The transcriptome of SARS-CoV-2-infected cells that reflects the interplay between host and virus has provided valuable insights into mechanisms underlying SARS-CoV-2 infection and COVID-19 disease progression. In this study, we show that SARS-CoV-2 can establish a robust infection in HEK293T cells that overexpress human angiotensin-converting enzyme 2 (hACE2) without triggering significant host immune response. Instead, endoplasmic reticulum stress and unfolded protein response-related pathways are predominantly activated. By comparing our data with published transcriptome of SARS-CoV-2 infection in other cell lines, we found that the expression level of hACE2 directly correlates with the viral load in infected cells but not with the scale of immune responses. Only cells that express high level of endogenous hACE2 exhibit an extensive immune attack even with a low viral load. Therefore, the infection route may be critical for the extent of the immune response, thus the severity of COVID-19 disease status.
【저자키워드】 immunology, Microbiology, Diseases, Pathogenesis, Molecular biology, Computational biology and bioinformatics, Systems biology, Cell Biology, 【초록키워드】 Transcriptome, SARS-CoV-2, immune response, Stress, SARS-COV-2 infection, Infection, progression, virus, hACE2, COVID-19 disease, Endoplasmic reticulum, Protein, Host immune response, Viral load, severity of COVID-19, immune responses, pathway, Critical, mechanism, Infection route, cell lines, expression level, human Angiotensin-converting enzyme, disease status, immune attack, Express, infected cell, triggering, Host, Cell, robust, provided, activated, reflect, HEK293T cell, overexpress, SARS-CoV-2-infected cell, 【제목키워드】 SARS-CoV-2, innate immune response, transcriptomic analysis, Comparative, infected cell, model system, reveal,