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Differential immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung and intestinal cells: Implications for treatment with IFN-β and IFN inducer.
J Infect. 2020 Oct; 81(4):e1-e10.JI

Abstract

OBJECTIVES

Respiratory and intestinal tract are two primary target organs of SARS-CoV-2 infection. However, detailed characterization of the host-virus interplay in infected human lung and intestinal epithelial cells is lacking.

METHODS

We utilized immunofluorescence assays, flow cytometry, and RT-qPCR to delineate the virological features and the innate immune response of the host cells against SARS-CoV-2 infection in two prototype human cell lines representing the human lung (Calu3) and intestinal (Caco2) epithelium when compared with SARS-CoV.

RESULTS

Lung epithelial cells were significantly more susceptible to SARS-CoV-2 compared to SARS-CoV. However, SARS-CoV-2 infection induced an attenuated pro-inflammatory cytokines/chemokines induction and type I and type II IFN responses. A single dose of 10 U/mL interferon-β (IFNβ) pretreatment potently protected both Calu3 and Caco2 against SARS-CoV-2 infection. Interestingly, SARS-CoV-2 was more sensitive to the pretreatment with IFNβ and IFN inducer than SARS-CoV in Calu3.

CONCLUSIONS

Despite robust infection in both human lung and intestinal epithelial cells, SARS-CoV-2 could attenuate the virus-induced pro-inflammatory response and IFN response. Pre-activation of the type I IFN signaling pathway primed a highly efficient antiviral response in the host against SARS-CoV-2 infection, which could serve as a potential therapeutic and prophylactic maneuver to COVID-19 patients.

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Authors+Show Affiliations

Shuai H
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Chu H
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Hou Y
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Yang D
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Wang Y
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Hu B
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Huang X
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Zhang X
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Chai Y
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Cai JP
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Chan JF
State Key Laboratory of Emerging Infectious Diseases, Carol Yu Centre for Infection, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region; Department of Microbiology, Queen Mary Hospital, Pokfulam, Hong Kong Special Administrative Region; Department of Clinical Microbiology and Infection Control, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China; Hainan Medical University-The University of Hong Kong Joint Laboratory of Tropical Infectious Diseases, Hainan Medical University, Haikou, Hainan, and The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China. Electronic address: jfwchan@hku.hk.
Yuen KY
Department of Clinical Microbiology and Infection Control, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China; Hainan Medical University-The University of Hong Kong Joint Laboratory of Tropical Infectious Diseases, Hainan Medical University, Haikou, Hainan, and The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China. Electronic address: kyyuen@hku.hk.

MeSH

Antiviral AgentsBetacoronavirusCOVID-19Caco-2 CellsCell Line, TumorCoronavirus InfectionsEpithelial CellsHumansImmunity, InnateInterferon InducersInterferon-betaIntestinal MucosaLungPandemicsPneumonia, ViralRespiratory MucosaSevere acute respiratory syndrome-related coronavirusSARS-CoV-2Severe Acute Respiratory SyndromeCOVID-19 Drug Treatment

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

32707230

Citation

Shuai, Huiping, et al. "Differential Immune Activation Profile of SARS-CoV-2 and SARS-CoV Infection in Human Lung and Intestinal Cells: Implications for Treatment With IFN-β and IFN Inducer." The Journal of Infection, vol. 81, no. 4, 2020, pp. e1-e10.
Shuai H, Chu H, Hou Y, et al. Differential immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung and intestinal cells: Implications for treatment with IFN-β and IFN inducer. J Infect. 2020;81(4):e1-e10.
Shuai, H., Chu, H., Hou, Y., Yang, D., Wang, Y., Hu, B., Huang, X., Zhang, X., Chai, Y., Cai, J. P., Chan, J. F., & Yuen, K. Y. (2020). Differential immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung and intestinal cells: Implications for treatment with IFN-β and IFN inducer. The Journal of Infection, 81(4), e1-e10. https://doi.org/10.1016/j.jinf.2020.07.016
Shuai H, et al. Differential Immune Activation Profile of SARS-CoV-2 and SARS-CoV Infection in Human Lung and Intestinal Cells: Implications for Treatment With IFN-β and IFN Inducer. J Infect. 2020;81(4):e1-e10. PubMed PMID: 32707230.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differential immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung and intestinal cells: Implications for treatment with IFN-β and IFN inducer. AU - Shuai,Huiping, AU - Chu,Hin, AU - Hou,Yuxin, AU - Yang,Dong, AU - Wang,Yixin, AU - Hu,Bingjie, AU - Huang,Xiner, AU - Zhang,Xi, AU - Chai,Yue, AU - Cai,Jian-Piao, AU - Chan,Jasper Fuk-Woo, AU - Yuen,Kwok-Yung, Y1 - 2020/07/21/ PY - 2020/5/19/received PY - 2020/7/16/accepted PY - 2020/7/25/pubmed PY - 2020/10/6/medline PY - 2020/7/25/entrez KW - COVID-19 KW - IFN KW - Innate immune response KW - SARS-CoV-2 SP - e1 EP - e10 JF - The Journal of infection JO - J Infect VL - 81 IS - 4 N2 - OBJECTIVES: Respiratory and intestinal tract are two primary target organs of SARS-CoV-2 infection. However, detailed characterization of the host-virus interplay in infected human lung and intestinal epithelial cells is lacking. METHODS: We utilized immunofluorescence assays, flow cytometry, and RT-qPCR to delineate the virological features and the innate immune response of the host cells against SARS-CoV-2 infection in two prototype human cell lines representing the human lung (Calu3) and intestinal (Caco2) epithelium when compared with SARS-CoV. RESULTS: Lung epithelial cells were significantly more susceptible to SARS-CoV-2 compared to SARS-CoV. However, SARS-CoV-2 infection induced an attenuated pro-inflammatory cytokines/chemokines induction and type I and type II IFN responses. A single dose of 10 U/mL interferon-β (IFNβ) pretreatment potently protected both Calu3 and Caco2 against SARS-CoV-2 infection. Interestingly, SARS-CoV-2 was more sensitive to the pretreatment with IFNβ and IFN inducer than SARS-CoV in Calu3. CONCLUSIONS: Despite robust infection in both human lung and intestinal epithelial cells, SARS-CoV-2 could attenuate the virus-induced pro-inflammatory response and IFN response. Pre-activation of the type I IFN signaling pathway primed a highly efficient antiviral response in the host against SARS-CoV-2 infection, which could serve as a potential therapeutic and prophylactic maneuver to COVID-19 patients. SN - 1532-2742 UR - https://www.unboundmedicine.com/medline/citation/32707230/Differential_immune_activation_profile_of_SARS_CoV_2_and_SARS_CoV_infection_in_human_lung_and_intestinal_cells:_Implications_for_treatment_with_IFN_β_and_IFN_inducer_ DB - PRIME DP - Unbound Medicine ER -