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  1. Article: Maintenance of Alveolar Ridge Dimensions Utilizing an Extracted Tooth Dentin Particulate Autograft and PlateletRich Fibrin: A Retrospective Radiographic ConeBeam Computed Tomography Study.

    Pohl, Snjezana / Binderman, Itzhak / Tomac, Jelena

    Materials (Basel, Switzerland)

    2020  Volume 13, Issue 5

    Abstract: This study utilized radiographic comparative analysis in order to evaluate dimensional ridge changes four months after tooth extraction and immediate grafting with mineralized dentin particulate autograft and chopped plateletrich fibrin. Fiftyeight ... ...

    Abstract This study utilized radiographic comparative analysis in order to evaluate dimensional ridge changes four months after tooth extraction and immediate grafting with mineralized dentin particulate autograft and chopped plateletrich fibrin. Fiftyeight extraction sockets with up to 2 mm of missing buccal bone in the coronal aspect compared to the lingual bone were included. Graft material was covered with either a plateletrich fibrin membrane or collagen sponge with no effort to achieve primary closure. The dimensional changes of the ridge were assessed on conebeam computed tomography (CBCT) images acquired prior to extraction and four months later. The reduction in the buccal bone plate thickness 1 mm, 3 mm, and 5 mm below the buccal crest was -0.87 ± 0.84 mm, -0.60 ± 0.70 mm, and -0.41 ± 0.55 mm, respectively. The mean ridge width changes 1 mm, 3 mm, and 5 mm below the crest were -1.38 ± 1.24 mm, -0.82 ± 1.13 mm, and -0.43 ± 0.89 mm, respectively. The average midbuccal bone height gain was +1.1%, while the midlingual height gain was 5.6%. A mineralized dentin autograft with plateletrich fibrin is effective in preserving postextraction alveolar ridge dimensions.
    Language English
    Publishing date 2020-02-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2487261-1
    ISSN 1996-1944
    ISSN 1996-1944
    DOI 10.3390/ma13051083
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Rodent Models of Congenital Cytomegalovirus Infection.

    Lisnić, Berislav / Tomac, Jelena / Cekinović, Djurdjica / Jonjić, Stipan / Juranić Lisnić, Vanda

    Methods in molecular biology (Clifton, N.J.)

    2021  Volume 2244, Page(s) 365–401

    Abstract: Human cytomegalovirus (HCMV) is a leading viral cause of congenital infections in the central nervous system (CNS) and may result in severe long-term sequelae. High rates of sequelae following congenital HCMV infection and insufficient antiviral therapy ... ...

    Abstract Human cytomegalovirus (HCMV) is a leading viral cause of congenital infections in the central nervous system (CNS) and may result in severe long-term sequelae. High rates of sequelae following congenital HCMV infection and insufficient antiviral therapy in the perinatal period makes the development of an HCMV-specific vaccine a high priority of modern medicine. Due to the species specificity of HCMV, animal models are frequently used to study CMV pathogenesis. Studies of murine cytomegalovirus (MCMV) infections of adult mice have played a significant role as a model of CMV biology and pathogenesis, while MCMV infection of newborn mice has been successfully used as a model of perinatal CMV infection. Newborn mice infected with MCMV have high levels of viremia during which the virus establishes a productive infection in most organs, coupled with a robust inflammatory response. Productive infection in the brain parenchyma during early postnatal period leads to an extensive nonnecrotizing multifocal widespread encephalitis characterized by infiltration of components of both innate and adaptive immunity. As a result, impairment in postnatal development of mouse cerebellum leads to long-term motor and sensor disabilities. This chapter summarizes current findings of rodent models of perinatal CMV infection and describes methods for analysis of perinatal MCMV infection in newborn mice.
    MeSH term(s) Animals ; Animals, Newborn ; Brain/immunology ; Central Nervous System/virology ; Cytomegalovirus/immunology ; Cytomegalovirus/metabolism ; Cytomegalovirus/pathogenicity ; Cytomegalovirus Infections/immunology ; Disease Models, Animal ; Encephalitis ; Fetal Diseases ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Muromegalovirus/immunology ; Primary Cell Culture
    Language English
    Publishing date 2021-02-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1111-1_18
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Augmentation mit partikelförmigem Dentin im Oberkiefer

    Pohl, Snjezana / Golemac, Mijo / Grgic Miljanic, Daniela / Petrakakis, Pantelis / Tomac, Jelena

    Implantologie-Journal

    2021  Volume 25, Issue 5, Page(s) 22

    Language German
    Document type Article
    ZDB-ID 1464637-7
    ISSN 1435-6139
    Database Current Contents Medicine

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  4. Article ; Online: Viral infection of the ovaries compromises pregnancy and reveals innate immune mechanisms protecting fertility.

    Tomac, Jelena / Mazor, Marija / Lisnić, Berislav / Golemac, Mijo / Kveštak, Daria / Bralić, Marina / Bilić Zulle, Lidija / Brinkmann, Melanie M / Dölken, Lars / Reinert, Line S / Paludan, Soren R / Krmpotić, Astrid / Jonjić, Stipan / Juranić Lisnić, Vanda

    Immunity

    2021  Volume 54, Issue 7, Page(s) 1478–1493.e6

    Abstract: Viral infections during pregnancy are a considerable cause of adverse outcomes and birth defects, and the underlying mechanisms are poorly understood. Among those, cytomegalovirus (CMV) infection stands out as the most common intrauterine infection in ... ...

    Abstract Viral infections during pregnancy are a considerable cause of adverse outcomes and birth defects, and the underlying mechanisms are poorly understood. Among those, cytomegalovirus (CMV) infection stands out as the most common intrauterine infection in humans, putatively causing early pregnancy loss. We employed murine CMV as a model to study the consequences of viral infection on pregnancy outcome and fertility maintenance. Even though pregnant mice successfully controlled CMV infection, we observed highly selective, strong infection of corpus luteum (CL) cells in their ovaries. High infection densities indicated complete failure of immune control in CL cells, resulting in progesterone insufficiency and pregnancy loss. An abundance of gap junctions, absence of vasculature, strong type I interferon (IFN) responses, and interaction of innate immune cells fully protected the ovarian follicles from viral infection. Our work provides fundamental insights into the effect of CMV infection on pregnancy loss and mechanisms protecting fertility.
    MeSH term(s) Animals ; Corpus Luteum/immunology ; Corpus Luteum/virology ; Cytomegalovirus/immunology ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/virology ; Female ; Fertility/immunology ; Gap Junctions/immunology ; Immunity, Innate/immunology ; Interferon Type I/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Pregnancy ; Progesterone/immunology
    Chemical Substances Interferon Type I ; Progesterone (4G7DS2Q64Y)
    Language English
    Publishing date 2021-05-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.04.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: NK/ILC1 cells mediate neuroinflammation and brain pathology following congenital CMV infection.

    Kveštak, Daria / Juranić Lisnić, Vanda / Lisnić, Berislav / Tomac, Jelena / Golemac, Mijo / Brizić, Ilija / Indenbirken, Daniela / Cokarić Brdovčak, Maja / Bernardini, Giovanni / Krstanović, Fran / Rožmanić, Carmen / Grundhoff, Adam / Krmpotić, Astrid / Britt, William J / Jonjić, Stipan

    The Journal of experimental medicine

    2021  Volume 218, Issue 5

    Abstract: Congenital human cytomegalovirus (cHCMV) infection of the brain is associated with a wide range of neurocognitive sequelae. Using infection of newborn mice with mouse cytomegalovirus (MCMV) as a reliable model that recapitulates many aspects of cHCMV ... ...

    Abstract Congenital human cytomegalovirus (cHCMV) infection of the brain is associated with a wide range of neurocognitive sequelae. Using infection of newborn mice with mouse cytomegalovirus (MCMV) as a reliable model that recapitulates many aspects of cHCMV infection, including disseminated infection, CNS infection, altered neurodevelopment, and sensorineural hearing loss, we have previously shown that mitigation of inflammation prevented alterations in cerebellar development, suggesting that host inflammatory factors are key drivers of neurodevelopmental defects. Here, we show that MCMV infection causes a dramatic increase in the expression of the microglia-derived chemokines CXCL9/CXCL10, which recruit NK and ILC1 cells into the brain in a CXCR3-dependent manner. Surprisingly, brain-infiltrating innate immune cells not only were unable to control virus infection in the brain but also orchestrated pathological inflammatory responses, which lead to delays in cerebellar morphogenesis. Our results identify NK and ILC1 cells as the major mediators of immunopathology in response to virus infection in the developing CNS, which can be prevented by anti-IFN-γ antibodies.
    MeSH term(s) Animals ; Animals, Newborn ; Brain/immunology ; Brain/pathology ; Brain/virology ; Chemokine CXCL10/genetics ; Chemokine CXCL10/immunology ; Chemokine CXCL10/metabolism ; Chemokine CXCL9/genetics ; Chemokine CXCL9/immunology ; Chemokine CXCL9/metabolism ; Cytomegalovirus/immunology ; Cytomegalovirus/physiology ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/virology ; Gene Expression Regulation/immunology ; Humans ; Immunity, Innate/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/virology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Mice, 129 Strain ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia/immunology ; Microglia/metabolism ; Microglia/virology ; Receptors, CXCR3/genetics ; Receptors, CXCR3/immunology ; Receptors, CXCR3/metabolism ; Mice
    Chemical Substances Chemokine CXCL10 ; Chemokine CXCL9 ; Cxcr3 protein, mouse ; Receptors, CXCR3
    Language English
    Publishing date 2021-02-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20201503
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin.

    Domitrović, Robert / Jakovac, Hrvoje / Tomac, Jelena / Sain, Ivana

    Toxicology and applied pharmacology

    2009  Volume 241, Issue 3, Page(s) 311–321

    Abstract: Hepatic fibrosis is effusive wound healing process in which excessive connective tissue builds up in the liver. Because specific treatments to stop progressive fibrosis of the liver are not available, we have investigated the effects of luteolin on ... ...

    Abstract Hepatic fibrosis is effusive wound healing process in which excessive connective tissue builds up in the liver. Because specific treatments to stop progressive fibrosis of the liver are not available, we have investigated the effects of luteolin on carbon tetrachloride (CCl(4))-induced hepatic fibrosis. Male Balb/C mice were treated with CCl(4) (0.4 ml/kg) intraperitoneally (i.p.), twice a week for 6 weeks. Luteolin was administered i.p. once daily for next 2 weeks, in doses of 10, 25, and 50 mg/kg of body weight. The CCl(4) control group has been observed for spontaneous reversion of fibrosis. CCl(4)-intoxication increased serum aminotransferase and alkaline phosphatase levels and disturbed hepatic antioxidative status. Most of these parameters were spontaneously normalized in the CCl(4) control group, although the progression of liver fibrosis was observed histologically. Luteolin treatment has increased hepatic matrix metalloproteinase-9 levels and metallothionein (MT) I/II expression, eliminated fibrinous deposits and restored architecture of the liver in a dose-dependent manner. Concomitantly, the expression of glial fibrillary acidic protein and alpha-smooth muscle actin indicated deactivation of hepatic stellate cells. Our results suggest the therapeutic effects of luteolin on CCl(4)-induced liver fibrosis by promoting extracellular matrix degradation in the fibrotic liver tissue and the strong enhancement of hepatic regenerative capability, with MTs as a critical mediator of liver regeneration.
    MeSH term(s) Actins/metabolism ; Animals ; Carbon Tetrachloride Poisoning/drug therapy ; Carbon Tetrachloride Poisoning/pathology ; Chemical and Drug Induced Liver Injury/pathology ; Copper/metabolism ; Expectorants/therapeutic use ; Glial Fibrillary Acidic Protein/metabolism ; Glutathione/metabolism ; Hydroxyproline/metabolism ; Immunohistochemistry ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/pathology ; Luteolin/therapeutic use ; Male ; Matrix Metalloproteinases/metabolism ; Metallothionein/metabolism ; Mice ; Mice, Inbred BALB C ; Superoxide Dismutase/metabolism ; Vitamin A/metabolism ; Zinc/metabolism
    Chemical Substances Actins ; Expectorants ; Glial Fibrillary Acidic Protein ; alpha-smooth muscle actin, mouse ; Vitamin A (11103-57-4) ; Copper (789U1901C5) ; Metallothionein (9038-94-2) ; Superoxide Dismutase (EC 1.15.1.1) ; Matrix Metalloproteinases (EC 3.4.24.-) ; Glutathione (GAN16C9B8O) ; Zinc (J41CSQ7QDS) ; Luteolin (KUX1ZNC9J2) ; Hydroxyproline (RMB44WO89X)
    Language English
    Publishing date 2009-12-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2009.09.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: The specific NK cell response in concert with perforin prevents CD8(+) T cell-mediated immunopathology after mouse cytomegalovirus infection.

    Arapović, Jurica / Arapović, Maja / Golemac, Mijo / Traven, Luka / Tomac, Jelena / Rumora, Dijana / Ražić, Edvard / Krmpotić, Astrid / Jonjić, Stipan

    Medical microbiology and immunology

    2015  Volume 204, Issue 3, Page(s) 335–344

    Abstract: Natural killer (NK) and CD8(+) T cells play a crucial role in the control of mouse cytomegalovirus (MCMV) infection. These effector cells exert their functions by releasing antiviral cytokines and by cytolytic mechanisms including perforin activation. In ...

    Abstract Natural killer (NK) and CD8(+) T cells play a crucial role in the control of mouse cytomegalovirus (MCMV) infection. These effector cells exert their functions by releasing antiviral cytokines and by cytolytic mechanisms including perforin activation. In addition to their role in virus control, NK cells play an immunoregulatory role since they shape the CD8(+) T cell response to MCMV. To investigate the role of perforin-dependent cytolytic mechanism in NK cell modulation of CD8(+) T cell response during acute MCMV infection, we have used perforin-deficient C57BL/6 mice (Prf1(-/-)) and have shown that virus control by CD8(+) T cells in Prf1(-/-) mice is more efficient if NK cells are activated by the engagement of the Ly49H receptor with the m157 MCMV protein. A lack of perforin results in severe liver inflammation after MCMV infection, which is characterized by immunopathological lesions that are more pronounced in Prf1(-/-) mice infected with virus unable to activate NK cells. This immunopathology is caused by an abundant infiltration of activated CD8(+) T cells. The depletion of CD8(+) T cells has markedly reduced pathohistological lesions in the liver and improved the survival of Prf1(-/-) mice in spite of an increased viral load. Altogether, the results of our study suggest that a lack of perforin and absence of the specific activation of NK cells during acute MCMV infection lead to an unleashed CD8(+) T cell response that is detrimental for the host.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cytokines/metabolism ; Gene Deletion ; Herpesviridae Infections/immunology ; Herpesviridae Infections/mortality ; Herpesviridae Infections/pathology ; Herpesviridae Infections/virology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Liver/immunology ; Liver/pathology ; Liver/virology ; Lymphocyte Activation/immunology ; Lymphocyte Depletion ; Mice ; Mice, Knockout ; Muromegalovirus/genetics ; Muromegalovirus/immunology ; Mutation ; Perforin/deficiency ; Perforin/genetics ; Perforin/metabolism ; T-Cell Antigen Receptor Specificity/genetics ; T-Cell Antigen Receptor Specificity/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Viral Load
    Chemical Substances Cytokines ; Perforin (126465-35-8)
    Language English
    Publishing date 2015-06
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120933-4
    ISSN 1432-1831 ; 0300-8584
    ISSN (online) 1432-1831
    ISSN 0300-8584
    DOI 10.1007/s00430-015-0409-y
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  8. Article ; Online: Accumulation of defective interfering viral particles in only a few passages in Vero cells attenuates mumps virus neurovirulence.

    Šantak, Maja / Markušić, Maja / Balija, Maja Lang / Kopač, Sandra Keć / Jug, Renata / Örvell, Claes / Tomac, Jelena / Forčić, Dubravko

    Microbes and infection

    2015  Volume 17, Issue 3, Page(s) 228–236

    Abstract: Immunization programs have implemented live attenuated mumps vaccines which reduced mumps incidence ≥97%. Some of the vaccine strains were abandoned due to unwanted side effects and the genetic marker of attenuation has not been identified so far. Our ... ...

    Abstract Immunization programs have implemented live attenuated mumps vaccines which reduced mumps incidence ≥97%. Some of the vaccine strains were abandoned due to unwanted side effects and the genetic marker of attenuation has not been identified so far. Our hypothesis was that non-infectious viral particles, in particular defective interfering particles (DIPs), contribute to neuroattenuation. We showed that non-infectious particles of the mumps vaccine L-Zagreb attenuated neurovirulence of wild type mumps virus 9218/Zg98. Then, we attenuated recent wild type mumps virus MuVi/Zagreb.HRV/28.12 in Vero cells through 16 passages but already the fifth passage (p5) showed accumulation of DIPs and attenuated neurovirulence in a newborn rat model when compared to the second passage (p2). Sequence analysis of the p2 and p5 revealed a single mutation in the 5' untranslated region of the HN gene. Analysis of the expression level of the HN protein showed that this mutation does not affect the expression of the protein. We conclude that the passages of MuVi/Zagreb.HRV/28.12 in Vero cells for only three passages accumulated DIPs which attenuate neurovirulence. These findings reveal DIPs as a very promising and general neuroattenuating factor which should be considered in the rational design of the new mumps vaccine.
    MeSH term(s) Animals ; Base Sequence ; Cell Line, Tumor ; Cercopithecus aethiops ; Defective Viruses/immunology ; Humans ; Molecular Sequence Data ; Mumps virus/genetics ; Mumps virus/immunology ; Rats ; Vaccines, Attenuated/genetics ; Vero Cells/immunology ; Vero Cells/virology ; Virion ; Virulence/genetics
    Chemical Substances Vaccines, Attenuated
    Language English
    Publishing date 2015-03
    Publishing country France
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1465093-9
    ISSN 1769-714X ; 1286-4579
    ISSN (online) 1769-714X
    ISSN 1286-4579
    DOI 10.1016/j.micinf.2014.11.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Brain-resident memory CD8

    Brizić, Ilija / Šušak, Božo / Arapović, Maja / Huszthy, Peter C / Hiršl, Lea / Kveštak, Daria / Juranić Lisnić, Vanda / Golemac, Mijo / Pernjak Pugel, Ester / Tomac, Jelena / Oxenius, Annette / Britt, William J / Arapović, Jurica / Krmpotić, Astrid / Jonjić, Stipan

    European journal of immunology

    2018  Volume 48, Issue 6, Page(s) 950–964

    Abstract: Congenital HCMV infection is a leading infectious cause of long-term neurodevelopmental sequelae. Infection of newborn mice with mouse cytomegalovirus (MCMV) intraperitoneally is a well-established model of congenital human cytomegalovirus infection, ... ...

    Abstract Congenital HCMV infection is a leading infectious cause of long-term neurodevelopmental sequelae. Infection of newborn mice with mouse cytomegalovirus (MCMV) intraperitoneally is a well-established model of congenital human cytomegalovirus infection, which best recapitulates the hematogenous route of virus spread to brain and subsequent pathology. Here, we used this model to investigate the role, dynamics, and phenotype of CD8
    MeSH term(s) Adoptive Transfer ; Animals ; Animals, Newborn ; Brain/immunology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/transplantation ; Cells, Cultured ; Congenital Abnormalities ; Cytomegalovirus/physiology ; Cytomegalovirus Infections/immunology ; Disease Models, Animal ; Humans ; Immunologic Memory ; Mice ; Mice, Inbred C57BL ; Muromegalovirus/physiology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/transplantation ; Virus Activation/immunology
    Language English
    Publishing date 2018-03-23
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.201847526
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  10. Article ; Online: Altered development of the brain after focal herpesvirus infection of the central nervous system.

    Koontz, Thad / Bralic, Marina / Tomac, Jelena / Pernjak-Pugel, Ester / Bantug, Glen / Jonjic, Stipan / Britt, William J

    The Journal of experimental medicine

    2008  Volume 205, Issue 2, Page(s) 423–435

    Abstract: Human cytomegalovirus infection of the developing central nervous system (CNS) is a major cause of neurological damage in newborn infants and children. To investigate the pathogenesis of this human infection, we developed a mouse model of infection in ... ...

    Abstract Human cytomegalovirus infection of the developing central nervous system (CNS) is a major cause of neurological damage in newborn infants and children. To investigate the pathogenesis of this human infection, we developed a mouse model of infection in the developing CNS. Intraperitoneal inoculation of newborn animals with murine cytomegalovirus resulted in virus replication in the liver followed by virus spread to the brain. Virus infection of the CNS was associated with the induction of inflammatory responses, including the induction of a large number of interferon-stimulated genes and histological evidence of focal encephalitis with recruitment of mononuclear cells to foci containing virus-infected cells. The morphogenesis of the cerebellum was delayed in infected animals. The defects in cerebellar development in infected animals were generalized and, although correlated temporally with virus replication and CNS inflammation, spatially unrelated to foci of virus-infected cells. Specific defects included decreased granular neuron proliferation and migration, expression of differentiation markers, and activation of neurotrophin receptors. These findings suggested that in the developing CNS, focal virus infection and induction of inflammatory responses in resident and infiltrating mononuclear cells resulted in delayed cerebellar morphogenesis.
    MeSH term(s) Animals ; Animals, Newborn ; Brain/immunology ; Brain/pathology ; Brain/virology ; Cell Differentiation ; Cell Movement ; Central Nervous System Diseases/immunology ; Central Nervous System Diseases/pathology ; Central Nervous System Diseases/virology ; Cytomegalovirus Infections/immunology ; Cytomegalovirus Infections/pathology ; Cytomegalovirus Infections/virology ; Leukocytes, Mononuclear/immunology ; Mice ; Muromegalovirus ; Nerve Growth Factors/immunology ; Neuroglia/virology ; Neurons/cytology ; Neurons/virology ; Receptor Protein-Tyrosine Kinases/immunology
    Chemical Substances Nerve Growth Factors ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2008-02-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20071489
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