. Issel, R. F. Cook, S. J. Cook, M. L. Raabe, Y-H. Chong, L. Costa, and R. C. Montelaro. "Enhancement of EIAV replication and disease by immunization with a baculovirus-expressed recombinant envelope surface glycoprotein." Virology 199, no. 1 (1994): 247-251. https://www.sciencedirect.com/science/article/abs/pii/S0042682284711202
Mascola, John R., Bonnie J. Mathieson, Philip M. Zack, MARY CLARE WALKER, Scott B. Halstead, and Donald S. Burke. "Summary report: workshop on the potential risks of antibody-dependent enhancement in human HIV vaccine trials." AIDS research and human retroviruses 9, no. 12 (1993): 1175-1184. https://apps.dtic.mil/dtic/tr/fulltext/u2/a275482.pdf
Burke, Donald S. "Human HIV vaccine trials: does antibody-dependent enhancement pose a genuine risk?." Perspectives in Biology and Medicine 35, no. 4 (1992): 511-530. https://muse.jhu.edu/article/459161/pdf
Guzman, Maria G., Mayling Alvarez, Rosmari Rodriguez-Roche, Lídice Bernardo, Tibaire Montes, Susana Vazquez, Luis Morier et al. "Neutralizing antibodies after infection with dengue 1 virus." Emerging infectious diseases 13, no. 2 (2007): 282. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725871/
Dejnirattisai, Wanwisa, Amonrat Jumnainsong, Naruthai Onsirisakul, Patricia Fitton, Sirijitt Vasanawathana, Wannee Limpitikul, Chunya Puttikhunt et al. "Cross-reacting antibodies enhance dengue virus infection in humans." Science 328, no. 5979 (2010): 745-748. https://europepmc.org/article/PMC/3837288
Dutry, Isabelle, Hui-ling Yen, Horace Lee, Malik Peiris, and Martial Jaume. "Antibody-dependent enhancement (ADE) of infection and its possible role in the pathogenesis of influenza." In BMC proceedings, vol. 5, no. 1, p. P62. BioMed Central, 2011. https://bmcproc.biomedcentral.com/track/pdf/10.1186/1753-6561-5-S1-P62?site=http://bmcproc.biomedcentral.com
Takada, Ayato, Heinz Feldmann, Thomas G. Ksiazek, and Yoshihiro Kawaoka. "Antibody-dependent enhancement of Ebola virus infection." Journal of virology 77, no. 13 (2003): 7539-7544. https://jvi.asm.org/content/jvi/77/13/7539.full.pdf
Lurie N, Saville M et al. Developing Covid-19 Vaccines at Pandemic Speed. NEJM Mar. 31, 2020.
Fisher BL. COVID-19 Meltdown & Big Pharma’s Big Money Win. The Vaccine Reaction Apr. 13, 2020.
van Doremalen B, Lambe T et al. ChAdOx1 nCoV-19 vaccination prevents SARS-Cov-2 pneumonia in rhesus macaques. bioRxiv May 13, 2020.
Times of India. Coronavirus vaccine current status: Oxford vaccine failed in animal trials; here is what happened. May 21, 2020.
Fisher BL, Raines K Inovio COVID-19 Vaccine Uses Electricity to Drive DNA into Body Cells. The Vaccine Reaction Apr. 18, 2020.
Zimmer, Kathrina. COVID-19 Vaccine Researchers Mindful of Immune Enhancement, The Scientist, 5-26-2020.
KIM, HYUN WHA, JOSE G. CANCHOLA, CARL D. BRANDT, GLORIA PYLES, ROBERT M. CHANOCK, KEITH JENSEN, and ROBERT H. PARROTT. "Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine." American journal of epidemiology 89, no. 4 (1969): 422-434. http://sa.uploads.ru/SU2xL.pdf
Gauger PC, Vincent AL, Loving CL, Lager KM, Janke BH, Kehrli ME Jr., and Roth JA: Enhanced pneumonia and disease in pigs vaccinated with an inactivated human-like (delta-cluster) H1N2 vaccine and challenged with pandemic 2009 H1N1 influenza virus. Vaccine 2011;29:2712–2719. https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1075&context=vmpm_pubs
KAPIKIAN, ALBERT Z., REGINALD H. MITCHELL, ROBERT M. CHANOCK, RUTH A. SHVEDOFF, and C. ELEANOR STEWART. "An epidemiologic study of altered clinical reactivity to respiratory syncytial (RS) virus infection in children previously vaccinated with an inactivated RS virus vaccine." American journal of epidemiology 89, no. 4 (1969): 405-421. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.855.1446&rep=rep1&type=pdf
Rajão, Daniela S., Hongjun Chen, Daniel R. Perez, Matthew R. Sandbulte, Phillip C. Gauger, Crystal L. Loving, G. Dennis Shanks, and Amy Vincent. "Vaccine-associated enhanced respiratory disease is influenced by haemagglutinin and neuraminidase in whole inactivated influenza virus vaccines." Journal of General Virology 97, no. 7 (2016): 1489-1499. https://www.microbiologyresearch.org/docserver/fulltext/jgv/97/7/1489_vir000468.pdf?expires=1591728632&id=id&accname=guest&checksum=5007EAF2D1FCFBE1C2DD06ED7D1C8FFE
CHIN, JAMES, ROBERT L. MAGOFFIN, LOIS ANN SHEARER, JACK H. SCHIEBLE, and EDWIN H. LENNETTE. "Field evaluation of a respiratory syncytial virus vaccine and a trivalent parainfluenza virus vaccine in a pediatric population." American journal of epidemiology 89, no. 4 (1969): 449-463. https://academic.oup.com/aje/article-abstract/89/4/449/198872
Influenza, Vaccination TWG, National Immunization Advisory Committee, and Technical Working Group. "Technical guidelines for seasonal influenza vaccination in China, 2019-2020." Zhonghua liu xing bing xue za zhi= Zhonghua liuxingbingxue zazhi 40, no. 11 (2019): 1333. https://pubmed.ncbi.nlm.nih.gov/31838802/
de St. Maurice, Annabelle, and Natasha Halasa. "Preparing for the 2019‐2020 influenza season." Pediatric Transplantation 24, no. 1 (2020): e13645. https://onlinelibrary.wiley.com/doi/full/10.1111/petr.13645
Costantino, Claudio, Vincenzo Restivo, Emanuele Amodio, Giuseppina Maria Elena Colomba, Francesco Vitale, and Fabio Tramuto. "A mid-term estimate of 2018/2019 vaccine effectiveness to prevent laboratory confirmed A (H1N1) pdm09 and A (H3N2) influenza cases in Sicily (Italy)." Vaccine 37, no. 39 (2019): 5812-5816. https://www.sciencedirect.com/science/article/pii/S0264410X19310643
Liu, Li, Qiang Wei, Qingqing Lin, Jun Fang, Haibo Wang, Hauyee Kwok, Hangying Tang et al. "Anti–spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection." JCI insight 4, no. 4 (2019). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478436/
Takano, Tomomi, Shinji Yamada, Tomoyoshi Doki, and Tsutomu Hohdatsu. "Pathogenesis of oral type I feline infectious peritonitis virus (FIPV) infection: Antibody-dependent enhancement infection of cats with type I FIPV via the oral route." Journal of Veterinary Medical Science (2019): 18-0702. https://www.jstage.jst.go.jp/article/jvms/advpub/0/advpub_18-0702/_pdf
Kam, Yiu Wing, François Kien, Anjeanette Roberts, Yan Chung Cheung, Elaine W. Lamirande, Leatrice Vogel, Shui Ling Chu et al. "Antibodies against trimeric S glycoprotein protect hamsters against SARS-CoV challenge despite their capacity to mediate FcγRII-dependent entry into B cells in vitro." Vaccine 25, no. 4 (2007): 729-740. http://www.hkupasteur.hku.hk/publications/pdf/Kam_et_al_2007.pdf
Jaume, Martial, Ming S. Yip, Chung Y. Cheung, Hiu L. Leung, Ping H. Li, Francois Kien, Isabelle Dutry et al. "Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH-and cysteine protease-independent FcγR pathway." Journal of virology 85, no. 20 (2011): 10582-10597. https://jvi.asm.org/content/jvi/85/20/10582.full.pdf
Lv N, Wu NC, Tsang OTY, Yuan M, Perera RAPM, Leung WS, et al. Cross-reactive antibody response between SARS-CoV-2 and SARS-CoV infections. BioRxiv 2020.03.15.993097 [Preprint]. 2020 [posted 2020 March 17, cited 2020 April 9]. Available from: https://www.biorxiv.org/content/10.1101/2020.03.15.993097v1