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Summary. -Study of murine gammaherpesvirus 68 (MHV-68), which was discovered in 1980 in Slovakia, has led to many important findings regarding gammaherpesviral properties in general. Nowadays, it is considered to be a universal model used for detailed studies to determine pathogenetic, immunological and molecular aspects of oncogenesis in analogy to Epstein-Barr virus (EBV) and Kaposi΄s sarcoma-associated virus (KSHV). The objective of this work is to characterize biological and pathogenetic properties of the virus with an emphasis on our prior results concerning ecology, epidemiology, viral persistence in peritoneal macrophages, detection of malign and benign lymphoproliferations accompanied by the presence of atypical lymphocytes in blood during IM-like and leukemia-like syndromes. We are trying to elucidate the role of virus-specific genes in virulence, pathogenicity and murine gammaherpesvirus oncogenesis by comparison of molecular-biological, pathogenetic and oncogenic potential of MHV-68 isolates and deletion mutant MHV-76 and therefore help to understand the analogical processes that occur in EBV infected patients.

Summary. -Murine gammaherpesvirus 68 (MHV-68), isolated from a bank vole (Clethrionomys glareolus)in Slovakia in 1976 is a natural pathogen of wild murid rodents. This review is focused to biological properties of this pathogen, the mode of its maintenance in murid rodents as reservoir animals, mechanisms of its spread to other animals in the same biotope as well as to livestock and household animals. Potential role of ticks as vectors and the possibility of infection of humans with this virus are considered as well. All the above evidence of the virus infection of various hosts is based on serological or molecular analytical data. The presented knowledge indicates important epizootologic consequences, namely harboring and permanent maintenance of the virus in murid rodents as reservoir animals with a real possibility of spread to other animals in the same biotope. These relationships imply a cross-species virus transmission with potential serious consequences for the infected animals or humans.

Murid gammaherpesvirus 4 (MuHV-4) provides a small animal model for the study of animal gammaherpesviruses. MHV-76 is a spontaneous deletion mutant as compared to the prototype strain of MuHV-4 (MHV-68). The MHV-76 genome lacks at least 12 ORFs at the 5´-end including the M1, M2, M3 and M4 genes and the eight viral t-RNA-like genes. During 27 months of experimental infection of BALB/c mice we followed their pathogenesis, immunology and oncogenic properties. After intranasal infection with MHV-76, the infectious virus was detected in the blood, thymus, lungs, heart, liver, spleen, bone marrow, peritoneal macrophages, lymph nodes, kidneys, mammary glands, brain and small intestine. The acute phase of infection was attenuated, but the chronic phase of infection was accompanied with long persistence of virus not only in the lymphatic, but in the neural and glandular tissue, as well. In comparison with the prototype strain, splenomegaly and lymphocytosis was very low. Surprisingly, during 27 months the BALB/c mice infected with MHV-76 did not develop lymphoproliferative disorders like infectious mononucleosis, leukaemia or lymphomas. We hypothesize that the M4 gene, present in all oncogenic MHV isolates, might be related (directly or indirectly) to their transforming properties.

Summary. -We have studied the impact of simultaneous infection of mice with murine gammaherpesvirus (MHV) and infl uenza A virus (IAV) on the immune response and pathogenesis of both infections. Aft er a persistent MHV-68 herpesviral infection had been established, the same mice were super-infected with IAV. Individual parameters of MHV infection (viral DNA detection in organs and blood) and numbers of leukocytes in lungs and spleens were determined. With regard to the assumed reactivation of MHV-68 (mainly in lungs, spleen, thymus and peritoneal exudate cells) we focused our attention on the detection of transcripts, typical either for lytic infection (ORF50) and/or for latency (ORF73). Herpesviral DNA was detected in above mentioned organs in several intervals during the acute phase of IAV co-infection, but the expression of monitored transcripts was lower, i.e. it has decreased. Th ough the reason for such limited expression during acute infl uenza superinfection remains unclear, it is unambiguous that lower MHV-68 expression was detected in lungs and peritoneal exudate cells (PECs) from 3 rd to 10 th day aft er co-infection with IAV. Furthermore, our study showed that the ongoing gammaherpesvirus latency in co-infected mice aff ected the number of cytotoxic T-lymphocytes and neutrophils during the acute IAV infection and lowered their deviations from that of non-infected mice. Th erefore, we suppose that co-infection with herpes and infl uenza viruses could be mutually benefi cial for the host by promoting its defense against both viruses.