Document Type
Article
Department
Department of Medicine; Pathology and Laboratory Medicine
Abstract
Understanding key host protective mechanisms against SARS-CoV-2 infection can help improve treatment modalities for COVID-19. We used a blood transcriptome approach to study biomarkers associated with differing severity of COVID-19, comparing severe and mild Symptomatic disease with Asymptomatic COVID-19 and uninfected Controls. There was suppression of antigen presentation but upregulation of inflammatory and viral mRNA translation associated pathways in Symptomatic as compared with Asymptomatic cases. In severe COVID-19, CD177 a neutrophil marker, was upregulated while interferon stimulated genes (ISGs) were downregulated. Asymptomatic COVID-19 cases displayed upregulation of ISGs and humoral response genes with downregulation of ICAM3 and TLR8. Compared across the COVID-19 disease spectrum, we found type I interferon (IFN) responses to be significantly upregulated (IFNAR2, IRF2BP1, IRF4, MAVS, SAMHD1, TRIM1), or downregulated (SOCS3, IRF2BP2, IRF2BPL) in Asymptomatic as compared with mild and severe COVID-19, with the dysregulation of an increasing number of ISGs associated with progressive disease. These data suggest that initial early responses against SARS-CoV-2 may be effectively controlled by ISGs. Therefore, we hypothesize that treatment with type I interferons in the early stage of COVID-19 may limit disease progression by limiting SARS-CoV-2 in the host.
Publication (Name of Journal)
Scientific Reports
Recommended Citation
Masood, K. I.,
Yameen, M.,
Ashraf, J.,
Shahid, S.,
Mahmood, S.,
Nasir, A.,
Nasir, N.,
Jamil, B.,
Ghanchi, N. K.,
Khanum, I.,
Razzak, S. A.,
Kanji, A.,
Hussain, R.,
Rottenberg, M. E.,
Hasan, Z.
(2021). Upregulated type I interferon responses in asymptomatic COVID-19 infection are associated with improved clinical outcome. Scientific Reports, 11(1), 22958.
Available at:
https://ecommons.aku.edu/pakistan_fhs_mc_pathol_microbiol/1369
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Comments
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