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master's thesis
MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM
2017. urn:nbn:hr:184:483842
Aničić, Josip
University of Rijeka
Faculty of Medicine
Department of Physiology, Immunology and Pathophxsiology

Cite this document

Aničić, J. (2017). MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM (Master's thesis). Rijeka: University of Rijeka, Faculty of Medicine. Retrieved from https://urn.nsk.hr/urn:nbn:hr:184:483842

Aničić, Josip. "MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM." Master's thesis, University of Rijeka, Faculty of Medicine, 2017. https://urn.nsk.hr/urn:nbn:hr:184:483842

Aničić, Josip. "MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM." Master's thesis, University of Rijeka, Faculty of Medicine, 2017. https://urn.nsk.hr/urn:nbn:hr:184:483842

Aničić, J. (2017). 'MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM', Master's thesis, University of Rijeka, Faculty of Medicine, accessed 18 April 2024, https://urn.nsk.hr/urn:nbn:hr:184:483842

Aničić J. MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM [Master's thesis]. Rijeka: University of Rijeka, Faculty of Medicine; 2017 [cited 2024 April 18] Available at: https://urn.nsk.hr/urn:nbn:hr:184:483842

J. Aničić, "MEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM", Master's thesis, University of Rijeka, Faculty of Medicine, Rijeka, 2017. Available at: https://urn.nsk.hr/urn:nbn:hr:184:483842

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Metadata
TitleMEHANIZMI AUTOFAGIJE U INFEKCIJI MIŠJIM CITOMEGALOVIRUSOM
AuthorJosip Aničić
MentorZlatko Trobonjača (mentor)
Committee memberIvana Marić (predsjednik povjerenstva)
Committee memberHana Mahmutefendić (član povjerenstva)
Committee memberHrvoje Jakovac (član povjerenstva)
GranterUniversity of Rijeka
Faculty of Medicine
(Department of Physiology, Immunology and Pathophxsiology)
Rijeka
Defense date and country2017-07-14, Croatia
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Immunology
Abstract
Autofagija je proces koji, pored svoje temeljne funkcije uklanjanja tvari koje stanici nisu potrebne, sudjeluje u nizu životno važnih procesa u organizmu. Upravo zbog toga smo, u eksperimentalnom mišjem modelu, odlučili promatrati kako oslabljena funkcija autofagije utječe na dinamiku i širenje virusne infekcije. Virus koji smo koristili u istraživanju jest mišji citomegalovirus (MCMV) i to njegova Δm157 mutanta koji ima svojstvo inhibicije stanica NK. Korišteni su miševi heterozigoti za gene koji kodiraju proteine Atg5 i LC3 za koje je poznato da imaju ključnu ulogu u procesu autofagije, a kao kontrolnu smo skupinu koristili smo C57bl/6 miševe divljeg tipa. Infekcija miševa provedena je interaperitonealnom inokulacijom 2x105 PFU MCMV Δm157 te žrtvovanjem, vađenjem i titracijom slezene, jetre i pluća sedmog dana od inokulacije. Broj virusa u organima kvantificirali smo metodom određivanja virusnih čistina in vitro nakon četverodnevne inkubacije čiji broj korelira s intenzitetom replikacije virusa u organizmu četvrtog dana od dana vađenja organa. Rezultati su pokazali statistički značajnu razliku u broju PFU u slezeni između sve tri ispitne skupine uz najveći broj virusnih čistina u LC3+/- miševa. U plućima i slezeni smo našli statistički značajno veći broj PFU u skupini LC3+/- miševa u odnosu kontrolne skupine, dok su jetra i slezena pokazale statistički značajno manji broj PFU u skupini Atg5+/- miševa u odnosu na kontrolne miševe. Zaključno, dobiveni rezultati dokazuju da oštećenje autofagije zbog deficijencije Atg5 i LC3 proteina utječe na intenzitet replikacije MCMV-a, što donosi doprinos poznavanju imunobiologije herpes virusa.
Abstract (english)
Autophagy is a mechanism of intracellular degradation which plays important roles in many physiological processes. This is the reason we performed an experiment in which function of autophagy was decreased. Virus used for the experiment was murine cytomegalovirus (MCMV) Δm157 mutant, which inhibits activation of the natural killer cells. Mice used in the experiment were heterozygous for the mutation of Atg5 and LC3 proteins which play key role in the process of autophagy, with C57bl/6 mice being the control group. The experiment was performed by intraperitoneal inoculation of 2x105 PFU MCMV Δm157. Mice were sacrificed and organs (lungs, liver and spleen) were titrated seven days after inoculation. The number of viral particles was quantified by plaque-forming unit (PFU) in vitro method. PFUs were counted and were considered to correlate with the intensity of the viral replication in the organism after a four-day incubation period. That was performed on the eleventh day. Results have shown that the spleen is a major site of viral replication. There is statistically significant difference among all three mouse groups in the spleen tissue with the highest PFU number in mice lacking LC3. Statistically significant higher results were obtained in the lung and spleen tissue of LC3+/- mice than in the control group. Atg5+/- mice obtained a statistically significant lower number of PFUs when compared to control group of mice. In conclusion, these results implicate that intensity of viral replication is strongly influenced by depletion of Atg5 or LC3 proteins. That contributes to a better knowledge of the immunobiology of the herpes viruses.
Keywords
Keywords (english)
Languagecroatian
URN:NBNurn:nbn:hr:184:483842
Study programmeTitle: Medicine
Study programme type: university
Study level: integrated undergraduate and graduate
Academic / professional title: doktor/doktorica medicine (doktor/doktorica medicine)
Type of resourceText
File originBorn digital
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2018-06-13 12:09:23