OBJECTIVETo observe the pathological changes and morphological alterations of ECV304 cells after the infection by herpes simplex virus type 2 (HSV-2) in vitro.

METHODSPassaged ECV304 cells were infected with HSV-2, TCID50 and morphological changes were observed by optical microscopy and tissue staining.

RESULTSOne day after HSV-2 infection, swelling, rounding, and increase of thickened cytoplasmic granules occurred in the ECV304 cells, and on day 2, cell fusion was observed with weakened nuclear staining.

CONCLUSIONECV304 cells mostly undergo necrosis after HSV-2 infection without obvious evidence of cell apoptosis.

Cells, Cultured ; Endothelium, Vascular ; pathology ; virology ; Herpesviridae Infections ; pathology ; Herpesvirus 2, Human ; Humans ; Necrosis ; Umbilical Veins ; pathology

Antigens, CD ; metabolism ; Diagnosis, Differential ; Epstein-Barr Virus Infections ; Herpesviridae Infections ; Humans ; Immunohistochemistry ; Lymphoma ; classification ; immunology ; pathology ; virology

In order to investigate the human cytomegalovirus (HCMV) infection, the mouse cytomegalovirus (MCMV) infected mice were experimentally studied. 6 to 8 week old female BALB/C mice with immunosuppression were selected to undergo the MCMV inoculations: intracranial inoculation and peritoneal inoculation. MCMV of the infected mice in various organs and tissues were detected by using beta-gal staining and in situ nucleic acid hybridization assay. The pathological changes were observed in HE staining paraffin-embedded sections. It was found that all the MCMV infected mice showed the retardation of growth and development, and feather looseness. Both intracranial inoculation of 10(4) PFU viruses or peritoneal inoculation of 10(6) PFU viruses resulted in the pathological changes, to some extent, of various organs and tissues in the mice. The pathological changes in liver were consistent with the amount of beta-gal staining positive cells, indicating the liver lesions were mainly caused by viral proliferation. It was also found that the viruses in the immunosuppressed mice subjected to intracranial inoculation could spread to whole body organs, while the viruses in the immunosuppressed mice subjected to intrapeitoneal inoculation couldn't spread to the brain, suggesting blood-brain barrier could prevent the virus from spreading to the brain.
Blood-Brain Barrier ; Brain/pathology ; Brain/virology ; Disease Models, Animal ; *Herpesviridae Infections/pathology ; *Herpesviridae Infections/virology ; Immunocompromised Host ; Liver/pathology ; Liver/virology ; Lung/pathology ; Lung/virology ; Mice, Inbred BALB C ; *Muromegalovirus

OBJECTIVETo establish a BALB/c mice model system of cytomegalovirus-induced myocarditis.

METHODSTwenty five specific pathogen-free inbred female BALB/c mice (5 weeks old, 16 - 18 g, seronegative for MCMV) were infected with 1 x 10(4) PFU MCMV by the intraperitoneal (i.p.) route. All experimental mice were sacrificed at 3, 5, 7, 10, 14 days i.p. (n = 5 per time point). Hearts were removed under aseptic conditions, and were transected along the midline. One part of each heart was processed with Bouin's fixative for histological examination. The other part of each heart was immediately frozen in liquid nitrogen and stored at -80 degrees C until MCMV titre was determined by plaque assay. Serum cTnI level was assayed by ELISA.

RESULTSMCMV was detected in the hearts at extremely low levels on 3 days i.p. and could not be detected on 10 days i.p. A mixed cellular infiltrate composed of polymorphonuclear neutrophils and mononuclear lymphocytes was observed on 3 days, which reached a peak at 7 to 10 days after MCMV infection and was maintained for at least 3 - 4 months postinfection. Serum cTnI levels were elevated on 3 days i.p., reaching a peak at 7 to 10 days i.p..

CONCLUSIONSThese data highlight the possible therapeutic uses of antiviral drugs in viral myocarditis as well as further elucidating the pathogenic nature of the disease.

Animals ; Disease Models, Animal ; Female ; Herpesviridae Infections ; pathology ; Mice ; Mice, Inbred BALB C ; Muromegalovirus ; Myocarditis ; virology ; Troponin I ; metabolism

This study was carried out to describe clinical, gross and histopathological findings in the respiratory tract in chickens infected intranasally with A96 strain of infectious laryngotracheitis virus (ILTV). In addition, the presence of ILTV antigens in formalin-fixed and paraffin-embedded larynx and trachea tissues was investigated with the immunoperoxidase (IP) method in the infected chickens. At various days of viral infection, nares, larynx, trachea, lungs and air sacs tissue samples of the infected chickens were obtained and fixed with formalin and embedded in paraffin. The cross sections were stained with hematoxylineosin, and the larynx and trachea sections were also stained with the IP method. Mild rales and gasping were observed in only 4 of 35 chickens. The virus caused mild inflammatory changes in the respiratory tract. It was shown that clinical, gross and histopathological findings were not specific for differential diagnosis of the disease. However, ILTV antigens were detected by the IP method in formalin-fixed and paraffin-embedded larynx and trachea sections. These results revealed that the study use of the IP method might be useful for the diagnosis of ILTV infections with non-specific lesions.
Animals ; Chickens ; Hemorrhage/pathology ; Herpesviridae Infections/*pathology ; Herpesvirus 1, Gallid/isolation & purification/*pathogenicity ; Immunohistochemistry ; Larynx/blood supply/pathology ; Mucous Membrane/pathology ; Virulence

In order to investigate the human cytomegalovirus (HCMV) infection, the mouse cytomegalovirus (MCMV) infected mice were experimentally studied. 6 to 8 week old female BALB/C mice with immunosuppression were selected to undergo the MCMV inoculations: intracranial inoculation and peritoneal inoculation. MCMV of the infected mice in various organs and tissues were detected by using beta-gal staining and in situ nucleic acid hybridization assay. The pathological changes were observed in HE staining paraffin-embedded sections. It was found that all the MCMV infected mice showed the retardation of growth and development, and feather looseness. Both intracranial inoculation of 10(4) PFU viruses or peritoneal inoculation of 10(6) PFU viruses resulted in the pathological changes, to some extent, of various organs and tissues in the mice. The pathological changes in liver were consistent with the amount of beta-gal staining positive cells, indicating the liver lesions were mainly caused by viral proliferation. It was also found that the viruses in the immunosuppressed mice subjected to intracranial inoculation could spread to whole body organs, while the viruses in the immunosuppressed mice subjected to intrapeitoneal inoculation couldn't spread to the brain, suggesting blood-brain barrier could prevent the virus from spreading to the brain.
Animals ; Blood-Brain Barrier ; Brain ; pathology ; virology ; Disease Models, Animal ; Female ; Herpesviridae Infections ; pathology ; virology ; Immunocompromised Host ; Liver ; pathology ; virology ; Lung ; pathology ; virology ; Mice ; Mice, Inbred BALB C ; Muromegalovirus

Antiviral Agents ; therapeutic use ; Castleman Disease ; drug therapy ; metabolism ; pathology ; virology ; Dendritic Cells, Follicular ; pathology ; Herpesviridae Infections ; virology ; Herpesvirus 8, Human ; isolation & purification ; Humans ; Interleukin-6 ; blood ; Receptor, Epidermal Growth Factor ; metabolism

Castleman's disease represents an atypical lymphoproliferative disorder, infrequently associated with various immunologic abnormalities or subsequent development of malignancy such as Kaposi sarcoma, malignant lymphoma and plasmacytoma. Its clinicopathologic features depend on various etiologic factors such as Kaposi sarcoma herpesvirus (KSHV), oversecretion of IL-6, adhesion molecule and follicular dendritic cell dysplasia, etc. To investigate the relationship of Castleman's disease (CD) and the above factors, we reviewed 22 cases of CD. Four cases of KSHV positive CD were detected, all multicentric, plasma cell type, and these cases displayed prominent vascular proliferation, characteristic 'Kaposi-like lesion'. IL-6 and CD54 positive mononuclear cells were scattered in interfollicular areas of KSHV positive cases. Follicular dendritic cell hyperplasia, vascular proliferation, expression of IL-6 and CD54 did not show any significant difference between solitary vs multicentric type, and plasma cell type vs hyaline vascular type. Our study suggests that KSHV positive CD reveals unique pathologic features, and the probable relationship of KSHV and IL-6 and CD54 is discussed.
Adolescence ; Adult ; Biological Markers ; Dendritic Cells, Follicular/pathology ; Epstein-Barr Virus Infections/virology ; Epstein-Barr Virus Infections/epidemiology ; Female ; Germinal Center/pathology ; Giant Lymph Node Hyperplasia/virology ; Giant Lymph Node Hyperplasia/pathology+ACo- ; Giant Lymph Node Hyperplasia/epidemiology ; Giant Lymph Node Hyperplasia/classification ; Herpesviridae Infections/virology ; Herpesviridae Infections/epidemiology ; Herpesvirus 4, Human/isolation +ACY- purification ; Herpesvirus, Kaposi Sarcoma-Associated/isolation +ACY- purification ; Human ; Hyperplasia ; Intercellular Adhesion Molecule-1/analysis ; Interleukin-6/analysis ; Korea/epidemiology ; Lymph Nodes/virology ; Lymph Nodes/pathology ; Lymph Nodes/chemistry ; Male ; Middle Age ; Neovascularization, Pathologic ; Receptors, Complement 3d/analysis ; Retrospective Studies ; Tumor Virus Infections/virology ; Tumor Virus Infections/epidemiology

Kaposi sarcoma herpes virus (KSHV), also known as human herpesvirus-8, plays an important role in the pathogenesis of Kaposi sarcoma (KS), multicentric Castleman disease (MCD) of the plasma cell type, and primary effusion lymphoma. KSHV is rarely associated with the hemophagocytic syndrome (HPS), but when it does occur, it most occurs in immunocompromised patients. We report herein an unusual case of KSHV-associated HPS in an immunocompetent patient. A previously healthy 62-yr-old male was referred for evaluation of leukocytopenia and multiple lymphadenopathies. After a lymph node biopsy, he was diagnosed with MCD of the plasma cell type. KSHV DNA was detected in the lymph node tissue by polymerase chain reaction. Following a short-term response of the leukocytopenia to prednisolone, mental change, left side weakness, fever, thrombocytopenia, hemolytic anemia, and renal failure developed. Despite intravenous immunoglobulin therapy and plasmapheresis, he expired. The lymph nodes were infiltrated by hemophagocytic histiocytes in the sinuses. Pulmonary nodules and gastric erosions were shown to be KS. KSHV DNA was detected in the stomach, lung, and liver. This is the first case of multiple KSHV associated diseases including MCD and KS with KSHV-associated hemophagocytic syndrome in an HIV-negative, non-transplant, immunocompetent patient.
Autopsy ; Giant Lymph Node Hyperplasia/complications/*diagnosis/pathology ; HIV Seronegativity ; Herpesviridae Infections/*diagnosis ; Herpesvirus 8, Human/*isolation & purification ; Humans ; Immunocompetence ; Lymphohistiocytosis, Hemophagocytic/*diagnosis/etiology ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Polymerase Chain Reaction ; Sarcoma, Kaposi/complications/*diagnosis

UNLABELLEDTo provide a reliable animal model for study of human CMV disease in gastrointestinal track, we tried to infect with murine cytomegalovirus (MCMV) in mice that were received allogenetic skin transplantation under immunosuppression. (1) Skin transplantation was performed between 18 donor C57BL/6 mice and 72 recipient BALB/c mice. (2) All recipient mice were then given Cyclosporine at 12 mg/kg daily for 2 weeks by intraperitoneal injection. Mice were randomly divided into 3 groups. Two experimental groups were received MCMV-infected mouse embryonic fibroblasts (MEF) at 10(4) PFU and 10(5) PFU respectively, and the control group received MEF only. We observed any possibly pathophysiological behavior changes and recorded the changes in body weight. The mice were sacrificed at 5d, 9d, 14d, 21d post infection and colon tissue was collected for analysis.

RESULTSMice infected with MCMV at 10(5) PFU group showed anorexia, lethargy and degression in locomotor activity. This group of mice showed significant decrease in body weight than that of other groups. Colon tissues were collected 14 days after infection. Histological examination revealed that the mucous layer became thinner in the proximal colon and increased number of lymphoid follicles in distal colon in infected animals. The changes in the mucosal structure was most prominent in the group 10(5) PFU MCMV. Viral DNA was present in the colon by in situ hybridization for IE1 gene, and viral gB transcript was positive by RT-PCR. One of the viral major proteins, pp65, was widely distributed in the colon by immunohistochemistry. These data demonstrated that MCMV established infection in colon of the mice after allogenetic skin transplantation. Electron microscopy showed that there were herpes virus particles in the colon tissue.

CONCLUSIONInfection with MCMV in mouse after allogenetic skin transplantation by nasal cavity inoculation resulted in the pathological changes in colon tissue similar to that of inflammation in human colon. The small animal model of colon inflammation may provide a platform for further study of pathogenesis as well as medical intervention of HCMV involved inflammation of human bowel.

Animals ; Colon ; immunology ; pathology ; virology ; Cytomegalovirus Infections ; immunology ; pathology ; virology ; Disease Models, Animal ; Female ; Herpesviridae Infections ; immunology ; pathology ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Muromegalovirus ; genetics ; immunology ; isolation & purification ; Random Allocation ; Skin Transplantation ; adverse effects ; immunology ; pathology ; Transplantation, Homologous ; adverse effects ; immunology ; pathology ; Viral Proteins ; genetics ; metabolism