In-Depth Ethical Analysis of the COVID-19 Vaccine Rollout for Migrant Workers in the Gulf Countries.

During the initial COVID-19 vaccine rollout, supplies were scarce, necessitating rationing. Gulf countries, hosting millions of migrant workers, prioritized nationals over migrants for vaccination. As it turned out, many migrant workers found themselves waiting behind nationals to get vaccinated for COVID-19. Here, we discuss the public health ethical concerns surrounding this approach and call for fair and inclusive vaccine allocation policies. First, we examine global justice through the lens of statism, where distributive justice applies only to sovereign state members, and cosmopolitanism, advocating equal justice distribution for all humans. We propose a cooperativist perspective, suggesting that new justice obligations can arise between people beyond national ties. In cases of mutually beneficial cooperation, such as migrant workers contributing to a nation's economy, equal concern for all parties is required. Second, the principle of reciprocity further supports this stance, as migrants significantly contribute to host countries' societies and economies. Additional ethical principles-equity, utilitarianism, solidarity, and nondiscrimination-are essentially violated when excluding non-nationals in vaccine distribution. Finally, we argue that prioritizing nationals over migrants is not only ethically indefensible, but it also fails to ensure full protection for nationals and hampers efforts to curb COVID-19 community spread.

Conditional deletion of dnaic1 in a murine model of primary ciliary dyskinesia causes chronic rhinosinusitis.

Studies of primary ciliary dyskinesia (PCD) have been hampered by the lack of a suitable animal model because disruption of essential ciliary genes in mice results in a high incidence of lethal hydrocephalus. To develop a viable mouse model for long-term studies of PCD, we have generated a transgenic mouse line in which two conserved exons of the mouse intermediate dynein chain gene, Dnaic1, are flanked by loxP sites (Dnaic1(flox/flox)). Dnaic1 is the murine homolog of human DNAI1, which is mutated in approximately 10% of human PCD cases. These mice have been crossed with mice expressing a tamoxifen-inducible Cre recombinase (CreER). Treatment of adult Dnaic1(flox/flox)/CreER(+/-) mice with tamoxifen results in an almost complete deletion of Dnaic1 with no evidence of hydrocephalus. Treated animals have reduced levels of full-length Dnaic1 mRNA, and electron micrographs of cilia demonstrate a loss of outer dynein arm structures. In treated Dnaic1(flox/flox)/CreER(+/-) animals, mucociliary clearance (MCC) was reduced over time. After approximately 3 months, no MCC was observed in the nasopharynx, whereas in the trachea, MCC was observed for up to 6 months, likely reflecting a difference in the turnover of ciliated cells in these tissues. All treated animals developed severe rhinosinusitis, demonstrating the importance of MCC to the health of the upper airways. However, no evidence of lung disease was observed up to 11 months after Dnaic1 deletion, suggesting that other mechanisms are able to compensate for the lack of MCC in the lower airways of mice. This model will be useful for the study of the pathogenesis and treatment of PCD.