RESUMEN
Background: Public hesitancy towards Covid-19 vaccines remains a major hurdle for mass vaccination programs today. While mRNA vaccines are more efficacious than conventional vaccines, it is unknown how much the novelty of this technology increases hesitancy. Methods: We quantify this "novelty penalty" in a large online experiment with 35,173 adults in nine countries. Subjects were randomly selected and assigned to one of two vaccine groups (conventional or mRNA), and one of five hypothetical inoculation rate groups (0%, 20%, 40%, 60%, or 80%). Subjects reported their willingness to accept the Covid-19 vaccine on a five-point Likert scale. Results: The novelty of the mRNA vaccine technology reduces the odds of a higher level of vaccine acceptance by 14.2% (odds ratio 0.858; p < 0.001). On the other hand, we find that social conformity reduces vaccine hesitancy. At a 0% inoculation rate, 31.7% report that they are "very likely" to get a mRNA vaccine while at a 20% inoculation rate, willingness jumps to 49.6%. Conclusions: The novelty of the mRNA vaccine increases hesitancy, but social conformity reduces it. A small group of early adopters can provide momentum for vaccination.
RESUMEN
We previously reported that the p53 tumor suppressor protein plays an essential role in the induction of tetraploid G1 arrest in response to perturbation of the actin cytoskeleton, termed actin damage. In this study, we investigated the role of p53, ataxia telangiectasia mutated protein (ATM), and catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) in tetraploid G1 arrest induced by actin damage. Treatment with actin- damaging agents including pectenotoxin-2 (PTX-2) increases phosphorylation of Ser-15 and Ser-37 residues of p53, but not Ser-20 residue. Knockdown of ATM and DNA-PKcs do not affect p53 phosphorylation induced by actin damage. However, while ATM knockdown does not affect tetraploid G1 arrest, knockdown of DNA-PKcs not only perturbs tetraploid G1 arrest, but also results in formation of polyploidy and induction of apoptosis. These results indicate that DNA-PKcs is essential for the maintenance of actin damage induced- tetraploid G1 arrest in a p53-independent manner. Furthermore, actin damage-induced p53 expression is not observed in cells synchronized at G1/S of the cell cycle, implying that p53 induction is due to actin damage-induced tetraploidy rather than perturbation of actin cytoskeleton. Therefore, these results suggest that p53 and DNA- PKcs independently function for tetraploid G1 arrest and preventing polyploidy formation.