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Review
. 2023 Aug 29;11(9):2179.
doi: 10.3390/microorganisms11092179.

Interferons-Implications in the Immune Response to Respiratory Viruses

Harrison C Bergeron  1 , Matthew R Hansen  1 , Ralph A Tripp  1
Affiliations
Review

Interferons-Implications in the Immune Response to Respiratory Viruses

Harrison C Bergeron et al. Microorganisms. .

Abstract

Interferons (IFN) are an assemblage of signaling proteins made and released by various host cells in response to stimuli, including viruses. Respiratory syncytial virus (RSV), influenza virus, and SARS-CoV-2 are major causes of respiratory disease that induce or antagonize IFN responses depending on various factors. In this review, the role and function of type I, II, and III IFN responses to respiratory virus infections are considered. In addition, the role of the viral proteins in modifying anti-viral immunity is noted, as are the specific IFN responses that underly the correlates of immunity and protection from disease.

Keywords: COVID-19; IFN; RSV; SARS-CoV-2; immunity; influenza; interferons; respiratory syncytial virus.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Overview of viral protein interactions. Viral proteins from RSV, SARS-CoV-2, and IAV antagonize or agonize IFN responses using a variety of mechanisms. An abridged illustration of the viral proteins and host factors involved is pictured summarizing those mentioned throughout the text. RIG-I (retinoic acid-inducible gene 1), EGF (epidermal growth factor), TLR (toll-like receptor), JAK (Janus kinase), MAVS (mitochondrial antiviral-signalizing protein), TRIM25 (tripartite motif-containing protein 25), CARD (caspase recruitment domains), CPSF30 (cleavage and polyadenylation specificity factor subunit 4), IAV (influenza A virus), RSV (respiratory syncytial virus), S-CoV-2 (SARS-CoV-2), NS/NSP (non-structural/non-structural protein), IRF (interferon regulatory transcription factor), TBK1 (TANK-binding kinase), U (ubiquitination), P (phosphorylation). Created with BioRender and Microsoft PowerPoint.
See this image and copyright information in PMC

References

    1. Isaacs A., Lindenmann J. Virus interference. I. The interferon. Proc. R. Soc. Lond. B Biol. Sci. 1957;147:258–267. doi: 10.1098/rspb.1957.0048. - DOI - PubMed
    1. Taylor M.W. Interferons. Springer International Publishing; Berlin/Heidelberg, Germany: 2014. pp. 101–119.
    1. Lazear H.M., Schoggins J.W., Diamond M.S. Shared and Distinct Functions of Type I and Type III Interferons. Immunity. 2019;50:907–923. doi: 10.1016/j.immuni.2019.03.025. - DOI - PMC - PubMed
    1. Wells A.I., Coyne C.B. Type III Interferons in Antiviral Defenses at Barrier Surfaces. Trends Immunol. 2018;39:848–858. doi: 10.1016/j.it.2018.08.008. - DOI - PMC - PubMed
    1. Pervolaraki K., Rastgou Talemi S., Albrecht D., Bormann F., Bamford C., Mendoza J.L., Garcia K.C., McLauchlan J., Höfer T., Stanifer M.L., et al. Differential induction of interferon stimulated genes between type I and type III interferons is independent of interferon receptor abundance. PLoS Pathog. 2018;14:e1007420. doi: 10.1371/journal.ppat.1007420. - DOI - PMC - PubMed

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