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

OBJECTIVETo investigate whether simian virus 40 (SV40) was related to patients of malignant mesothelioma in China.

METHODSParaffin-embeded samples of 17 patients with malignant mesothelioma were collected. After isolation of DNA from paraffin blocks, polymerase chain reaction (PCR) analyses were performed using three different sets of primer for detection of SV40 large T antigen gene. These samples were also immunohistochemically evaluated for expression of SV40 TAg protein with two different anti-SV40 Tag (Pab101 and Ab-2).

RESULTSOnly one of the three primer pairs successfully amplified SV40 genome in three malignant mesothelioma samples. No immunopositive staining for SV40 TAg was found in any of the samples.

CONCLUSIONSThe study shows that malignant mesothelioma in China may be independent of SV40 infection.

Adult ; Aged ; Antigens, Viral, Tumor ; genetics ; metabolism ; China ; Female ; Host-Pathogen Interactions ; Humans ; Immunohistochemistry ; Male ; Mesothelioma ; pathology ; virology ; Middle Aged ; Polymerase Chain Reaction ; Polyomavirus Infections ; pathology ; virology ; Simian virus 40 ; genetics ; immunology ; physiology ; Tumor Virus Infections ; pathology ; virology ; Young Adult

The pathogenesis of endocervical glandular lesions are not clearly understood. The aims of this study are to evaluate the etiologic role of human papillomavirus (HPV) 16/18 and the relationship of HPV 16/18, p53 and MIB-1 expressions in endocervical glandular dysplasia (EGD), adenocarcinoma in situ (AIS) and adenocarcinoma. The materials included 14 endocervical adenocarcinoma and 5 AIS and 18 high grade EGD and 39 low grade EGD. Immunohistochemistry for p53 and MIB-1, and in situ PCR for HPV 16/18 were done. HPV 16/18 positivity was 84.2%, 16.7% and 17.9% in malignant glandular lesion (adenocarcinoma and AIS), high grade EGD and low grade EGD, respectively. P53 protein expression rates of malignant glandular lesions, high grade EGD and low grade EGD were 31.6%, 11.1%, and 0%, respectively. High MIB-1 labelling index was found in 73.7% of malignant glandular lesions, but in only 5.7% and 3.6% of high and low grade EGD, respectively. There were statistically significant differences in HPV 16/18, p53 and MIB-1 expressions between malignant endocervical glandular lesions and EGD, but no significant difference in p53 and MIB-1 expressions in relation to HPV 16/18 expression. In malignant endocervical glandular lesions, HPV 16/18 infection may be a major causative factor, but not be related to p53 and MIB-1 expressions.
Adenocarcinoma/pathology/physiopathology/*virology ; Carcinoma, Squamous Cell/pathology/physiopathology/virology ; Cervix Neoplasms/pathology/physiopathology/*virology ; Female ; Human ; Nuclear Proteins/analysis/*genetics ; Oncogene Proteins, Viral/genetics ; *Papillomavirus, Human ; Papovaviridae Infections/*pathology/physiopathology ; Protein p53/analysis/*genetics ; Tumor Virus Infections/*pathology/physiopathology

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

Histologic changes suggesting HPV infection are occasionally found adjacent to squamous cell carcinoma or in squamous papilloma of the esophagus, but the relationship between HPV infection and benign and malignant squamous lesions of the esophagus is not yet dear. The aim of this study was to examine the role of HPV in squamous lesions of the esophagus. Microscopic examination with emphasis on HPV infection was done on 15 cases of squamous cell carcinoma and 26 cases of squamous papilloma. In situ hybridization technique for wide-spectrum HPV probe was performed on 35 endoscopically biopsied esophageal tissues. Among the histologic parameters suggesting HPV infection, acanthosis was the most frequent finding: 100.0% in benign and malignant esophageal lesions, and koilocytosis and intraepithelial capillary loops were the second (92.7%).: Dyskeratosis, basal cell hyperplasia and bi- or multinucleation were 52.3%, 44.0% and 34.1% in frequency, respectively. On in situ hybridization study, the HPV DNA expression rates of 10 squamous cell carcinomas with evidence of HPV infection and 15 carcinomas without evidence of HPV infection were 60.0% and 33.3%, respectively. In contrast to the carcinoma cases, only one (10.0%) of 10 squamous papillomas revealed positive signal. In conclusion, HPV infection is strongly associated with squamous cell carcinoma, but the causal relation of HPV to squamous papilloma is inconspicous.
DNA, Viral/*analysis ; Esophageal Neoplasms/pathology/*virology ; Human ; *In Situ Hybridization ; Neoplasms, Squamous Cell/pathology/*virology ; Papillomavirus, Human/genetics/*isolation & purification ; Papovaviridae Infections/pathology/*virology ; Tumor Virus Infections/pathology/*virology

Histologic changes suggesting HPV infection are occasionally found adjacent to squamous cell carcinoma or in squamous papilloma of the esophagus, but the relationship between HPV infection and benign and malignant squamous lesions of the esophagus is not yet dear. The aim of this study was to examine the role of HPV in squamous lesions of the esophagus. Microscopic examination with emphasis on HPV infection was done on 15 cases of squamous cell carcinoma and 26 cases of squamous papilloma. In situ hybridization technique for wide-spectrum HPV probe was performed on 35 endoscopically biopsied esophageal tissues. Among the histologic parameters suggesting HPV infection, acanthosis was the most frequent finding: 100.0% in benign and malignant esophageal lesions, and koilocytosis and intraepithelial capillary loops were the second (92.7%).: Dyskeratosis, basal cell hyperplasia and bi- or multinucleation were 52.3%, 44.0% and 34.1% in frequency, respectively. On in situ hybridization study, the HPV DNA expression rates of 10 squamous cell carcinomas with evidence of HPV infection and 15 carcinomas without evidence of HPV infection were 60.0% and 33.3%, respectively. In contrast to the carcinoma cases, only one (10.0%) of 10 squamous papillomas revealed positive signal. In conclusion, HPV infection is strongly associated with squamous cell carcinoma, but the causal relation of HPV to squamous papilloma is inconspicous.
DNA, Viral/*analysis ; Esophageal Neoplasms/pathology/*virology ; Human ; *In Situ Hybridization ; Neoplasms, Squamous Cell/pathology/*virology ; Papillomavirus, Human/genetics/*isolation & purification ; Papovaviridae Infections/pathology/*virology ; Tumor Virus Infections/pathology/*virology

OBJECTIVETo investigate the correlation between the presence of human papillomavirus (HPV) DNA in the lymph nodes and histopathologically confirmed metastasis of early-stage cervical carcinoma.

METHODSHPV L1 gene fragment in paraffin-embedded tissue specimens of the primary tumor and pelvic lymph nodes from 31 patients with cervical cancer was amplified using HPV-specific PCR with general consensus primers GP5+/GP6+. The type of HPV was identified by sequence analysis of the PCR products, and the correlation between the presence of HPV DNA in the lymph node and the clinicopathological indices of cervical carcinoma was analyzed.

RESULTSThe positivity rate of HPV DNA in the pelvic lymph nodes was 58.1% in the 31 patients, and in 13 of the patients with confirmed metastasis, the detection rate was 84.6% as compared with the rate of 27.8% in the other 18 patients without metastases. The presence of HPV DNA in the lymph node was associated with histologically confirmed metastases. The results of both HPV DNA detection and pathological examination indicated that the obturator, internal iliac and external iliac lymph nodes were more liable to be positive for HPV DNA, accounting for over 90% of the positivity.

CONCLUSIONHPV DNA detection in the pelvic lymph nodes is a helpful predictive factor of metastases, and the obturator, internal iliac and external iliac lymph nodes are the among the most vulnerable lymph nodes of metastatic involvement by early-stage cervical carcinoma.

Adult ; DNA, Viral ; analysis ; genetics ; Female ; Host-Pathogen Interactions ; Humans ; Lymph Nodes ; pathology ; virology ; Lymphatic Metastasis ; Middle Aged ; Papillomaviridae ; genetics ; physiology ; Papillomavirus Infections ; pathology ; virology ; Polymerase Chain Reaction ; Tumor Virus Infections ; pathology ; virology ; Uterine Cervical Neoplasms ; pathology ; virology

Reactivation of polyoma virus (BK virus) is a significant cause of morbidity in kidney transplant patients. This seemingly insignificant viral infection that affects the majority of population at a young age, once reactivated by immunosuppression, is a major factor contributing to graft loss. Screening techniques have been developed for early prediction of BK virus reactivation. These include plasma and urine assays for detection of BK virus DNA by PCR, urine cytology for detection of "decoy cells" and electron microscopy. Combining urine cytology and serology screening can be more effective for early detection of BK virus reactivation. Immunohistochemistry can be utilized as an additional tool to support the diagnosis. Once screening tests reveal a suspicious BK virus reactivation, tissue biopsy should be performed to confirm the diagnosis, rule out acute cellular rejection and plan treatment approaches. Treatment normally includes decreasing immunosuppression and the use of antiviral drug therapy. Unfortunately, disease outcome is often unfavorable and can culminate with eventual graft loss. Renal retransplantation has been performed with mixed results. As new data emerges, we will gain a better understanding of the disease caused by BK virus and respond with improved early diagnosis and treatment to preserve graft function.
Antiviral Agents/therapeutic use ; *BK Virus ; Humans ; Immunosuppression/*adverse effects ; Kidney Diseases/pathology/*virology ; *Kidney Transplantation ; Polyomavirus Infections/*complications/drug therapy/etiology ; Tumor Virus Infections/*complications/drug therapy/etiology

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

The ability of viral oncoproteins to subvert cell cycle checkpoints may constitute a mechanism by which viral oncoproteins induce genetic instability. HPV 16 E6 and E7 disrupt cell cycle checkpoints, particularly affecting nearly all cyclin-dependent kinase inhibitors linked to the G1- and G2- checkpoints, in each case by means of a different mechanism. HPV 16 E7 shows homology with the pRb binding sites of cyclin D1, which consequently releases E2F. In addition, E7 directly binds to p21, and releases PCNA and other S-phase promoting genes. In turn, released E2F activates cyclin E, and cyclin E accelerates p27 proteolysis as a function of the antagonistic reaction of its own inhibitor. The induction of p16 expression is assumed to be indirectly associated with E7, which is upregulated only after prolonged inactivation of Rb. HPV 16 E6 decreased the fidelity of multiple checkpoints controlling both entry into and exit from mitosis, with the mechanism of p53 inactivation. In addition, HPV 16 E6 increased the sensitivity to chemically induced S-phase premature mitosis and decreased mitotic spindle assembly checkpoint function. Alongside the impressive advances made in the understanding of the molecular mechanisms, which HPV disrupts, the validity of these conclusions should be evaluated in the diagnostic and prognostic fields.
Cervix Neoplasms/*pathology/virology ; Cyclin-Dependent Kinases/*antagonists & inhibitors ; Cyclins/analysis ; Female ; *G1 Phase ; *G2 Phase ; Human ; Microfilament Proteins/analysis ; Papillomavirus Infections/*pathology ; *Papillomavirus, Human ; Proliferating Cell Nuclear Antigen/analysis ; Protein p16/analysis ; Tumor Virus Infections/*pathology