Differential immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung and intestinal cells: Implications for treatment with IFN-ß and IFN inducer.
J Infect
; 81(4): e1-e10, 2020 10.
Article
in English
| MEDLINE | ID: covidwho-665494
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 10â¯U/mL interferon-ß (IFNß) pretreatment potently protected both Calu3 and Caco2 against SARS-CoV-2 infection. Interestingly, SARS-CoV-2 was more sensitive to the pretreatment with IFNß 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.Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pneumonia, Viral
/
Interferon Inducers
/
Interferon-beta
/
Coronavirus Infections
/
Respiratory Mucosa
/
Severe Acute Respiratory Syndrome
/
Intestinal Mucosa
Topics:
Vaccines
Limits:
Humans
Language:
English
Journal:
J Infect
Year:
2020
Document Type:
Article
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