Objectives: The aim of this study was to establish experimental model that will enable us to follow constitutive internalization of MHC class I. molecules and other cell surface expressed molecules in uninfected or in the cell infected with either MCMV wild-type or with different MCMV deletion mutant. It is well known that MHC-I molecules are downregulated with higher rate from infected cell than from uninfected cell, so we measured the kinetics of MHC-I molecules downregulation. Additionally, we investigated the principles of MHC-I molecules endocytosis, their recycling pathway and also MHC-I molecules entrance in degradation pathway respectively, in late endosomes. Material and methods: Experiments were performed on murine embrional fibroblasts (MEFs). In our experiment we used uninfected and cell infected with numerous MCMV: Δm138-MCMV (ΔMC95.15) with the deletion of the fcr1 (m138) gene, Δie1-MCMV with the deletion of exon 4 ie1 gene, Δie2-MCMV with the deletion of the ie2 (m128) gene, Δie3-MCMV with the deletion of the ie3 gene, Δm4m6m152-MCMV with deletion of three well known immunoevasins that affect MHC-I molecules maturation. The MCMV wild-type and MCMV deletion mutants were propagated on BALB/c MEFs. The Δie3-MCMV was grown on the complementing cell line NIH3T3 BAM25. In order to follow MHC-I molecules, we have used a monoclonal antibodies (mAbs): MA-215 for conformed Kd molecules and 34-5-8S for conformed Dd molecules. Transferrin receptor (TfR) was followed by mAb R17, and GM1 molecules with labeled cholera toxin B subunits. In order to determine which pathways are involved in endocytosis, endosomal trafficking, recycling and degradation of these molecules, we used different chemical inhibitors of endocytosis. The kinetics of surface molecules was followed by flow citometry and their intracellular trafficking by confocal microscopy after binding of appropriate mAbs. Internalized molecules were colocalized with each other as well as with specific endosomal markers. After rearranging two different protocols from the literature we followed molecules recycling by flow citometry and confocal microscopy. In order to monitor the kinetics of degradation, we used the method of surface biotinilation and imunoprecipitation, electrophoresis on polyacrylamide gels (SDS-PAGE), Western-blot and chemiluminiscence. Results: The pattern of MHC-I molecules expression on the cell surface and intracellular was changing during the infection. MHC-I molecules were downregulated from the surface of infected cell with process that is not specific for them since the other cell surface expressed molecules have also been downregulated. After their downregulation MHC-I molecules were accumulated in hybrid compartment which is positive on various markers of endosomal pathways and compartments (EEA-1+, TfR, GM130). Kinetics of MHC-I molecules internalization were significantly faster in infected cells than in uninfected cells following the pathway that is dynamin independent. Neither of the tested chemical inhibitors (chlorpromazine, imipramin, filipin and AlF4-) did not block internalization of MHC-I molecules. Downregulation of cell surface expressed MHC-I molecules is process that is 5-6 times faster than constitutive internalization and it is probably induced with viral proteins. MCMV directs after internalization from the cell surface MHC-I molecules in the retention compartment. Internalized MHC-I+ vesicles are unable to release EEA-1 respectively early endosomal membrane what could clarify their delayed entry into endolysosomal route in the process of degradation. In MCMV-infected cells many of the internalized molecules have been accumulated in the retention compartment from which recycling was possible although the capacity of the recycling was reduced. Retention compartment contains most of the membrane of early endosomes since only small amount of the molecules was capable to recycle on 16 °C even in the presence of LY294002, which are the characteristics juxtanuclear recycling compartment. The most likely cause of changes in the recycling of MCMV-infected cells was reduction of the total amount of Rab11 molecules that decreased the possibility of creating recycling membrane domains. Degradation pathway has been affected in MCMV-infected cells for numerous molecules regardless to their pathway of entry into the cell. Besides the amount of the Rab11 molecules in MCV-infected cells the level of other Rab molecules was altered. The level of Rab5 in infected cells didn’t decrease like other Rab molecules, leading to the difficult conversion of Rab5 to Rab7, as well as a reduction in the level of Rab7 in infected cells, resulting in a delayed removal of molecules in the degradation pathway. The function that rapidly down-regulate cell surface MHC-I is either related to the effect of ie3 protein or viral early function that are under ie3 regulation. m06/gp48 protein redirects both newly synthesized and internalized MHC-I molecules in the process of degradation. Conclusion: Endosomal remodeling is a mechanism evolved for the purpose of MCMV morphogenesis in infected cell since it does not affect only MHC-I molecules, but also all endocytosed cargo that uses sorting endosomal route. This remodeling, however, supplements the block of MHC-I export from the secretory pathway leading to the accelerated loss of MHC-I from the cell surface in the early phase of infection.