Editing Interferon (section)

==Coronavirus response==
[[Coronavirus]]es evade [[Innate immune system|innate immunity]] during the first ten days of viral infection.<ref name="pmid32726355">{{cite journal | vauthors = Sa Ribero M, Jouvenet N, Dreux M, Nisole S | title = Interplay between SARS-CoV-2 and the type I interferon response | journal = PLOS Pathogens | volume = 16 | issue = 7 | pages = e1008737 | date = July 2020 | pmid = 32726355 | pmc = 7390284 | doi = 10.1371/journal.ppat.1008737 | doi-access = free }}</ref> In the early stages of infection, [[Severe acute respiratory syndrome coronavirus 2|SARS-CoV-2]] induces an even lower [[interferon type I]] (IFN-I) response than [[Severe acute respiratory syndrome coronavirus 1|SARS-CoV]], which itself is a weak IFN-I inducer in human cells.<ref name="pmid32726355" /><ref name="pmid34571706">{{cite journal | vauthors = Palermo E, Di Carlo D, Sgarbanti M, Hiscott J | title = Type I Interferons in COVID-19 Pathogenesis | journal = Biology | volume = 10 | issue = 9 | page = 829 | date = August 2021 | pmid = 34571706 | pmc = 8468334 | doi = 10.3390/biology10090829 | doi-access = free }}</ref> SARS-CoV-2 limits the IFN-III response as well.<ref name="pmid32935333">{{cite journal | vauthors = Toor SM, Saleh R, Sasidharan Nair V, Taha RZ, Elkord E | title = T-cell responses and therapies against SARS-CoV-2 infection | journal = Immunology | volume = 162 | issue = 1 | pages = 30–43 | date = January 2021 | pmid = 32935333 | pmc = 7730020 | doi = 10.1111/imm.13262 }}</ref> Reduced numbers of [[plasmacytoid dendritic cell]]s with age is associated with increased [[COVID-19]] severity, possibly because these cells are substantial interferon producers.<ref name="pmid34746804">{{cite journal | vauthors = Bartleson JM, Radenkovic D, Covarrubias AJ, Furman D, Winer DA, Verdin E | title = SARS-CoV-2, COVID-19 and the Ageing Immune System | journal = Nature Aging | volume = 1 | issue = 9 | pages = 769–782 | date = September 2021 | pmid = 34746804 | pmc = 8570568 | doi = 10.1038/s43587-021-00114-7 }}</ref>

Ten percent of patients with life-threatening COVID-19 have [[Autoantibody|autoantibodies]] against type I interferon.<ref name="pmid34746804" />

Delayed IFN-I response contributes to the pathogenic inflammation ([[cytokine storm]]) seen in later stages of [[COVID-19]] disease.<ref name="pmid32464097">{{cite journal | vauthors = Park A, Iwasaki A | title = Type I and Type III Interferons - Induction, Signaling, Evasion, and Application to Combat COVID-19 | journal = Cell Host & Microbe | volume = 27 | issue = 6 | pages = 870–878 | date = June 2020 | pmid = 32464097 | pmc = 7255347 | doi = 10.1016/j.chom.2020.05.008 }}</ref> Application of IFN-I prior to (or in the very early stages of) viral infection can be protective,<ref name="pmid32726355" /> which should be validated in randomized clinical trials.<ref name="pmid32464097" />

With pegylated IFN lambda, the relative risk for hospitalization with the Omicron strains is reduced by about 80 %.<ref>{{cite journal | vauthors = Reis G, Moreira Silva EA, Medeiros Silva DC, Thabane L, Campos VH, Ferreira TS, Santos CV, Nogueira AM, Almeida AP, Savassi LC, Figueiredo-Neto AD, Dias AC, Freire Júnior AM, Bitarães C, Milagres AC, Callegari ED, Simplicio MI, Ribeiro LB, Oliveira R, Harari O, Wilson LA, Forrest JI, Ruton H, Sprague S, McKay P, Guo CM, Limbrick-Oldfield EH, Kanters S, Guyatt GH, Rayner CR, Kandel C, Biondi MJ, Kozak R, Hansen B, Zahoor MA, Arora P, Hislop C, Choong I, Feld JJ, Mills EJ, Glenn JS | title = Early Treatment with Pegylated Interferon Lambda for Covid-19 | journal = The New England Journal of Medicine | volume = 388 | issue = 6 | pages = 518–528 | date = February 2023 | pmid = 36780676 | pmc = 9933926 | doi = 10.1056/NEJMoa2209760 }}</ref>