And the simple reason why younger people
get more blood clots is statistical - many of those with this rare
vulnerability have already died before getting old.
the 1960s, scientists found that antiviral antisera might result in an
exceptional increase in viral infectivity of animal viruses. This
phenomenon that viral infection can be enhanced by internalization
associated with antibody Fc receptors, i.e antibody dependent
enhancement, was then widely reported in infections with flaviviruses
and other viruses. Later, more antibody FcR-mediated effects, such as
complement activation and release of inflammatory cytokines, were
reported to be involved in severer diseas. ADE has also been observed in
vaccinated animals after viral challenge with the corresponding virus.
Cats immunized with a vaccine expressing the feline infectious peritonitis virus S protein on a recombinant pox virus vector died earlier than control animals when challenged with FIPV25. Given that passive immunization with feline serum containing high-titre antibodies reactive with feline FIPV also resulted in a more rapid disease after FIPV challenge, the vaccine-induced disease exacerbation may be attributed to antibody dependent enhancement. Moreover, type 2 T helper cell based immunopathologic responses induced by homologous viral challenge after vaccination could also result in disease exacerbation.
Vaccine-associated disease enhancement involves both antibody-dependent and TH2 cell-dependent disease exacerbation. The history of the development of vaccines against respiratory syncytial virus, dengue virus, SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), each provides clues for better COVID-19 vaccine development.