Implemented occupational health surveillance limits the spread of SARS-CoV-2 Omicron at the workplace.

The global spread of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has put an enormous pressure on human societies, at both health and economic levels. Early diagnosis of SARS-CoV-2, the causative agent of 2019 coronavirus disease (COVID-19), has proved an efficient method to rapidly isolate positive individuals and reduce transmission rates, thus alleviating its negative impact on society's well-being and economic growth. In this work, through a coordinated and centralized effort to monitor SARS-CoV-2 circulation in companies from the State of Rio de Janeiro, Brazil, we have detected and linked an early rise of infection rates in January 2022 to the introduction of the Omicron variant of concern (VoC) (BA.1). Interestingly, when the Omicron genomic isolates were compared to correlates from public datasets, it was revealed that introduction events were multiple, with possible migration routes mapping to: Mali; Oman and United States; and Italy, Latin America, and United States. In addition, we have built a haplotype network with our genomic dataset and found no strong evidence of transmission chains, between and within companies. Considering Omicron's particularly high transmissibility, and that most of our samples (>87%) arose from 3 out of 10 companies, these findings suggest that workers from such environments were exposed to SARS-CoV-2 outside their company boundaries. Thus, using a mixed strategy in which quick molecular diagnosis finds support in comprehensive genomic analysis, we have shown that a successfully implemented occupational health program should contribute to document emerging VoC and to limit the spread of SARS-CoV-2 at the workplace.

Human endogenous retrovirus K in the respiratory tract is associated with COVID-19 physiopathology.

BACKGROUND: Critically ill 2019 coronavirus disease (COVID-19) patients under invasive mechanical ventilation (IMV) are 10 to 40 times more likely to die than the general population. Although progression from mild to severe COVID-19 has been associated with hypoxia, uncontrolled inflammation, and coagulopathy, the mechanisms involved in the progression to severity are poorly understood. METHODS: The virome of tracheal aspirates (TA) from 25 COVID-19 patients under IMV was assessed through unbiased RNA sequencing (RNA-seq), and correlation analyses were conducted using available clinical data. Unbiased sequences from nasopharyngeal swabs (NS) from mild cases and TA from non-COVID patients were included in our study for further comparisons. RESULTS: We found higher levels and differential expression of human endogenous retrovirus K (HERV-K) genes in TA from critically ill and deceased patients when comparing nasopharyngeal swabs from mild cases to TA from non-COVID patients. In critically ill patients, higher HERV-K levels were associated with early mortality (within 14 days of diagnosis) in the intensive care unit. Increased HERV-K expression in deceased patients was associated with IL-17-related inflammation, monocyte activation, and an increased consumption of clotting/fibrinolysis factors. Moreover, increased HERV-K expression was detected in human primary monocytes from healthy donors after experimental SARS-CoV-2 infection in vitro. CONCLUSION: Our data implicate the levels of HERV-K transcripts in the physiopathology of COVID-19 in the respiratory tract of patients under invasive mechanical ventilation. Video abstract.

Genetic Evidence and Host Immune Response in Persons Reinfected with SARS-CoV-2, Brazil.

The dynamics underlying severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfection remain poorly understood. We identified a small cluster of patients in Brazil who experienced 2 episodes of coronavirus disease (COVID-19) in March and late May 2020. In the first episode, patients manifested an enhanced innate response compared with healthy persons, but neutralizing humoral immunity was not fully achieved. The second episode was associated with different SARS-CoV-2 strains, higher viral loads, and clinical symptoms. Our finding that persons with mild COVID-19 may have controlled SARS-CoV-2 replication without developing detectable humoral immunity suggests that reinfection is more frequent than supposed, but this hypothesis is not well documented.