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. 2021 Oct 7;42(11):1009–1023. doi: 10.1016/j.it.2021.09.003

Figure 2.

Figure 2

Key figure. Key roles for type I, II, and III interferons in mucosal antiviral responses in mice and humans.

(A) Norovirus initiates infection within the gastrointestinal tract, wherein type III interferons (IFNs) are key for restricting viral growth [30]. Type I IFNs restrict dissemination of the virus from the gut to distal sites such as the liver and brain, wherein type II IFN further controls replication [69,89]. (B) Herpes simplex virus infections initiated in the female reproductive tract are controlled at the site of infection by type III IFNs, while type I IFNs drive inflammation [29,60]. Dissemination from this mucosal tissue to the central nervous system (CNS) is restricted by type I IFNs [32,73]. Herpesviruses undergo latency, remaining mostly transcriptionally silent within neurons, with reactivation of the virus from latency restricted by type II IFN [92]. (C) SARS-CoV-2 is restricted within the respiratory tract by type I and III IFNs [83,84,113]. Conversely, type I IFNs may be drivers of inflammation in the respiratory tract during SARS-CoV-2 infection [28,83,86]. The role of type II IFN is currently less understood, but it may be proviral in some sites by inducing expression of the viral receptor and may also drive inflammation [100]. Figure created using BioRender (https://biorender.com/). Abbreviation: SARS-CoV-2, severe acute respiratory virus coronavirus 2.