An article recently published in the journal, Nature, gives evidence of the phenomenon of Antibody Dependent Enhancement (ADE), with the Covid vaxxes, where a vaccine produces sub-optimal antibodies that can enhance disease enabling a more severe infection, of the same disease or others. The mainstream medical profession, and Big Pharma have denied that the Covid vaxxes could produce ADE, as indicated by the wiki material cited below for an introduction. But, as indicated, this position now seems to be dated.  

https://en.wikipedia.org/wiki/Antibody-dependent_enhancement

“Antibody-dependent enhancement (ADE), sometimes less precisely called immune enhancement or disease enhancement, is a phenomenon in which binding of a virus to suboptimal antibodies enhances its entry into host cells, followed by its replication.^[1][2] The suboptimal antibodies can result from natural infection or from vaccination. ADE may cause enhanced respiratory disease, but is not limited to respiratory disease.^[3] It has been observed in HIV, RSV virus and Dengue virus and is monitored for in vaccine development.^[4]

In ADE, antiviral antibodies promote viral infection of target immune cells by exploiting the phagocytic FcγR or complement pathway.^[5] After interaction with a virus, the antibodies bind Fc receptors (FcR) expressed on certain immune cells or complement proteins. FcγRs bind antibodies via their fragment crystallizable region (Fc).

The process of phagocytosis is accompanied by virus degradation, but if the virus is not neutralized (either due to low affinity binding or targeting to a non-neutralizing epitope), antibody binding may result in virus escape and, therefore, more severe infection. Thus, phagocytosis can cause viral replication and the subsequent death of immune cells. Essentially, the virus “deceives” the process of phagocytosis of immune cells and uses the host's antibodies as a Trojan horse.

ADE may occur because of the non-neutralizing characteristic of an antibody, which binds viral epitopes other than those involved in host-cell attachment and entry. It may also happen when antibodies are present at sub-neutralizing concentrations (yielding occupancies on viral epitopes below the threshold for neutralization),^[6][7] or when the strength of antibody-antigen interaction is below a certain threshold.^[8][9] This phenomenon can lead to increased viral infectivity and virulence.

ADE can occur during the development of a primary or secondary viral infection, as well as with a virus challenge after vaccination.^[1][10][11] It has been observed mainly with positive-strand RNA viruses, including flaviviruses such as dengue, yellow fever, and Zika;^[12][13][14] alpha- and betacoronaviruses;^[15] orthomyxoviruses such as influenza;^[16] retroviruses such as HIV;^[17][18][19] and orthopneumoviruses such as RSV.^[20][21][22] The viruses that cause it frequently share common features such as antigenic diversity, replication ability, or ability to establish persistence in immune cells.^[1]

The mechanism that involves phagocytosis of immune complexes via the FcγRII/CD32 receptor is better understood compared to the complement receptor pathway.^[23][24][25] Cells that express this receptor are represented by monocytes, macrophages, and some categories of dendritic cells and B-cells. ADE is mainly mediated by IgG antibodies,^[24] but IgM^[26] and IgA antibodies^[18][19] have also been shown to trigger it.

Coronavirus

COVID-19

Prior to the pandemic, ADE was observed in animal studies of laboratory rodents with vaccines for SARS-CoV, the virus that causes severe acute respiratory syndrome (SARS). However, as of 27 January 2022 there have been no observed incidents with vaccines for COVID-19 in trials with nonhuman primates, in clinical trials with humans, or following the widespread use of approved vaccines.^{[27][28][29][30][31]}

But this Wiki entry is out of date:

https://www.nature.com/articles/s41598-022-19993-w

“Reevaluation of antibody-dependent enhancement of infection in anti-SARS-CoV-2 therapeutic antibodies and mRNA-vaccine antisera using FcR- and ACE2-positive cells

• Jun Shimizu, 
• Tadahiro Sasaki, 
• Ritsuko Koketsu, 
• Ryo Morita, 
• Yuka Yoshimura, 
• Ami Murakami, 
• Yua Saito, 
• Toshie Kusunoki, 
• Yoshihiro Samune, 
• Emi E. Nakayama, 
• Kazuo Miyazaki& 
• Tatsuo Shioda

Scientific Reports volume 12, Article number: 15612 (2022) 

Abstract

Many therapeutic antibodies (Abs) and mRNA vaccines, both targeting SARS-CoV-2 spike protein (S-protein), have been developed and approved in order to combat the ongoing COVID-19 pandemic. In consideration of these developments, a common concern has been the potential for Ab-dependent enhancement (ADE) of infection caused by inoculated or induced Abs. Although the preventive and therapeutic effects of these Abs are obvious, little attention has been paid to the influence of the remaining and dwindling anti-S-protein Abs in vivo. Here, we demonstrate that certain monoclonal Abs (mAbs) approved as therapeutic neutralizing anti-S-protein mAbs for human usage have the potential to cause ADE in a narrow range of Ab concentrations. Although sera collected from mRNA-vaccinated individuals exhibited neutralizing activity, some sera gradually exhibited dominance of ADE activity in a time-dependent manner. None of the sera examined exhibited neutralizing activity against infection with the Omicron strain. Rather, some ADE of Omicron infection was observed in some sera. These results suggest the possible emergence of adverse effects caused by these Abs in addition to the therapeutic or preventive effect.”