ABSTRACT
Background: COVID-19 has exacerbated health inequalities worldwide. Yet, such a perspective has not been investigated in specific healthcare workers and their resulting inclusion as a priority group for vaccination have been an important focus of political and social discussion. This study aimed at investigating whether SARS-CoV-2-seropositivity in healthcare workers in a public hospital in Rio de Janeiro, Brazil, was influenced by social determinants of health and the social vulnerability in subgroups of workers. Methods: A serological survey was conducted in 1,154 healthcare workers in June and July 2020. The association between the serological test results for detection of IgG antibodies to SARS-CoV-2 and socioeconomic, occupational characteristics and transportation used by the workers to commute was assessed using the Pearson´s chi-square test and Carmer’s V. Findings: Overall, the serum prevalence for the virus in the healthcare workers was 30%. Non-white workers with lower income and schooling, as well as users of the mass transportation system showed the highest infection rates. Importantly they mostly corresponded to hospital support workers, in particular the cleaning personnel. Accordingly, income, schooling and work modality appeared as negative predictors, as ascertained by forest plot analysis. Interpretations: The data clearly illustrate the inequality in SARS-CoV-2 infection in the Brazilian population, comprising even healthcare workers of the Brazilian unified health system.Funding Information: This study was financed by Fiocruz, CNPq, Faperj, Capes, FOCEM/Mercosur and the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES) – Finance Code 001.Declaration of Interests: The authors declare no competing financial interests.Ethics Approval Statement: “Clinical and immunological characteristics of children, adolescents, and adults with COVID-19 diagnosis: COVID-19 Kids Project” was submitted to the Institutional Review Board of IFF (CEP/IFF) under identification number 30487120.2.0000.0008 and approved under review number 4.100.148. There was no discrimination in the selection of research subjects or exposure to unnecessary risks.
Subject(s)
Porphyria, Erythropoietic , COVID-19 , Gerstmann SyndromeABSTRACT
Background: Many SARS-CoV-2 variants of concern have emerged since the Covid-19 outburst, notably the lineages detected in the UK, South Africa, and Brazil. Their increased transmissibility and higher viral load put them in the spotlight. Much has been investigated on the ability of those new variants to evade antibody recognition. However, not enough attention has been given to pre-existing and induced SARS-CoV-2-specific CD8+ T cell responses during the natural course of infection by new lineages. Methods: In this work, we investigated the SARS-CoV-2-specific CD8+ T cell epitopes from the main variants of concern and the potential of associated mutations to trigger or hinder CD8+ T-cells response. We also estimated the population's coverage of these different lineages, considering peptide binding predictions to class I HLA alleles from 29 countries to investigate differences in the fraction of individuals expected to respond to a given epitope set from new and previous lineages. Results: We observed a lower populational coverage for 20B/S.484K (P2 lineage) in contrast to an increased coverage found for 20H/501Y.V2 (B.1.351 Lineage) and 20J/501Y.V3 (P1 lineage) compared to a reference lineage. Moreover, mutations such as Spike N501Y and Nucleocapsid T205I were predicted to have an overall higher affinity through HLA-I than the reference sequence. Conclusions: In summary, the data in this work provided evidence for the existence of potentially immunogenic and conserved epitopes across new SARS-CoV-2 variants, but also highlights the reduced populational's coverage for the Brazilian lineage P.1, suggesting its potential to evade from CD8+ T-cell responses. Our results also may guide efforts to characterize and validate relevant peptides to trigger CD8+ T-cell responses, and design new universal T-cell-inducing vaccine candidates that minimize detrimental effects of viral diversification and at the same time induce responses to a broad human population.