The association of OASL and type I interferons in the pathogenesis and survival of intracellular replicating bacterial species

dc.contributor.authorLeisching, Ginaen_ZA
dc.contributor.authorWiid, Ianen_ZA
dc.contributor.authorBaker, Bienyameenen_ZA
dc.date.accessioned2018-08-27T14:15:31Z
dc.date.available2018-08-27T14:15:31Z
dc.date.issued2017
dc.descriptionCITATION: Leisching, G., Wiid, I. & Baker, B. 2017. The association of OASL and type I interferons in the pathogenesis and survival of intracellular replicating bacterial species. Frontiers in Cellular and Infection Microbiology, 7:196, doi:10.3389/fcimb.2017.00196.
dc.descriptionThe original publication is available at https://www.frontiersin.org
dc.description.abstractThe type I IFN response quickly became associated with its role in the innate immune response to viral infection. The past few years have seen the significance of IFNs expand in breadth to include non-viral pathogens. Previous work has identified that following viral infection, type I IFN signaling induces the production of the 2′-5′-oligoadenylate synthetase (OAS) family, which include OAS1, OAS2, OAS3, and OAS-like (OASL) protein. OASL was identified to be strongly induced following viral infection through engaging the RNA sensor RIG-I and increasing signaling through this pathway to enhance the anti-viral type I IFN response. Surprisingly, infection with viral dsDNA revealed an IFN inhibitory role and therefore pro-viral function of OASL through the inhibition of the cGAS cytosolic DNA sensing mechanism. Intracellular bacteria are able to activate the cytosolic DNA sensing pathway, however the role of OASL during bacterial infection is largely unknown. Vacuolar pathogenic microbes such as mycobacteria induce OASL early post infection, where it functions in a prosurvival fashion by inhibiting autophagic mechanisms and antimicrobial peptide expression. This suggests an underestimated role of OASL in the innate immune response to infection with a variety of pathogens and points to OASL-associated modulation of the type I IFN response. OASL may therefore play a critical role in defining the outcome of infection. We provide a brief update on the recent developments of the OAS family of proteins in response to DNA and RNA virus infections, as well as discuss evidence of Oasl expression in response to a number of cytosolic and vacuolar replicating bacterial pathogens.en_ZA
dc.description.urihttps://www.frontiersin.org/articles/10.3389/fcimb.2017.00196/full
dc.description.versionPublisher's version
dc.format.extent6 pages
dc.identifier.citationLeisching, G., Wiid, I. & Baker, B. 2017. The association of OASL and type I interferons in the pathogenesis and survival of intracellular replicating bacterial species. Frontiers in Cellular and Infection Microbiology, 7:196, doi:10.3389/fcimb.2017.00196
dc.identifier.issn2235-2988 (online)
dc.identifier.otherdoi:10.3389/fcimb.2017.00196
dc.identifier.urihttp://hdl.handle.net/10019.1/104353
dc.language.isoen_ZAen_ZA
dc.publisherFrontiers Media
dc.rights.holderAuthors retain copyright
dc.subjectAtypical mycobacteriaen_ZA
dc.subjectPathogenesisen_ZA
dc.titleThe association of OASL and type I interferons in the pathogenesis and survival of intracellular replicating bacterial speciesen_ZA
dc.typeArticleen_ZA
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