SARS-CoV-2 Blocks Innate Immune Activation to Cause COVID-19 Infection, Study Suggests

A recent review article in Journal of Interferon & Cytokine Research (JICR) by researchers at the University of Texas Medical Branch at Galveston (Galveston, TX, USA) has summarized that SARS-CoV-2 blocks the processes of innate immune activation that normally direct the production and/or signaling of type I interferon (IFN-I) by the infected cell and tissues. IFN-I is a key component of host innate immunity that is responsible for eliminating the virus at the early stage of infection. By suppressing innate immunity, the virus replicates and spreads in the body unchecked, leading to COVID-19.

"SARS-CoV-2 utilizes various approaches to evade host IFN-I response, including suppression of IFN-I production and IFN-I signaling," said Hongjie Xia and Pei-Yong Shi, University of Texas Medical Branch at Galveston. "Viruses defective in antagonizing IFN-I response, in combination with replication-defective mutations, could potentially be developed as live attenuated vaccine candidates."

"Targeting innate immunity is highly attractive for therapeutic and vaccine strategies aimed at controlling SARS-CoV-2 infection and protecting against COVID-19. By revealing how the virus blocks innate immune programs we can then build approaches to restore these processes and enhance antiviral immunity," added Journal of Interferon & Cytokine Research Editor-in-Chief Michael Gale Jr., Department of Immunology and Center for Innate Immunity and Immune Disease, University of Washington.

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University of Texas Medical Branch at Galveston