SVIBOR - Papers quoted in CC - project code: 3-01-169

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Papers quoted in Current Contents on project 3-01-169

Quoted papers: 12
Other papers: 24
Total: 36

Title:

Authors:: Jonjić, Stipan (95583); Pavić, Ivica (163242); Polić, Bojan (173636); Crnković, Irena (194586); Lučin, Pero (142314); Koszinowski, Ulrich

Journal: Journal of Experimental Medicine
ISSN: 0022-1007
Volume: 179
Year: 1994
Pages: from 1713 to 1717
Number of references: 23
Language: engleski
Summary: Virus shedding from the epithelial cells of the serous acini ofsalivary glands is a major source for the horizontaltransmission of cytomegalovirus. These cells are, different toother tissues, exempt from CD8+ T lymphocyte control. CD4 Tlymphocytes are essential to terminate the productive infection.Here, we prove that T-B cooperation and the production ofantibodies are not required for this process. For the infectionwith murine cytomegalovirus (MCMV) mutant mice were used which tonot produce antibodies due to a disrupted membrane exon of theimmunoglobulin u-chain gene. Also in these mice the virusclearance from salivary glands is a function of CD4 Tlymphocytes. Yet, these mice clear the virus and establish virallatency with a kinetics that is indistinguishable from normalmice. Reactivation from virus latency is the only stage at whichthe absence of antibodies alters the phenotype of infection. Inimmunoglobulin-deficient mice virus recurrence results in highhervirus titers. The adoptive serum transfer proved that antibody isthe limiting factor which prevents virus dissemination in theimmunodeficient host.
Keywords: Cytomegalovirus, Antibodies, Viral latency, ractivation.

Title:

Authors:: Koszinowski, Ulrich; Jonjić, Stipan (95583); Lučin, Pero (142314)

Journal: Seminars in Virology
ISSN: 1044-5773
Volume: 5
Year: 1994
Pages: from 297 to 305
Number of references: 60
Language: engleski
Summary: Cytomegaloviruses (CMV) are members of the ubiquitous family of herpesviruses. The infection is characterized by a highly variable course of disease. the virus-host balance is dependent upon the state of the immune system. Several immune mechanisms independently contribute to virus control. The virus escapes immunological clearence and persists throughout life in the infected host. CMV apparently encodes more than one function which modulate the host surveillance. Some tissues are exempt from control and alow local virus persistance. Other host-interactive genes can be directly monitored by their interaction with proteins of defined immunological function. Sequence homology indicates the existence of additional patative host-interactive genes.
Keywords: antigen presentation, cytokines , cytemegalovirus, immune evasion, virus persistence

Title:

Authors:: Lučin, Pero (142314); Jonjić, Stipan (95583); Hengel, Hartmut; Pavić, Ivica (163242); Polić, Bojan (173636); Crnković, Irena (194586); Polić, Bojan (173636); Crnković, Irena (194586); Koszinowski, Ulrich; Thale, Regine; Zorica, Irena

Journal: Regional Immunology
Number: 5-6
ISSN: 0896-0623
Volume: 6
Year: 1994
Pages: from 391 to 396
Number of references: 31
Language: engleski
Summary: Cytomegaloviruses (CMV) are members of the ubiquitous herpesvirus family. The course of CMV infection is dependent upon the status of the immune system. In immunocompetent hosts the infection is efficiently controlled and the virus escapes into the state of latency, whereas in immunodeficient hosts the replication of CMV is pathogenic resulting in a highly variable course of disease. In most tissues the productive infection with murine CMV (MCMV) is controlled by CD8 T lymphocytes. Lack of CD8 T cells can be efficaciously compensated by CD4 T cells which engage remaining immune mechanisms to clear the virus. Expection to this rule are acinar epithelial cells of the salivary gland where CD8 T cells are insufficient and the function of CD4 T cells is required for generation of an effector mechanism. In this organ the virus escapes immune control resulting in persistent infection which can continue for life if CD4 T lymphocytes are absent. Two mechanisms for CMV evasion from immune control are recognized so far: block in antigen presentation and coding for a protein with FC-receptor function. The possible role of these mechanisms in the salivary gland persistance of MCMV is discussed.
Keywords: cytomegalovirus, cytotoxic T lymphocytes, interferon, murine cytomegalovirus, major histocompatibility complex, natural killer, tumor necrosis factor

Title:

Authors:: Polić, Bojan (173636); Jonjić, Stipan (95583); Pavić, Ivica (163242); Dujmović, Milivoj; Crnković, Irena (194586); Zorica, Irena; Hengel, Hartmut; Kučić, Natalija; Lučin, Pero (142314); Koszinowski, Ulrich

Journal: Scandinavian Journal of Infectious Diseases
ISSN: 0300-8878
Volume: 0
Year: 1995
Pages: from 00 to 00
Number of references: 6
Language: engleski

Title:

Authors:: Polić, Bojan (173636); Jonjić, Stipan (95583); Pavić, Ivica (163242); Crnković, Irena (194586); Zorica, Irena; Hengel, Hartmut; Lučin, Pero (142314); Koszinowski, Ulrich

Journal: Journal of General Virology
ISSN: 0022-1317
Pages: from 00 to 00
Number of references: 44
Language: engleski
Summary: It has been claimed that MHC class I proteins serve as receptor for murine cytomegalovirus (MCMV) and that this interaction is the most important mechanism for virus entry in a majority of cells. This idea was fostered by the observation that the MHC haplotype contributes to the susceptibility to CMV infection in vivo. In vitro studies provided support for the concept that stable expression of correctly folded MHC class I molecules contributes to infection, since the individual properties of MHC class I alleles, the availability of b3-microglobulin (b2m) and also the degree of peptide charging of the MJHC class I heavy chain - b2m heterodimers determined the infection phenotype of cell lines. To assess the biological relevance of proper MHC class I expression we investigated CMV infection in b2m deficient mice, which fail to express ternary MHC class I complexes and lack peripheral CD8+ T lymphocytes. We find that virus organ titers and virus clearance kinetics are not altered in b2m mutant mice. In addition, there was no indication for a diminished virus propagation in b-/- embryonic fibroblasts. b-/- mice suffered from the lack of CD8+ T lymphocytes that was partially compensated by the function of CD4+ T lymphocytes. An organ specific antiviral function of NK cells was observed independent from the b2m deletion. The immune control unique for salivary gland infection was maintained. Altogether, the data confirm the role of MHC class I molecules in the immune surveillance of CMV infection but question the biological impact of correct MHC class I complexes for productive infection.
Keywords: murine cytomegalovirus, b2-microglobulin deficient mice, MHC class I deficiency, viral receptors

Title:

Authors:: Thale, Regine; Szepan, Uwe; Hengel, Hartmut; Geginat, Gernot; Lučin, Pero (142314); Koszinowski, Ulrich

Journal: Journal of Virology
Number: 10
ISSN: 0022-538x
Volume: 69
Year: 1995
Pages: from 6098 to 6105
Number of references: 44
Language: engleski
Summary: Mouse cytomegalovirus (MCMV) functions expressed at the beginning of the early phase of the viral replication cycle interfere with the major histocompatibility complex (MHC) class I-restricted pathway of antigen presentation. Nascent MHC class I heavy chains associate with b2-microglobulin and peptide, but the assembled trimolecular complex is retained in the endoplasmatic reticulum/cis-Golgi compartment. To locate the responsible genomic region, the cytoplasmic retention of MHC class I molecules after injection of MCMV DNA was tested. The function was mapped to the HindIII E fragment. A recombinant MCMV delection mutant dMS94.5 lacking 15.8 kb in HindIII-E was constructed. Restoration of MHC class I molecule maturation and recognition of antigenic peptides by cytolytic T lymphocytes during the first hours of the early phase in mutant virus-infected cells proved the correct location to a 6.8-kb region in the HindIII E fragment. At later stages of the early phase, membrane-resident MHC class I molecules and cytolytic T lymphocyte recognition disappeared in dMS94.5 mutant virus-infected cells. These results demonstrate that more than one early-gene function of MCMV affects the MHC class I pathway of antigen presentation. The redundant MHC class I-reactive functions target the transport of MHC class I molecules at different steps.


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