Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
The Center for Bioinformatics and Functional Genomics, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Viruses. 2022 Oct 1;14(10):2182. doi: 10.3390/v14102182.
Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19) is known to cause mild to acute respiratory infection and sometimes progress towards respiratory failure and death. The mechanisms driving the progression of the disease and accumulation of high viral load in the lungs without initial symptoms remain elusive. In this study, we evaluated the upper respiratory tract host transcriptional response in COVID-19 patients with mild to severe symptoms and compared it with the control COVID-19 negative group using RNA-sequencing (RNA-Seq). Our results reveal an upregulated early type I interferon response in severe COVID-19 patients as compared to mild or negative COVID-19 patients. Moreover, severely symptomatic patients have pronounced induction of interferon stimulated genes (ISGs), particularly the oligoadenylate synthetase (OAS) family of genes. Our results are in concurrence with other studies depicting the early induction of IFN-I response in severe COVID-19 patients, providing novel insights about the ISGs involved.
SARS-CoV-2 感染导致的 2019 年冠状病毒病（COVID-19）已知可引起轻度至急性呼吸道感染，有时会进展为呼吸衰竭和死亡。导致疾病进展和肺部高病毒载量积累而没有初始症状的机制仍不清楚。在这项研究中，我们使用 RNA 测序（RNA-Seq）评估了有轻度至重度症状的 COVID-19 患者的上呼吸道宿主转录反应，并将其与 COVID-19 阴性对照组进行了比较。我们的结果表明，与轻度或阴性 COVID-19 患者相比，严重 COVID-19 患者的早期 I 型干扰素反应上调。此外，症状严重的患者诱导产生干扰素刺激基因（ISGs），特别是寡聚腺苷酸合成酶（OAS）家族基因。我们的结果与其他研究一致，表明严重 COVID-19 患者中 IFN-I 反应的早期诱导，为涉及的 ISGs 提供了新的见解。
