Journal
MICROBIOME
Volume 10, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s40168-022-01260-9
Keywords
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Categories
Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ)
- Fundacao Oswaldo Cruz [VPGDI-054-Fio-20-02-13]
- Mercosur Fund for Structural Convergence (FOCEM, Mercosur) [03/11]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES, Brazil) [001]
- CNPq
- CAPES
- FAPERJ through the National Institutes of Science and Technology Program (INCT)
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This study found that critically ill COVID-19 patients had higher expression levels of HERV-K genes in tracheal aspirates. Increased HERV-K levels were associated with early mortality, inflammation, and coagulopathy.
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.
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