No, the 2012 study says nothing about Covid-19 vaccines. In fact, it's been so over-used by the anti-vaxxers that one of the study's authors was interviewed by Reuters back in February 2021:
A video which uses a research paper to argue that mRNA vaccines will make people fatally weakened to other diseases makes untrue claims about the study, according to the paper’s lead author. [...]
The recommendation for caution is indeed the final line of the study’s conclusion [...], but the lead author of the study, Prof Chien-Te (Kent) Tseng, told Reuters by email that the animals in the study did not die. [...]
He said that when the animals were exposed to the live virus, they developed eosinophilia (a high count of a type of white blood cells) but, despite this, they “found that mice survived the lethal challenge without showing any readily noticeable weight loss and other signs of illness.” [...]
However, Tseng, said the vaccines they had studied in the 2012 paper and the mRNA technology used in the COVID-19 vaccines are “very different vaccine platforms.”
Tseng also said that, while people should always be cautious about the safety of new vaccines, they should not be alarmed by his paper.
He wrote: “I feel our earlier report has raised that safety issue which has been taken seriously within the vaccine developers worldwide by different Institutions, including the World Health Organisation and the National Institute of Allergy and Infectious Diseases.”
Also, from a perspective article in which Tseng's study is ref 78:
The first RSV vaccine, based on formalin-inactivated RSV (FI-RSV), entered a clinical trial in 1965, a time when several other inactivated or attenuated virus-based vaccines had already been successfully developed, such as vaccines against smallpox and polio The FI-RSV vaccine was well tolerated and appeared to be moderately immunogenic at first. However, instead of protecting study participants, the FI-RSV vaccine exhibited a paradoxical disease-strengthening effect (enhanced respiratory disease (ERD); Box 1) during subsequent natural RSV infection. Among the 20 infants who received the FI-RSV vaccine, 16 required hospitalization, including two who subsequently died, whereas only one of the 21 participants in the control group was hospitalized. The FDA then urgently suspended all clinical studies of RSV vaccines. [...]
Thus, throughout the 50-year history of exploring RSV vaccines, we have learnt the absolute necessity of tracking the comprehensive safety of vaccines before large-scale application, no matter the urgency of the moment. From the RSV experience, we still do not know what features of an antigen will create disease exacerbation, although we do know that antigen conformation and prefusion versus fusion states are important. We have also learnt that a TH2 cell-biased immune response is harmful. For example, an antigen-induced TH2 cell-like cytokine profile, such as IL-5 and IL-13, could activate CD4+ T cells but poorly stimulate natural killer cells and CD8+ T cells in an animal model or human. Such a TH2 cell-biased immune response might result in VADE under viral challenge. Furthermore, we have learnt that the induction of NAbs over binding antibodies is crucial. [...]
A recombinant modified vaccinia virus Ankara vector expressing SARS-CoV S protein elicited a rapid and vigorous NAb response in ferrets; however, a strong inflammatory response in the liver of immunized ferrets occurred after challenge with SARS-CoV74,75. More studies then demonstrated that SARS vaccines, based on either inactivated virus or a recombinant vector, could induce eosinophils and TH2 cell-skewed immune responses on subsequent challenge with SARS-CoV in a mouse model76,77, 78, which is reminiscent of RSV vaccine-induced ERD in infants. Similarly, an inactivated SARS-CoV vaccine and a SARS-CoV S protein-derived peptide vaccine both induced severer lung damage in rhesus macaques after SARS-CoV challenge79. A DNA vaccine encoding the S protein of SARS-CoV induced CD4+ and CD8+ T cell and NAb responses in a mouse model and in a phase I clinical trial80,81.
ADE was also observed in SARS vaccines. A SARS vaccine based on recombinant SARS-CoV S protein protected hamsters from SARS-CoV infection; however, the S protein-specific antibodies could mediate FcR-dependent entry into B cells in vitro82,83.
The road to useable vaccines was paved with many failures, mostly in animal testing, but as the above story demonstrates, also some human victims when the effect was ADE/ERD effect was first discovered during the 1965 human trials of a vaccine candidate against RSV. For those who need a term dictionary:
[Box 1] Key terms in disease enhancement
Antibody-dependent enhancement (ADE) can be mediated by antibody Fc receptor-associated internalization of a virus, thus resulting in more extensive viral replication and cytokine release in the presence of virus-specific antibodies. ADE was widely reported in flavivirus and other viral infections, such as HIV and influenza virus infections.
Enhanced respiratory disease (ERD) describes severer clinical symptoms after respiratory virus infection, such as with respiratory syncytial virus and influenza virus, due to previous immune responses. ERD usually manifests itself as peribronchiolar monocytic infiltration with an excess of eosinophils. ERD can happen during homotypic or heterotypic serotype virus infection after vaccination, natural infection or transfer of maternal passive immunity.
Vaccine-associated disease enhancement (VADE) partially overlaps with ADE and ERD. In contrast to ERD, VADE involves only the vaccine-associated situation, and, more importantly, it is not limited to respiratory disease. For example, heterotypic-serotype dengue virus infection may cause severer dengue haemorrhagic fever in vaccinated individuals. This phenomenon is related to VADE, but does not include ERD. VADE can be attributed to antibody-dependent and type 2 T helper cell-dependent mechanisms.
In the months before the Covid-19 phase III vaccine trials were published there were in fact quite a few papers (e.g. 1, 2) seriously discussing the possibility that we might see ADE/ERD with Covid-19 vaccines, despite the extensive screening studies in animal models. But that hasn't really materialized once the phase-III trial data was published, although some ADE/ERD doubts still remain in the minds of some with respect to Covid-19 variants (again not supported by data insofar).
It's true on the other hand that we might have discovered something new with the TTS/VIPIT adverse events (which do involve clots) with the adenovirus-based Covid-19 vaccines. But this is a rare side effect that wasn't common enough to spot in clinical trials. And it's not really related to TH2 (ADE/RDE) in any way that I could find, although there is a similarity between TTS/VIPIT and HIT (heparin-induced thrombocytopenia) autoimmune disorders. So there may be some problems with some Covid-19 vaccines, but they aren't the same problems as were discussed in that 2012 Tseng paper on SARS vaccine candidates. Only the clueless outsiders seem to throw all of them in the same basket. In particular, TTS/VIPIT happen just after vaccine administration, with no subsequent Covid-19 infection needed/noted in any of the TTS/VIPIT cases.