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master's thesis
Uloga optineurina u infekciji herpes simpleks virusa
2018. urn:nbn:hr:193:986708
Vidulić, Ana
University of Rijeka
Faculty of Biotechnology and Drug Development

Cite this document

Vidulić, A. (2018). Uloga optineurina u infekciji herpes simpleks virusa (Master's thesis). Rijeka: University of Rijeka. Retrieved from https://urn.nsk.hr/urn:nbn:hr:193:986708

Vidulić, Ana. "Uloga optineurina u infekciji herpes simpleks virusa." Master's thesis, University of Rijeka, 2018. https://urn.nsk.hr/urn:nbn:hr:193:986708

Vidulić, Ana. "Uloga optineurina u infekciji herpes simpleks virusa." Master's thesis, University of Rijeka, 2018. https://urn.nsk.hr/urn:nbn:hr:193:986708

Vidulić, A. (2018). 'Uloga optineurina u infekciji herpes simpleks virusa', Master's thesis, University of Rijeka, accessed 17 November 2024, https://urn.nsk.hr/urn:nbn:hr:193:986708

Vidulić A. Uloga optineurina u infekciji herpes simpleks virusa [Master's thesis]. Rijeka: University of Rijeka; 2018 [cited 2024 November 17] Available at: https://urn.nsk.hr/urn:nbn:hr:193:986708

A. Vidulić, "Uloga optineurina u infekciji herpes simpleks virusa", Master's thesis, University of Rijeka, Rijeka, 2018. Available at: https://urn.nsk.hr/urn:nbn:hr:193:986708

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Metadata
TitleUloga optineurina u infekciji herpes simpleks virusa
Title (english)Roles of optineurin in herpes simplex virus 1 infection
AuthorAna Vidulić
MentorIgor Jurak (mentor)
Committee memberŽeljka Maglica (predsjednik povjerenstva)
Committee memberAntonija Jurak Begonja (član povjerenstva)
Committee memberIgor Jurak (član povjerenstva)
Committee memberIvana Munitić (član povjerenstva)
GranterUniversity of Rijeka
(Faculty of Biotechnology and Drug Development)
Rijeka
Defense date and country2018-09-26, Croatia
Scientific / art field,
discipline and subdiscipline		BIOTECHNICAL SCIENCES
Biotechnology
Abstract
Optineurin je multifunkcionalni protein čija se uloga pokazala bitnom u IRF3/7 signalnom putu, važnim za obranu od patogena. Nedostatak optineurina ili njegove ubikvitin vežuće regije ima za posljedicu slabiju aktivaciju TBK1 i smanjenu sekreciju interferona tipa 1. Herpes simpleks virus 1 (HSV-1) je virus iz obitelji alphaherpesviridae, koji inficira ljude uspješno izbjegavajući imunosni odgovor domaćina različitim mehanizmima. Kako bismo ispitali ima li optineurin ulogu u infekciji HSV- 1, pratili smo tijek infekcije u divljem tipu mišjih embrionalnih fibroblasta u usporedbi s mišjim embrionalnim fibroblastima u kojima je u genu za optineurin deletirana ubikvitin vežuća regija. Kod infekcije divljeg tipa stanica primijetili smo da razina optineurina pada s progresijom infekcije i to u ovisnosti o količini virusa koji se koristi. Ovaj rezultat ukazuje na virusom posredovano aktivno uklanjanje optineurina. U skladu s prethodno opisanom ulogom optineurina u pozitivnoj regulaciji TBK1, uočili smo da je TBK1 slabije fosforiliran tijekom infekcije kod stanica s nedostatkom optineurina u odnosu na divlji tip stanica. Međutim, u stanicama sa mutiranim optineurinom, virusna replikacija je, usprkos oslabljenoj TBK1 aktivaciji interferona, bila otežana u usporedbi sa stanicama divljeg tipa. Nadalje, nismo uočili značajne razlike kod replikacije HSV-1 kod divljeg tipa ili mutiranog nakon indukcije autofagije izgladnjivanjem. Preliminarni rezultati ovog istraživanja sugeriraju da optineurin olakšava replikaciju HSV-1, ali su potrebna daljnja istraživanja da bi se razjasnio točan mehanizam kojim se to postiže.
Abstract (english)
Optineurin is a multifunctional protein, which plays an important role in the IRF3/7 signaling pathway, an important mechanism through which the host defends itself against pathogens. The lack of optineurin or his ubiquitin binding domain results in attenuated activation of TBK1 and decreased secretion of type 1 interferons. Herpes simplex virus (HSV-1) is a virus from the alphaherpesviridae family which infects people while successfully evading the hosts immune response through various mechanisms. To study the role of optineurin in HSV-1 infection, we compared the progression of the infection in wild tipe mouse embryonic fibroblasts, and compared them to mouse embryonic fibroblasts whose ubiquitin binding domain has been deleted. We noticed that the level of optineurin in wild type infected cells decreased as the infection progressed depending on the amount of virus used. This result points to the active removal of optineurin mediated by the virus. In accordance with the previously described role of optineurin in the positive regulation TBK1, we noticed that TBK1 phosphorylation is weaker in cells with lacking optineurin than in wild type cells. However, viral replication in cells with mutated optineurin was impeded, despite the impaired TBK1 mediated interferon activation, compared to wild type cells. Moreover, we did not notice a significant difference in viral replication in wild type and mutated cells after the induction of autophagy. The preliminary results in this study suggest that optineurin facilitates HSV-1 replication, but more research is needed to clarify the mechanism behind it.
Keywords
Keywords (english)
Languagecroatian
URN:NBNurn:nbn:hr:193:986708
Study programmeTitle: Biotechnology in medicine
Study programme type: university
Study level: graduate
Academic / professional title: magistar/magistra biotehnologije u medicini (magistar/magistra biotehnologije u medicini)
Type of resourceText
File originBorn digital
Access conditionsClosed access
Terms of useLicence In copyright icon
Created on2018-10-31 08:58:37