Enteroviruses are small, non-enveloped, single-stranded RNA-viruses. They are one of the most common human pathogens. They cause a wide variety of mild and severe symptoms and diseases, such as common cold, myocarditis and different chronic diseases. Typically enterovirus infection quickly leads to the release of virus particles via cell death called cell lysis. However, research indicates that enteroviruses are also capable of causing persistent infection in which the cell culture stays alive despite of virus infection. This form of infection is not yet widely studied and for example it is not known how the infection spreads from these cells. Persistent enterovirus infection has been linked to type I diabetes making it an interesting research subject. The goal of this study was to examine two different enteroviruses (CVB3, CVB5) that belong to the family of coxsackieviruses, in two human cell lines that represent two different cell types (A549, RD). The goal was to determine the kinetics of forming new virus particles and replication, the timing of the cell death and the spreading mechanism of the infection. Cell viability test based on luminescence showed that both viruses killed A549 cell cultures quickly: CVB3 by 24 hours and CVB5 by 72 hours. This showed that the infection in question was lytic. RD cell cultures stayed alive for several days despite of the virus infection which indicates persistent infection model. Immunofluorescence labelling and confocal microscopy showed that in A549 cells the replication and the production of new virus particles were efficient with both viruses despite the viruses behaving differently in regards of time. CVB5 was considerably slower with significant virus production appearing only 12 hours post infection. The CVB3 was in a similar situation already in 6 hours post infection. In RD cells both viruses were slower than in A549 cells. Only a subpopulation off RD cells seemed to be infected with the viruses. This was shown in CVB3 with less than 20 % and in CVB5 with less than 10 % infected cells in a time span of 6-96 hours during which the replication was examined. Similar results were shown with production of capsids in CVB3. In CVB5 infection less than 20 % of cells showed positive for capsids labeling during a time span of 6-48 hours. Surprisingly though, 96 hours post infection 58 % of the RD cell population were CVB5 capsid positive cells. This surprising spike was not seen in the replication positive cells, which means that these were probably viruses transferred from the cells that show replication. This phenomenon was not seen during CVB3 infection meaning that the viruses have different spreading mechanisms in this cell line. The location of the capsids label was also different in CVB3 and CVB5 infections suggesting that these viruses have different spreading mechanisms. Additionally, preliminary tests indicate that RD cells produce viruses during CVB3 and CVB5 infections without cell lysis. All in all, in this study two different infection mechanisms (lytic and persistent) were examined. In both models viruses were observed to transfer to new cells without cell death, possibly via vesicle spreading. The persistent CVB5 infection of RD cells needs additional testing as to understand the spreading of new virus particles into majority of cells suddenly several days post infection.