Human cytomegalovirus (HCMV) is a widely-spread virus in the human population which, after the primary, establishes latent infection and remains present in the host organism throughout its life. Although in immunologically competent individuals does not cause the disease, HCMV is an important and dangerous opportunistic pathogen in people with a low or immature immune system, such as infants or people on immunosuppressive therapy. HCMV infects only humans and, therefore, other related animal cytomegaloviruses are used in studies with experimental animals. Of these, murine cytomegalovirus (MCMV) is most commonly used. Recently conducted transcriptional MCMV analysis indicated that the most strongly expressed regions of the MCMV genome are characterized very poorly. One of them is the M116 region. Recently, it has also been shown that the HCMV gene UL116 encodes the glycoprotein located on the virion surface and interacts with the gH protein that is important for the adherence and entry of the virus into the cell and hence can also affect viral tropism. Therefore, as part of this paper, research has been carried out to investigate the deletion of M116 gene on MCMV tropism in vitro. Using the MCMV mutant with deleted M116 gene region and its wild type I checked whether the mutant was attenuated in relation to the wild type and on which types of cells. I phenotypized the cells at which the virus was attenuated and checked for any difference in the expression of mouse inflammatory cytokines.