Interferon at the crossroads of SARS-CoV-2 infection and COVID-19 disease
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Updated: Jul 25, 2025
High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
Published on: March 24, 2015
1Department of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara, California, USA.
Abstract:
A novel coronavirus now known as SARS-CoV-2 emerged in late 2019, possibly following a zoonotic crossover from a coronavirus present in bats. This virus was identified as the pathogen responsible for the severe respiratory disease, coronavirus disease-19 (COVID-19), which as of May 2023, has killed an estimated 6.9 million people globally according to the World Health Organization. The interferon (IFN) response, a cornerstone of antiviral innate immunity, plays a key role in determining the outcome of infection by SARS-CoV-2. This review considers evidence that SARS-CoV-2 infection leads to IFN production; that virus replication is sensitive to IFN antiviral action; molecular mechanisms by which the SARS-CoV-2 virus antagonizes IFN action; and how genetic variability of SARS-CoV-2 and the human host affects the IFN response at the level of IFN production or action or both. Taken together, the current understanding suggests that deficiency of an effective IFN response is an important determinant underlying some cases of critical COVID-19 disease and that IFNλ and IFNα/β have potential as therapeutics for the treatment of SARS-CoV-2 infection.
Insights
A weakened interferon (IFN) response contributes to severe COVID-19. Enhancing IFNλ and IFNα/β may offer effective treatments for SARS-CoV-2 infection.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) causes COVID-19, a global health crisis.
- The interferon (IFN) response is critical for innate antiviral immunity.
- Understanding the interplay between SARS-CoV-2 and the IFN system is crucial for managing COVID-19.
Purpose of the Study:
- To review the role of the IFN response in SARS-CoV-2 infection.
- To explore mechanisms of viral antagonism of IFN.
- To assess the impact of genetic variability on the IFN response.
Main Methods:
- Literature review of studies on SARS-CoV-2 and IFN.
- Analysis of evidence for IFN production and sensitivity to IFN action.
- Examination of viral antagonism mechanisms.
- Investigation of host and viral genetic factors influencing the IFN response.
Main Results:
- SARS-CoV-2 infection elicits an IFN response, and viral replication is sensitive to IFN.
- SARS-CoV-2 employs molecular mechanisms to antagonize IFN action.
- Host and viral genetic variations can modulate the IFN response.
- Impaired IFN response is linked to critical COVID-19 outcomes.
Conclusions:
- Deficiency in the IFN response is a key factor in severe COVID-19.
- Interferon lambda (IFNλ) and Interferon alpha/beta (IFNα/β) show therapeutic potential against SARS-CoV-2.
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