This is the part that gets me, the vaccinated experienced severe disease and death... Sounds pretty safe to me.

Discussion The emergence of the disease SARS and the rapid identification of its severity and high risk for death prompted a rapid mobilization for control at the major sites of occurrence and at the international level. Part of this response was for development of vaccines for potential use in control, a potential facilitated by the rapid identification of the causative agent, a new coronavirus [8]–[9]. Applying the principles of infection control brought the epidemic under control but a concern for reemergence naturally or a deliberate release supported continuation of a vaccine development effort so as to have the knowledge and capability necessary for preparing and using an effective vaccine should a need arise. For this purpose, the National Institute of Allergy and Infectious Diseases supported preparation of vaccines for evaluation for potential use in humans. This effort was hampered by the occurrence in the initial preclinical trial of an immunopathogenic-type lung disease among ferrets and Cynomolgus monkeys given a whole virus vaccine adjuvanted with alum and challenged with infectious SARS-CoV [14]. That lung disease exhibited the characteristics of a Th2-type immunopathology with eosinophils in the lung sections suggesting hypersensitivity that was reminiscent of the descriptions of the Th2-type immunopathologic reaction in young children given an inactivated RSV vaccine and subsequently infected with naturally-occurring RSV [32]–[33]. Most of these children experienced severe disease with infection that led to a high frequency of hospitalizations; two children died from the infection [33], [40], [41]. The conclusion from that experience was clear; RSV lung disease was enhanced by the prior vaccination. Subsequent studies in animal models that are thought to mimic the human experience indicate RSV inactivated vaccine induces an increased CD4+ T lymphocyte response, primarily of Th2 cells and the occurrence of immune complex depositions in lung tissues [32], [42], [43]. This type of tissue response is associated with an increase in type 2 cytokines including IL4, IL5, and IL13 and an influx of eosinophils into the infected lung; [32], [33], [42], [44]. Histologic sections of tissues exhibiting this type of response have a notable eosinophilic component in the cellular infiltrates. Recent studies indicate that the Th2-type immune response has both innate and adaptive immune response components [33], [43].

In addition to the RSV experience, concern for an inappropriate response among persons vaccinated with a SARS-CoV vaccine emanated from experiences with coronavirus infections and disease in animals that included enhanced disease among infected animals vaccinated earlier with a coronavirus vaccine [31]. Feline infectious peritonitis coronavirus (FIPV) is a well-known example of antibody-mediated enhanced uptake of virus in macrophages that disseminate and increase virus quantities that lead to enhanced disease [31], [45]. Antigen-antibody complex formation with complement activation can also occur in that infection and some other coronavirus infections in animals. Thus, concern for safety of administering SARS-CoV vaccines to humans became an early concern in vaccine development