Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients. Issue 1 (1st January 2020)

• Record Type: Journal Article
• Authors: Xiong, Yong; Liu, Yuan; Cao, Liu; Wang, Dehe; Guo, Ming; Jiang, Ao; Guo, Dong; Hu, Wenjia; Yang, Jiayi; Tang, Zhidong; Wu, Honglong; Lin, Yongquan; Zhang, Meiyuan; Zhang, Qi; Shi, Mang; Liu, Yingle; Zhou, Yu; Lan, Ke; Chen, Yu
• Is Part Of: Emerging microbes & infections. Volume 9:Issue 1(2020)
• Page Start: 761
• Page End: 770
• Publication Date: 2020-01-01
• Subjects: COVID-19 -- transcriptome profiling -- inflammation -- cytokine -- lymphopenia; Medical microbiology -- Periodicals; Communicable diseases -- Periodicals; Infection -- Periodicals; 616.9041
• DOI: 10.1080/22221751.2020.1747363
• Languages: English
• ISSNs: 2222-1751

Abstract

ABSTRACT: Circulating in China and 158 other countries and areas, the ongoing COVID-19 outbreak has caused devastating mortality and posed a great threat to public health. However, efforts to identify effectively supportive therapeutic drugs and treatments has been hampered by our limited understanding of host immune response for this fatal disease. To characterize the transcriptional signatures of host inflammatory response to SARS-CoV-2 (HCoV-19) infection, we carried out transcriptome sequencing of the RNAs isolated from the bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cells (PBMC) specimens of COVID-19 patients. Our results reveal distinct host inflammatory cytokine profiles to SARS-CoV-2 infection in patients, and highlight the association between COVID-19 pathogenesis and excessive cytokine release such as CCL2/MCP-1, CXCL10/IP-10, CCL3/MIP-1A, and CCL4/MIP1B. Furthermore, SARS-CoV-2 induced activation of apoptosis and P53 signalling pathway in lymphocytes may be the cause of patients' lymphopenia. The transcriptome dataset of COVID-19 patients would be a valuable resource for clinical guidance on anti-inflammatory medication and understanding the molecular mechansims of host response.