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Author:Arilahti, Veera-Lauriina
Title:Influenssa A-viruksien laukaisema antiviraalinen signalointi dendriittisoluissa
Antiviral signalling in human dendritic cells induced by influenza A viruses
Publication type:Master's thesis
Publication year:2012
Pages:vii + 80 + [23]      Language:   fin
Department/School:Biotekniikan ja kemian tekniikan laitos
Main subject:Biokemia ja mikrobiologia   (Kem-30)
Supervisor:Nordström, Katrina
Instructor:Österlund, Pamela ; Julkunen, Ilkka
OEVS:
Electronic archive copy is available via Aalto Thesis Database.
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Location:P1 Ark Aalto  2022   | Archive
Keywords:influenza A
cytokines
immune response
innate immunity
influenssa A -virus
immuunivaste
sytokiinit
luonnollinen immuniteetti
Abstract (eng): The literature part of this thesis discusses the general structure of influenza A viruses, the variation of influenza A viruses and the immune response to influenza virus infection.
In addition, the literature part introduces the generation of a recombinant influenza A virus.

Because clinical studies have shown that H3N2 subtypes of the influenza A viruses cause more severe infection than H1 viruses, the purpose of this thesis was to study the difference between these two subtypes.
In the experimental part of the thesis the difference in cytokine responses and the activation of transcription factors induced by A/Finland/643/2009 (H1N1), A/Brisbane/59/07 (H1N1) and A/Wisconsin/67/05 (H3N2) viruses was observed.
The infectivity of the viruses was determined by plaque assay and flow cytometry.
Based on these results the virus dilutions used in the infection experiments were chosen.
The expression of transcription factors was detected by western blot technique and cytokine gene expression was analysed by quantitative real time polymerase chain reaction.
The plasmids of the recombinant A/Finland/554/2009 were generated from cloned complementary DNA.

The H3N2 virus induced more robust IFN-a1 and -ß1 cytokine responses and phosphorylation of IRF3 transcription factor than H1N1 viruses.
Instead, CXCL 10 and IFN-A1 cytokine gene expression was stronger in H1N1 virus-infected cells than in the cells infected with the H3N2 virus.
In the cells infected with H1N1 viruses the amount of IRF7 decreased during the infection, while in the cells infected with the H3N2 virus the amount of IRF7 increased during infection.
There were no differences seen in the levels of phosphorylated p38 MAP kinase induced by H1N1 and H3N2 viruses.

The results of this study were significant because H1N1 and H3N2 subtypes cause periodic epidemics but still the comparison of the immune responses induced by these viruses has not been extensively studied in an appropriate way.
Abstract (fin): Työn kirjallisessa osiossa on kuvattu influenssa A -viruksien yleinen rakenne, influenssa A -viruksien muuntuminen sekä influenssavirusinfektion immunologiaa.
Lisäksi kirjallisuusosuudessa on esitelty rekombinanttisen influenssa A -viruksen konstruointi.

Koska kliiniset tutkimukset ovat osoittaneet influenssa A -viruksien H3-alatyypin aiheuttavan vakavamman taudinkuvan kuin H1-viruksien, työn tarkoituksena oli tutkia näiden kahden alatyypin välisiä eroja.
Työn kokeellisessa osuudessa tutkittiin A/Finland/643/2009 (H1N1), A/Brisbane/59/07 (H1N1) ja A/Wisconsin/67105 (H3N2) viruksien laukaiseman sytokiinivasteen ja transkriptiotekijöiden aktivaation eroja.
Viruksien infektiivisyys määritettiin plakkititrauksen ja virtaussytometrian avulla, joiden tulosten perusteella pääteltiin käytetyt viruslaimennokset infektiokokeissa.
Transkriptiotekijöiden ilmentymistä tutkittiin Western blot -menetelmällä ja sytokiinigeenien ilmentymistä kvantitatiivisella reaaliaikaisella polymeraasiketjureaktiolla.
Rekombinanttisen A/Finland/554/2009 -viruksen plasmidit valmistettiin kloonatusta komplementaarisesta DNA:sta.

H3N2-virus laukaisi vahvemman IFN-a1 ja -ß1 sytokiinigeenien ilmentymisen ja fosforyloituneen IRF3-transkriptiotekijän aktivaation kuin H1N1-virukset.
Sen sijaan CXCL10 ja IFN-A1 sytokiinigeenien ilmentyminen oli voimakkaampaa H1N1-viruksilla infektoiduissa dendriittisoluissa kuin H3N2-viruksella.
H1N1-viruksilla infektoiduissa soluissa IRF7 määrä väheni infektion edetessä, kun taas H3N2-viruksella infektoiduissa soluissa IRF7 määrä nousi ajan myötä.
H1N1- ja H3N2-viruksien indusoimassa fosforyloituneen p38 MAP-kinaasin tasoissa ei ollut eroa viruksien välillä.

Työn tulokset olivat merkittäviä, koska H1N1ja H3N2-alatyypit aiheuttavat säännöllisiä epidemioita, mutta kuitenkaan näiden viruksien laukaisemien immuunivasteiden eroja ei ole tutkittu tarpeeksi ja tarkoituksen mukaisesti.
ED:2012-09-17
INSSI record number: 45258
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