@hamstersarse wasn’t the topic of this thread “why am I so sick despite being fully vaccinated?”
Answer: differences in genetics, point when vaccinated, waning immunity of vaccine and numerous other factors of host/virus/environment that contribute to various outcomes in individuals.
How has this turned into a pro-vax, anti-vac debate? Can people not stick to topic?!
Firstly, I find it alarming that you are using an accelerated preview article to substantiate points; it hasn’t been fully peer reviewed. Secondly, I would advise that you READ the paper that you have quoted as it directly contradicts the point you are trying to make re. vaccination and ADE….. in fact it refutes it:-
“ Plasma from vaccinated individuals did not promote monocyte infec- tion, indicating that ADE is not a concern with respect to vaccination”
There are concerns related to administration of antibodies to patients suffering from Covid outlined.
The authors themselves point out that the number of people included in the study (10 healthy and 60 covid) is too small.
“Larger cohorts are needed to better assess the relative importance of monocyte/macrophage pyroptosis in severe COVID-19 pathogenesis.”
For anyone not versed in cellular biology who does not fancy wading through the entire paper, here are the bits pertinent to the pro-vax/anti-vax argument:-
The paper’s focus is to elucidate the pathogenesis of covid specifically how excessive inflammation occurs.
They found that 6% of blood monocytes in COVID-19 patients are infected with SARS-CoV-2 and results suggest that antibody-mediated SARS-CoV-2 uptake by monocytes/macrophages triggers inflammatory cell death that aborts production of infectious virus but causes systemic inflammation that contributes to COVID-19 pathogenesis.
To assess whether disease severity or antibodies raised by vaccina- tion increased monocyte virus uptake, LPS-activated monocytes were infected in the presence of pooled plasma from uninfected donors, mRNA vaccine recipients or COVID-19 patients with mild or severe disease. Importantly, uninfected HD and post-vaccination plasma did not facilitate virus uptake or replication, even though plasma anti-RBD IgG was ~2-fold higher in HD vaccine recipients (6.5±1.1 μg/ml) than in COVID-19 patients (3.6±0.5 μg/ml) (Fig. 4f, g). However, non-COVID-19 patient pooled plasma slightly increased infection, but the increase was not significant, suggesting possible inefficient viral uptake by some non-COVID plasma component. Disease severity did not affect infection by COVID-19 patient plasma since pooled mild and/or severe plasma similarly facilitated infection.
Our findings, which implicate opsonizing antibodies in mono- cyte infection and inflammasome activation, suggest that antibod- ies may contribute to deleterious immune reactions associated with severe disease45. FcγR-mediated monocyte infection is an example of antibody-mediated enhancement (ADE) of infection. Nonetheless, over- whelming evidence shows that vaccine-generated neutralizing antibod- ies prevent infection and improve clinical outcome of breakthrough infections, suggesting that anti-spike antibodies are highly beneficial. Plasma from vaccinated individuals did not promote monocyte infec- tion, indicating that ADE is not a concern with respect to vaccination. Therapeutically administered anti-spike neutralizing monoclonal anti- bodies, however, only improve clinical outcome if given early, before hospitalization46,47, and antibody-containing convalescent sera have not shown clinical benefit48. Thus, it is worth considering whether some antibodies might have both protective and deleterious effects49. Anti- bodies are clearly beneficial for blocking infection of ACE2-expressing lung and airway epithelia, where the virus completes replication to produce infectious progeny. However, antibody properties that affect FcR-mediated cellular uptake, phagocytosis, cytotoxicity and comple-
28 ment activation, can affect disease pathogenesis.