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Exhaustion of Type I interferon response following an acute viral infection

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dc.contributor.authorAlsharifi, Mohammed
dc.contributor.authorRegner, Matthias
dc.contributor.authorBlanden, Robert
dc.contributor.authorLobigs, Mario
dc.contributor.authorLee, Eva
dc.contributor.authorKoskinen, Aulikki
dc.contributor.authorMullbacher, Arno
dc.date.accessioned2015-12-13T23:07:28Z
dc.date.issued2006
dc.date.updated2015-12-12T08:09:12Z
dc.description.abstractViral infections often cause a period of heightened susceptibility to a secondary infection but the cause of this phenomenon is unknown. We found that a primary viral infection in mice rapidly triggers an IFN-I-dependent partial activation state in the majority of B and T lymphocytes, which reverts to a resting phenotype within 5 days. When a secondary infection with an unrelated virus occurred 5 to 9 days after the primary infection, no recurrence of marked activation of lymphocytes was observed. This was not due to an inherent inability of the previously activated cells to undergo renewed partial activation, because they responded when challenged with virus after transfer into "naive" recipients. Instead, the failure to respond optimally resided in the original host's incapacity to mount an IFN-I response to the secondary infection during this time period. Thus, transient immunosuppression through exhaustion of IFN-I production during an acute viral infection creates a time period of enhanced susceptibility to secondary infection.
dc.identifier.issn0022-1767
dc.identifier.urihttp://hdl.handle.net/1885/86221
dc.publisherAmerican Association of Immunologists
dc.sourceJournal of Immunology
dc.subjectKeywords: alpha interferon; CD45 antigen; glycoprotein p 15095; animal cell; animal experiment; animal model; animal tissue; article; B lymphocyte; controlled study; cytokine production; female; immune deficiency; infection sensitivity; lymphocyte activation; mouse
dc.titleExhaustion of Type I interferon response following an acute viral infection
dc.typeJournal article
local.bibliographicCitation.lastpage33241
local.bibliographicCitation.startpage3235
local.contributor.affiliationAlsharifi, Mohammed, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationRegner, Matthias, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationBlanden, Robert, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationLobigs, Mario, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationLee, Eva, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationKoskinen, Aulikki, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationMullbacher, Arno, College of Medicine, Biology and Environment, ANU
local.contributor.authoremailu8102295@anu.edu.au
local.contributor.authoruidAlsharifi, Mohammed, a265709
local.contributor.authoruidRegner, Matthias, u3881430
local.contributor.authoruidBlanden, Robert, u7100504
local.contributor.authoruidLobigs, Mario, u8506091
local.contributor.authoruidLee, Eva, u8512358
local.contributor.authoruidKoskinen, Aulikki, u9108883
local.contributor.authoruidMullbacher, Arno, u8102295
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.description.refereedYes
local.identifier.absfor110799 - Immunology not elsewhere classified
local.identifier.ariespublicationMigratedxPub15021
local.identifier.citationvolume177
local.identifier.scopusID2-s2.0-33747753163
local.identifier.uidSubmittedByMigrated
local.type.statusPublished Version

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