Shasha Li1,2, Xiaoqiong Duan3, Yujia Li3, Ming Li1,2, Yong Gao2,4, Tuantuan Li2,4, Shilin Li3, Lin Tan1,2, Tuo Shao5, Andre J Jeyarajan5, Limin Chen3, Mingfeng Han2,6, Wenyu Lin5, Xiuyong Li2,7. 1. Department of Hepatology, The Second People's Hospital of Fuyang City, Fuyang 236015, Anhui Province, P.R. of China. 2. Fuyang Infectious Disease Clinical College of Anhui Medical University, Fuyang 236015, Anhui Province, P.R. of China. 3. Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu 610052, Sichuan Province, P.R. of China. 4. Clinical laboratory, The Second People's Hospital of Fuyang City, Fuyang 236015, Anhui Province, P.R. of China. 5. Liver Center and Gastrointestinal Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. 6. Department of Pneumology, The Second People's Hospital of Fuyang City, Fuyang 236015, Anhui Province, P.R. of China. 7. Hemodialysis center, The Second People's Hospital of Fuyang City, Fuyang 236015, Anhui Province, P.R. of China.
Abstract
BACKGROUND: Dysregulated immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are thought to underlie the progression of coronavirus disease 2019 (COVID-19). We sought to further characterize host antiviral and cytokine gene expression in COVID-19 patients based on illness severity. METHODS: In this case-control study, we retrospectively analyzed 46 recovered COVID-19 patients and 24 healthy subjects (no history of COVID-19) recruited from the Second People's Hospital of Fuyang City. Blood samples were collected from each study participant for RNA extraction and PCR. We assessed changes in antiviral gene expression between healthy controls and patients with mild/moderate (MM) and severe/critical (SC) disease. RESULTS: We found that type I interferon signaling (IFNA2, TLR8, IFNA1, IFNAR1, TLR9, IRF7, ISG15, APOBEC3G, and MX1) and genes encoding proinflammatory cytokines (IL12B, IL15, IL6, IL12A and IL1B) and chemokines (CXCL9, CXCL11 and CXCL10) were upregulated in patients with MM and SC disease. Moreover, we found that IFNA1, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G (APOBEC3G), and Fas-associated protein with death domain (FADD) were significantly downregulated (P < 0.05) in the SC group compared to the MM group. We also observed that microRNA (miR)-155 and miR-130a levels were markedly higher in the MM group compared to the SC group. CONCLUSION: COVID-19 is associated with the activation of host antiviral genes. Induction of the IFN system appears to be particularly important in controlling SARS-CoV-2 infection, as decreased expression of IFNA1, APOBEC3G and FADD genes in SC patients, relative to MM patients, may be associated with disease progression.
BACKGROUND: Dysregulated immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are thought to underlie the progression of coronavirus disease 2019 (COVID-19). We sought to further characterize host antiviral and cytokine gene expression in COVID-19patients based on illness severity. METHODS: In this case-control study, we retrospectively analyzed 46 recovered COVID-19patients and 24 healthy subjects (no history of COVID-19) recruited from the Second People's Hospital of Fuyang City. Blood samples were collected from each study participant for RNA extraction and PCR. We assessed changes in antiviral gene expression between healthy controls and patients with mild/moderate (MM) and severe/critical (SC) disease. RESULTS: We found that type I interferon signaling (IFNA2, TLR8, IFNA1, IFNAR1, TLR9, IRF7, ISG15, APOBEC3G, and MX1) and genes encoding proinflammatory cytokines (IL12B, IL15, IL6, IL12A and IL1B) and chemokines (CXCL9, CXCL11 and CXCL10) were upregulated in patients with MM and SC disease. Moreover, we found that IFNA1, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G (APOBEC3G), and Fas-associated protein with death domain (FADD) were significantly downregulated (P < 0.05) in the SC group compared to the MM group. We also observed that microRNA (miR)-155 and miR-130a levels were markedly higher in the MM group compared to the SC group. CONCLUSION:COVID-19 is associated with the activation of host antiviral genes. Induction of the IFN system appears to be particularly important in controlling SARS-CoV-2 infection, as decreased expression of IFNA1, APOBEC3G and FADD genes in SC patients, relative to MM patients, may be associated with disease progression.
Authors: Juliana M Serpeloni; Quirino Alves Lima Neto; Léia Carolina Lucio; Anelisa Ramão; Jaqueline Carvalho de Oliveira; Daniela Fiori Gradia; Danielle Malheiros; Adriano Ferrasa; Rafael Marchi; David L A Figueiredo; Wilson A Silva; Enilze M S F Ribeiro; Ilce M S Cólus; Luciane R Cavalli Journal: Immunobiology Date: 2021-08-17 Impact factor: 3.152
Authors: Shasha Li; Peng Huang; Andre J Jeyarajan; Chao Ma; Ke Zhu; Chuanlong Zhu; Ning Jiang; Ming Li; Tuo Shao; Mingfeng Han; Lin Tan; Wenyu Lin Journal: Front Med (Lausanne) Date: 2021-12-01