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Upregulated type I interferon responses in asymptomatic COVID-19 infection are associated with improved clinical outcome

Masood, KI (author)
Yameen, M (author)
Ashraf, J (author)
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Shahid, S (author)
Mahmood, SF (author)
Nasir, A (author)
Nasir, N (author)
Jamil, B (author)
Ghanchi, NK (author)
Khanum, I (author)
Razzak, SA (author)
Kanji, A (author)
Hussain, R (author)
Rottenberg, ME (author)
Karolinska Institutet
Hasan, Z (author)
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 (creator_code:org_t)
2021-11-25
2021
English.
In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 11:1, s. 22958-
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

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