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Infekcija HCMV-om, pripadnikom porodice β herpesvirusa, široko je rasprostranjena u ljudskoj populaciji. Kod imunokompetentnih pojedinaca infekcija uzrokuje blaže ili nikakve simptome, dok kod osoba sa oslabljenim ili nezrelim imunološkim sustavom može biti životno ugrožavajuća. Kao najčešći uzročnik kongenitalnih virusnih infekcija, HCMV uzrokuje teška strukturalna i funkcionalna oštećenja CNS-a. Trenutno ne postoji cjepivo za citomegalovirus, a dostupni terapijski postupci pokazuju ograničenu učinkovitost, stoga su istraživanja temeljnih mehanizama nastanka bolesti od izuzetne važnosti. Skoro sva dostupna istraživanja infekcije neurona CMV-om provedena su u in vitro uvjetima i pokazuju oprečne rezultate o sklonosti CMV-a prema neuronima. Svrha ovog rada bila je provesti in vivo istraživanje na mišjem modelu s reporterskim MCMV virusom kako bi se otkrilo mogu li neuroni biti produktivno inficirani. Rezultati su pokazali da u mozgu miševa dolazi do in vivo konverzije reporterskog virusa 14. dan nakon infekcije. Ovi rezultati ukazuju da inficirani neuroni produciraju virus, ali zbog niskog titra reporterskog virusa u mozgu korištenih miševa nismo saznali koliki postotak neurona ima sposobnost produkcije virusnih čestica. Stoga, ovo istraživanje služi kao preliminarno za daljnja in vivo istraživanja citomegalovirusne infekcije neurona., Infection with HCMV, a member of the β herpesvirus family, is widely distributed within the human population. In immunocompetent individuals the infection causes mild or none symptoms. On the other hand, it can be a life-threatening infection in people with weakened or immature immune system. As the most common cause of congenital viral infections, HCMV leads to severe structural and functional abnormalities of the CNS. At the moment there is no vaccine to prevent cytomegalovirus infection. Also, the available therapeutic procedures show limited efficacy. Therefore, the research on basic mechanisms of CMV infection are of great importance. Almost all the available research on CMV infection of neurons have been conducted in vitro and suggest conflicting results on CMV preference for neurons. The purpose of this paper was to conduct an in vivo research using mouse model with reporter MCMV virus to determine whether neurons can be productively infected. The results have demonstrated that in vivo conversion of the reporter virus occurs in the brain of mice 14 days after the infection. These results indicate that infected neurons can produce the virus. However, due to the low titer of reporter virus in the brain of mice, we haven't found out the exact percentage of neurons that has the ability to produce the virus. In conclusion, this paper serves as a preliminary research for necessary further in vivo research on CMV infection of neurons.