Adenovirus Infections, Human ; pathology ; virology ; Glomerulonephritis, Membranous ; pathology ; virology ; HIV Infections ; pathology ; virology ; Hepatitis B ; pathology ; virology ; Hepatitis C ; pathology ; virology ; Herpes Zoster ; pathology ; virology ; Herpesvirus 3, Human ; isolation & purification ; Humans ; Kidney ; pathology ; virology ; Kidney Diseases ; pathology ; virology ; Nephritis, Interstitial ; pathology ; virology ; Parvoviridae Infections ; pathology ; virology ; Parvovirus B19, Human ; isolation & purification

The tissue distribution and cellular localization of viral antigens in three cattle with persistent bovine viral diarrhea virus (BVDV) infection was studied. In three cases, necropsy findings of oral ulcers, abmasal ulcers and necrosis of Peyer's patches were suspected have been caused by BVDV infection. Non-cytopathic BVDV was isolated from a tissue pool of liver, kidneys and spleen. Immunohistochemical detection of BVDV showed that BVDV antigens were detected in both epithelial and nonepithelial cells in all examined organs, including the gastrointestinal tract, liver, pancreas, lung, lymphatic organs (spleen, lymph nodes), adrenal gland, ovary, uterus, and the mammary gland. These findings support the hypothesis that animals with persistent BVDV infection spread BVDV through all routes, and that infertility in BVDV infection is associated with the infection of BVDV in the ovaries and uteri.
Adrenal Glands/pathology/virology ; Animals ; Antigens, Viral/*isolation & purification ; Bovine Virus Diarrhea-Mucosal Disease/pathology/physiopathology/*virology ; Cattle ; Diarrhea Viruses, Bovine Viral/immunology/*isolation & purification ; Digestive System/pathology/virology ; Female ; Immunohistochemistry/veterinary ; Infertility, Female/virology ; Kidney/pathology/virology ; Lung/pathology/virology ; Lymphatic System/pathology/virology ; Mammary Glands, Animal/virology ; Ovary/pathology/virology ; Uterus/pathology/virology

OBJECTIVETo investigate the ultrastructural changes of the extraintestinal organs of newborn mice with human retrovirus (RV) infection to probe into the mechanism and clinical diagnose and therapy of extraintestinal RV infection.

METHODSHuman RV was inoculated into the abdominal cavity of the newborn mice, and the ultrastructural changes of the heart, lung, livers, and kidneys of the infected and control mice were observed by transmission electron microscope.

RESULTSThe mice with intraabdominal RV injection showed pathological changes of the cells in the small intestinal villus, liver, and kidneys. Shortened small intestinal villus, nuclear membrane disorganization, massive vacuolization, mitochondrial swelling and rough endoplasmic reticulum dilation were observed in the cells of the small intestinal. In the liver of the mice, marked mitochondrial swelling and agglutination, cell nucleus pyknosis or collapse, presence of numerous lipid droplets and vacuoles were seen in the liver cells, with lymphocyte and plasmacyte infiltration. Obvious dilatation and shedding of the microvillus were seen in cholangioles. The mitochondria of the proximal convoluted renal tubule showed mild swelling, but the cells in the heart and lung did not display obvious changes.

CONCLUSIONThe small intestinal villi were highly susceptible to RV infection, and systemic spread of human RV may cause damage of various extraintestinal organs especially the liver, which can also be susceptible to RV.

Animals ; Animals, Newborn ; Female ; Intestine, Small ; ultrastructure ; virology ; Kidney ; ultrastructure ; virology ; Liver ; ultrastructure ; virology ; Lung ; ultrastructure ; virology ; Male ; Mice ; Microscopy, Electron, Transmission ; Rotavirus Infections ; pathology ; virology

OBJECTIVEHepatitis B virus-associated membranous nephropathy (HBV-MN) is a disease characterized by podocytopathy. Podocyte is a terminally differentiated cell with limited capability of proliferation. Thus, damage of podocyte might result in decreased cell number, and then lead to the development of marked proteinuria and glomerulosclerosis. The present study aimed to investigate the changes of glomerular podocyte number in the children with hepatitis B virus-associated membranous nephropathy (HBV-MN), and their significance in the pathogenesis of HBV-MN.

METHODSPodocytes were identified through specific immunohistological staining of Wilms tumor gene protein 1 (WT1), a characteristic marker for podocyte nuclei, and podocyte numerical density (Nv), mean glomerular tuft volume (V) and the podocyte number per glomerulus (Npodo) were estimated through Weibel-Gomez method in 19 children with biopsy-proven HBV-MN and 8 children with thin basement membrane disease (control group), and analyses were made for possible correlation with clinical, serological and pathological data.

RESULTSAmong the 19 cases with HBV-MN, 3 showed microvillus-like foot process of podocytes, granular degeneration of podocyte were found in 4 cases, vacuolization in 1 case and podocyte detachment in 2 cases. Nv and Npodo were significantly decreased in children with HBV-MN compared with control group (t = 12.851, P = 0.0002 and t = 6.433, P = 0.0002, respectively). Moreover, the number of podocytes decreased more significantly in patients with stronger HBsAg deposition (> ++) than those with weak HBsAg deposition (< or = ++), P = 0.004, but no significant difference was found between patients with phase III or IV of HBV-MN and those with phase Ior II in podocyte number per glomerulus (P = 0.5262) and podocyte numerical density (P = 0.3564). Podocyte numerical density decreased more significantly in patients with massive proteinuria (> or = 2 g/24 h) than those with moderate proteinuria (< 2 g/24 h), P = 0.0488. The numbers of podocyte correlated significantly with serum levels of C(3) (r = 0.548, P = 0.028), but did not correlate with serum levels of albumin (r = -0.037, P = 0.891).

CONCLUSIONAll patients with HBV-MN showed podocyte damage and decreased number per glomerulus, which may play an important role in the pathogenesis of HBV-MN in children.

Cell Count ; Child ; Glomerulonephritis ; pathology ; Glomerulonephritis, Membranous ; complications ; virology ; Hepatitis B ; complications ; pathology ; Hepatitis B virus ; Humans ; Kidney Diseases ; pathology ; Kidney Glomerulus ; pathology ; Podocytes ; pathology ; Proteinuria ; pathology

BK virus (BKV) is a subtype of papovaviridae. The latent and asymptomatic infection of BKV is common among healthy people. The incidence of BKV re-activation in renal transplant recipients ranges 10%-68%. About 1%-7% of renal transplant recipients will suffer from BKV-associated nephropathy (BKVAN), and half of them will experience graft failure. This paper summarizes the re-activation mechanism of BKV as well as the risk factors, pathology, diagnosis, and treatment of BKVAN.
BK Virus ; physiology ; Humans ; Kidney ; pathology ; virology ; Kidney Transplantation ; Polyomavirus Infections ; diagnosis ; pathology ; therapy ; Postoperative Complications ; diagnosis ; pathology ; therapy ; virology ; Risk Factors ; Tumor Virus Infections ; diagnosis ; pathology ; therapy ; Virus Activation

In order to explore the morphological changes of Bovine Kidney (MDBK) cells induced by foot-and-mouth disease virus (FMDV) L protease, we induced the expression of FMDV L protease in bovine kidney cells (MDBK) artificially. All work is carried out on the basis of a stable MDBK cell line inducibly expresses the Lab gene under the control of tetracycline. We use cell morphology, Hoechst 33258 staining, AO-EB staining, and DNA Ladder abstraction to research the morphological changes of MDBK cells. 24 hours after FMDV L protease were induced and expressed in MDBK cells, cells shown the diminish of cell size, nuclear enrichment and the appearance of transparency circle under the light microscope. Apoptosis characteristics of nuclear condensation, fragmentation, accompanied by apoptotic bodies formation (Hoechst 33258 staining). 36 hours after the expression, nuclear staining of early lesions showed bright green plaque or debris-like dense, and advanced lesions showed Orange and dense plaques (AO-EB staining). 48 hours after the expression, DNA gel electrophoresis showed visible DNA ladder. Results indicate that FMDV L protease can induce apoptosis of MDBK and apoptosis plays an important role in the cytopathogenicity effect of FMDV.
Animals ; Cattle ; Cell Line ; Endopeptidases ; biosynthesis ; genetics ; Foot-and-Mouth Disease Virus ; pathogenicity ; Kidney ; cytology ; pathology ; virology ; Transfection

BK virus-associated nephropathy (BKVAN) is one of the major causes of allograft dysfunction in kidney transplant (KT) patients. We compared BKVAN combined with acute rejection (BKVAN/AR) with BKVAN alone in KT patients. We retrospectively analyzed biopsy-proven BKVAN in KT patients from 2000 to 2011 at Seoul National University Hospital. Among 414 biopsies from 951 patients, biopsy-proven BKVAN was found in 14 patients. Nine patients had BKVAN alone, while 5 patients had both BKVAN and acute cellular rejection. BKVAN in the BKVAN alone group was detected later than in BKVAN/AR group (21.77 vs 6.39 months after transplantation, P=0.03). Serum creatinine at diagnosis was similar (2.09 vs 2.00 mg/dL). Histological grade was more advanced in the BKVAN/AR group (P=0.034). Serum load of BKV, dose of immunosuppressants, and tacrolimus level showed a higher tendency in the BKVAN alone group; however it was not statistically significant. After anti-rejection therapy, immunosuppression was reduced in the BKVAN/AR group. Renal functional deterioration over 1 yr after BKVAN diagnosis was similar between the two groups (P=0.665). These findings suggest that the prognosis of BKVAN/AR after anti-rejection therapy followed by anti-BKV therapy might be similar to that of BKVAN alone after anti-BKV therapy.
Acute Disease ; Adult ; Antiviral Agents/therapeutic use ; BK Virus/*physiology ; Creatinine/blood ; Female ; *Graft Rejection/diagnosis/virology ; Humans ; Immunosuppressive Agents/administration & dosage ; Kidney/*virology ; Kidney Diseases/pathology/surgery/*virology ; *Kidney Transplantation ; Male ; Middle Aged ; Polyomavirus Infections/drug therapy/*etiology/pathology ; Retrospective Studies ; Tacrolimus/administration & dosage ; Time Factors ; Transplantation, Homologous/adverse effects ; Tumor Virus Infections/drug therapy/*etiology/pathology

OBJECTIVETo investigate the role of immunodeficiency and intestinal mixed infection on inducing extraintestinal dissemination of rotavirus (RV).

METHODSImmunodeficiency was induced in healthy Kunming mice by introperitoneal injection of cyclophosphamide, and RV was administered either orally or via intraperitoneal injection. In another group, toxigenic E. coli and human RV were given sequentially by intragastric administration to induce mixed infection. Three days later the organs of the mice were taken for pathological examination, and RV was detected by in situ PCR and hybridization. In children with or without viremia of rotavirus, blood tests for levels of tumor necrosis factor alpha (TNF-alpha), interleukin-2 (IL-2) and 7 trace elements (zinc, iron, copper, lead, calcium, manganese, and magnesium) were performed.

RESULTSIn immunodeficient mice, pathological changes were found in the small intestinal villus, gastric lamina propria and the cardiac cells of mice taking RV orally, and the mice with intraperitoneal RV injection showed additional liver and kidney pathologies. In mice with mixed infections, pathological changes occurred in the intestines, livers and kidneys. In situ hybridization detected RV in the intestinal villus of immunodeficient mice with oral RV administration, and in the intestinal villus and kidneys of the mice with mixed infections. In situ PCR revealed the presence of RV in the intestinal villus, intestinal gland cells, epithelial cells of the proximal convoluted tubules and collecting tubes in the kidneys of immunodeficient mice taking RV orally, in the intestinal villus, kidneys, livers, hearts and pancreases of those with RV injection, and in the intestines, kidneys, and livers of the mice with mixed infection. Children with rotavirus viremia had TNF-alpha level in comparison with those free of rotavirus viremia, and the majority of the former children showed disorder in trace elements.

CONCLUSIONImmunodeficiency, mixed infection and malnutrition can be important factors contributing to or exacerbating RV infection and extraintestinal RV dissemination.

Animals ; Cyclophosphamide ; administration & dosage ; toxicity ; DNA, Viral ; genetics ; Enzyme-Linked Immunosorbent Assay ; Female ; Immunocompromised Host ; drug effects ; immunology ; Interleukin-2 ; blood ; Intestines ; pathology ; virology ; Kidney ; pathology ; virology ; Liver ; pathology ; virology ; Male ; Mice ; Myocardium ; pathology ; Polymerase Chain Reaction ; Rotavirus ; genetics ; immunology ; Rotavirus Infections ; blood ; immunology ; virology ; Trace Elements ; blood ; Tumor Necrosis Factor-alpha ; blood

We report two cases of posttransplant malignant lymphoma(PTML) of B cell origin associated with Epstein-Barr virus(EBV) infection. They were a 52-year-old male and a 37 year-old-female, in whom intermediate-grade diffuse malignant lymphomas of large cell type developed in the submandibular area and jejunum, respectively. DNA and RNA in situ hybridization revealed the presence of EBV-specific DNA and RNA sequences in the tumor cells.
Adult ; Female ; *Herpesvirus 4, Human/isolation & purification ; Humans ; In Situ Hybridization ; Kidney Transplantation/*adverse effects/pathology ; Lymphoma/*complications/pathology/virology ; Male ; Middle Aged ; Transplantation, Homologous ; Tumor Virus Infections/*complications

Animals ; Child ; Epstein-Barr Virus Infections ; pathology ; Hodgkin Disease ; pathology ; virology ; Humans ; Infant, Newborn ; Kidney Neoplasms ; classification ; pathology ; Neuroblastoma ; classification ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rhabdomyosarcoma ; classification ; pathology ; Wilms Tumor ; classification ; pathology