Is a new COVID-19 social contract appropriate?
Ontology highlight
ABSTRACT:
SUBMITTER: Annweiler C
PROVIDER: S-EPMC8517571 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Most vaccines protect both the vaccinated individual and the society by reducing the transmission of infectious diseases. In order to eliminate infectious diseases, individuals need to consider social welfare beyond mere self-interest-regardless of ethnic, religious, or national group borders. It has therefore been proposed that vaccination poses a social contract in which individuals are morally obliged to get vaccinated. However, little is known about whether individuals indeed act upon this social contract. If so, vaccinated individuals should reciprocate by being more generous to a vaccinated other. On the contrary, if the other doesn't vaccinate and violates the social contract, generosity should decline. Three preregistered experiments investigated how a person's own vaccination behavior, others' vaccination behavior, and others' group membership influenced a person's generosity toward respective others. The experiments consistently showed that especially compliant (i.e., vaccinated) individuals showed less generosity toward nonvaccinated individuals. This effect was independent of the others' group membership, suggesting an unconditional moral principle. An internal metaanalysis (n = 1,032) confirmed the overall social contract effect. In a fourth experiment (n = 1,212), this pattern was especially pronounced among vaccinated individuals who perceived vaccination as a moral obligation. It is concluded that vaccination is a social contract in which cooperation is the morally right choice. Individuals act upon the social contract, and more so the stronger they perceive it as a moral obligation. Emphasizing the social contract could be a promising intervention to increase vaccine uptake, prevent free riding, and, eventually, support the elimination of infectious diseases.
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Project description:Black and Hispanic communities in the U.S. have endured a disproportionate burden of COVID-19-related morbidity and mortality. Racial and ethnic health disparities such as these are frequently aggravated by inequitable access to healthcare resources in disadvantaged communities. Yet, no known studies have investigated disadvantaged communities' access to COVID-19-related healthcare resources. The current study accordingly examined racial and ethnic differences in (1) April 2020 COVID-19 total and positive viral test rates across 177 New York City (NYC) ZIP Code Tabulation Areas (ZCTA); and (2) November 2019-April 2020 licensed and intensive care unit (ICU) hospital bed access across 194 NYC ZCTAs. Pairwise analyses indicated higher COVID-19 total and positive test rates per 1000 persons in majority Black and Hispanic vs. majority White ZCTAs (CI [0.117, 4.55]; CI [2.53, 5.14]). Multiple linear regression analyses indicated that higher percentage of Black and Hispanic residents predicted more total COVID-19 tests per 1000 persons (p < 0.05). In contrast, majority Black and Hispanic ZCTAs had fewer licensed and ICU beds (CI [6.50, 124.25]; CI [0.69, 7.16]), with social disadvantage predicting lower licensed and ICU bed access per 1000 persons (p < 0.01). While news reports of inequitable access to COVID-19-related healthcare resources in ethnocultural minority communities have emerged, this is the first study to reveal that social disadvantage may be a major driver of hospital resource inequities in Black and Hispanic communities. Thus, it will be imperative to enact policies that ensure equitable allocation of healthcare resources to socially disadvantaged communities to address current and future public health crises.
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Project description:Aging is identified as a significant risk factor for severe coronavirus disease-2019 (COVID-19), often resulting in profound lung damage and mortality. Yet, the biological relationship between aging, aging-related comorbidities, and COVID-19 remains incompletely understood. This study aimed to elucidate the age-related COVID19 pathogenesis using a Hutchinson-Gilford progeria syndrome (HGPS) mouse model with humanized ACE2 receptors. Pathological features were compared between young, aged, and HGPS hACE2 mice following SAR-CoV-2 challenge. We demonstrated that young mice display robust interferon response and antiviral activity, whereas this response is attenuated in aged mice. Viral infection in aged mice results in severe respiratory tract bleeding, likely contributing a higher mortality rate. In contrast, HGPS hACE2 mice exhibit milder disease manifestations characterized by minor immune cell infiltration and dysregulation of multiple metabolic processes. Comprehensive transcriptome analysis revealed both shared and unique gene expression dynamics among different mouse groups. Collectively, our studies evaluated the impact of SARS-CoV-2 infection on progeroid syndromes using a HGPS hACE2 mouse model, which holds promise as a valuable tool for investigating COVID-19 pathogenesis in individuals with premature aging.
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