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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Sci+Rep 2021 ; 11 (1): 22958 Nephropedia Template TP
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Upregulated type I interferon responses in asymptomatic COVID-19 infection are associated with improved clinical outcome #MMPMID34824360
Masood KI; Yameen M; Ashraf J; Shahid S; Mahmood SF; Nasir A; Nasir N; Jamil B; Ghanchi NK; Khanum I; Razzak SA; Kanji A; Hussain R; E Rottenberg M; Hasan Z
Sci Rep 2021[Nov]; 11 (1): 22958 PMID34824360show ga
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.
|Adult[MESH]
|Aged[MESH]
|Antiviral Agents[MESH]
|COVID-19/genetics/*immunology[MESH]
|Carrier State/*immunology[MESH]
|Computational Biology/methods[MESH]
|Female[MESH]
|Gene Expression Regulation/genetics[MESH]
|Gene Expression/genetics[MESH]
|Humans[MESH]
|Interferon Type I/genetics/*immunology/metabolism[MESH]