1/104. Oral wart associated with human papillomavirus type 2.More than 100 human papillomavirus (HPV) types have been identified to date. Of these, 24 types have been described as being associated with oral lesions. HPV-2 has been frequently associated with skin lesions, but the reports of oral lesions as features of mucosal infection are limited. A biopsy specimen of an oral wart on the right palate was taken from a 48-year-old man and examined for the presence of HPV The sections showed papillary growth of the epithelium with hyperkeratosis and parakeratosis, and koilocytotic changes of the cells located in the upper layers of the oral squamous cell epithelium. These histological features corresponded well to those of verruca vulgaris on the skin. Immunohistochemically, papillomavirus genus-specific capsid antigen was detected in most of the koilocytotic cells. In addition, Southern blot hybridization analysis revealed that the lesion harbored HPV-2 DNA. in situ hybridization with a biotinylated HPV-2 DNA probe clearly demonstrated viral DNA in the nuclei of squamous cells, which were located in a deeper layer of the epithelium than viral antigen-positive cells.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/104. Prominent hyperkeratotic plantar and palmar warts.We report the case of a 28-year-old man who had prominent hyperkeratotic plantar and palmar warts, and flat warts on his face and chest. By DNA hybridization, human papillomavirus 1 and/or 2, and 3 DNA were detected from the tissues of these skin lesions. Results of laboratory investigations revealed leukopenia, eosinophilia, anti-HBs antigen and anti-hepatitis c virus antibody, and decrease in the OKT4/OKT8 ratio. He had no abnormality in cellular immunity. He was treated with multiple modalities, but was successfully treated with electrocautery to the plantar and palmar warts, and cryotherapy with liquid nitrogen to the flat warts. Nine years after the initial treatment, almost no recurrence was recognized.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
3/104. Epstein-Barr virus-associated intravascular lymphomatosis within Kaposi's sarcoma in an AIDS patient.Intravascular lymphomatosis (IL) is an unusual neoplasm characterized by multifocal proliferation of lymphoma cells exclusively within the blood vessels. We report here a patient with acquired immunodeficiency syndrome (AIDS) and disseminated Kaposi's sarcoma. A 233-bp amplification product of HHV-8 was detected in the DNA extracted from specimens of Kaposi's sarcoma at different sites by polymerase chain reaction (PCR). At autopsy, the vessels within the Kaposi's sarcoma were dilated and filled with atypical large mononuclear cells. No such feature was seen in the vessels of non-Kaposi's sarcomatous regions. Immunohistochemically, the spindle cells of Kaposi's sarcoma were positive for CD31 (endothelial cell marker). The intravascular tumor cells were positive for CD45 (leukocyte common antigen) but negative for others, including chloroacetate esterase, CD45-RO (UCHL-1, Pan-T), CD3, CD43, CD20 (L26, Pan-B), CD30 (Ki-1), immunoglobulin heavy chains and light chains, CD56 (natural killer cell antigen), and CD31. Monoclonal rearrangement of immunoglobulin heavy chain gene was detected in the DNA extracts from fresh tissue of Kaposi's sarcoma by PCR, which indicated that the lymphoma cells within the Kaposi's sarcoma were of monoclonal B cell origin. in situ hybridization revealed that EBER-1 transcripts were present in the lymphoma cells of IL but not in the spindle cells of Kaposi's sarcoma. To the authors' best knowledge, this is the first instance of IL in an AIDS patient with direct evidence of EBV association.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
4/104. Perinatal Epstein Barr virus infection in a premature infant.This is a case of an infant boy born at 28 weeks gestational age who presented on the 42nd day of life with hepatosplenomegaly, haemolytic anaemia, thrombocytopenia and atypical lymphocytes on the peripheral blood smear. He had an Epstein Barr virus (EBV) viral capsid antigen (VCA) IgM antibody titre of 1:160 and a positive test for heterophil antibodies. The cytomegalovirus (CMV) IgM titre was 0.600 and CMV IgG 70 Au/ml. The infant died 10 d later and the autopsy showed CMV inclusion bodies in the lungs, liver and kidneys. EBV infection acquired perinatally, probably co-existing with CMV, may have led to a fatal disease.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
5/104. Genotypic and phenotypic alterations in Epstein-Barr virus-associated lymphoma.AIMS: Epstein-Barr virus (EBV) is associated with numerous reactive and neoplastic lymphoproliferative disorders. in vitro, EBV infection can transform b-lymphocytes and induce phenotypic alterations. This study presents the clinicopathological features of four cases with malignant lymphoma, which showed phenotypic and/or genotypic alterations during the course of the disease. methods AND RESULTS: To determine the type of EBV genotype, we performed polymerase chain reaction (PCR) for lymphocyte-defined membrane antigen (LYDMA) of EBV, subtype A/B and latent membrane protein (LMP)-1 deletion. In addition, we analysed the terminal repeat (TR) band of EBV and receptor genes (T-cell receptor gene, TCR; immunoglobulin gene heavy chain, IgH) for EBV-infected cell clonality. Double staining of cell markers (B, t-lymphocytes; histiocytes), and in-situ hybridization (ISH) for EBV were performed using tissues obtained during the course of the disease. The first case showed genotypic and phenotypic alterations of T-cell type to B-cell type. The first TCR rearrangement and T-cell markers (CD3 , CD4 , CD8-) were lost and IgH rearrangement and B-cell markers (CD19 , CD20 ) were identified. During the course of the disease, EBV-TR bands changed in size; however, the EBV genotype type B, LMP1 deletion type, and single LYDMA band remained the same. The initial T-cell lymphoma clone was considered to be different from the latter B-cell lymphoma clone. The second case showed phenotypic alterations. The first B-cell marker (CD19 , CD20 , CD68-) changed to histiocytic markers (CD19-, CD20-, CD68 ). However, IgH rearrangement and EBV-TR bands remained the same throughout the course of the disease and EBV genotype type A, LMP1 deletion type, and single LYDMA band remained unchanged. The third case showed phenotypic alterations. The B-cell marker (CD20 ) was lost; however, IgH rearrangement of PCR and EBV genotype remained the same. In the second and third cases, the initial lymphoma clones were considered to be same as the latter clones. The last case showed lineage alterations from Hodgkin's disease to natural killer (NK) cell leukaemia. However, EBV genotype did not change. The second case and Hodgkin's disease showed LMP expression, but the first and third cases showed no LMP, and EBNA2 was not detected in all cases. CONCLUSIONS: We report the genotypic and/or phenotypic alterations in four patients with EBV-associated lymphoma/leukaemia. However, EBV genotype did not change in all four. These findings suggest that EBV might induce the cell marker and lineage alteration in vivo, as in vitro.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
6/104. Conjunctival lymphocytic infiltrates associated with Epstein-Barr virus.PURPOSE: To describe the clinicopathologic features of two patients with Epstein-Barr virus (EBV) associated conjunctival lymphocytic infiltrates. DESIGN: Two case reports. methods: The clinical histories and pathologic findings of two patients with salmon-colored conjunctival infiltrates are described. MAIN OUTCOME MEASUREMENTS: Clinical observation and pathologic examination of conjunctival biopsy specimens with accompanying immunohistochemical staining, flow cytometric immunophenotyping, and polymerase chain reaction analysis when appropriate. RESULTS: One patient had ipsilateral preauricular lymphadenopathy, elevated serum EBV titers, and a unilateral reactive lymphocytic infiltrate resulting in a conjunctival mass. The other patient had bilateral conjunctival lymphocytic infiltrates causing conjunctival masses. There was an expanded clonal population of B lymphocytes in the conjunctival mass in the second patient. Both patients had EBV antigen in their conjunctival lymphocytic infiltrates. CONCLUSIONS: Conjunctival lymphocytic lesions associated with EBV represent a spectrum of reactive infiltrates to monoclonal populations.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
7/104. Virological and molecular characterisation of a new B lymphoid cell line, established from an AIDS patient with primary effusion lymphoma, harbouring both KSHV/HHV8 and EBV viruses.We report here a new case of primary effusion lymphoma (PEL), occurring in a French homosexual hiv-1 infected male with a pericardial, pleural and mesenteric tumour dissemination, and the establishment from his pleural effusion of a new cell line, Cra-BCBL, dually infected by EBV and KSHV/HHV8. Cra-BCBL cells are of B-cell origin as judged by their clonal immunoglobulin heavy chain (IgH) gene rearrangement, identical to that of the parental tumour. Both the cell line and the lymphoma cells expressed CD38 and CD45 antigens but no classical B-cell or T-cell lineage-restricted antigens. Cra-BCBL harbours a type I EBV virus, expressing a latency type II. Expression of KSHV/HHV8 ORF72 and ORF75 was detected by RT/PCR. In addition, KSHV lytic replication could be induced by treatment by n-butyrate. An equivalent and high copy number of KSHV genomes (20 to 200 copies by cell) was detected both in the primary tumour cells and in the cell line. Southern blot (SB) analysis of EBV terminal repeats (TR) displayed the same unique band in the cell line DNA and in the original tumour cells, consistent with a monoclonal infection of EBV. Furthermore, SB analysis of KSHV/HHV8 TR revealed the same hybridisation pattern between Cra-BCBL and the effusion cells, with a common band at around 30-40 kb corresponding to the fused termini of the viral episomes and a 5 Kb rearranged fragment. The new cell line characterised here could be a useful model to study interactions between two human herpes viruses and their contribution to lymphomagenesis.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
8/104. Tissue-specific expression of SV40 in tumors associated with the li-fraumeni syndrome.Inactivation of wild-type p53 tumor suppressor function is the primary mechanism of tumor initiation in li-fraumeni syndrome (LFS) individuals with germline p53 mutations. Tumors derived from LFS patients frequently retain the normal p53 allele, suggesting that alternative mechanisms in addition to gene deletion must be involved in inactivating wild-type p53 protein. dna tumor viruses, such as SV40, target p53 for inactivation through the action of viral oncoproteins. We studied the probands from two unrelated LFS families, each of whom presented with multiple malignant neoplasms. Patient 1 developed an embryonal rhabdomyosarcoma (RMS) and a choroid plexus carcinoma (CPC), while patient 2 developed a CPC and subsequently presented with both an osteosarcoma (OS) and renal cell carcinoma (RCC). We utilized DNA sequence analysis and immunohistochemistry to determine p53 gene status in the germline and tumors, as well as evidence for SV40 T-antigen oncoprotein expression. Each patient harbored a heterozygous germline p53 mutation at codons 175 and 273, respectively. In patient 1, the normal p53 gene was lost while the mutant p53 allele was reduced to homozygosity in the RMS. Both normal and mutant genes were maintained in the CPC. In patient 2, normal and mutant p53 alleles were retained in both the CPC and RCC. Both specific PCR and immunostaining detected SV40 T-antigen in both CPCs and the RCC. In addition to chromosomal alterations, epigenetic mechanisms may disrupt p53 function during tumorigenesis. In two LFS patients, we found SV40 DNA sequences and viral T-antigen expression that could account for inactivation of the normal p53 protein. Inactivation of p53 or other tumor suppressors by viral proteins may contribute to tumor formation in specific tissues of genetically susceptible individuals.- - - - - - - - - - ranking = 1.5keywords = antigen (Clic here for more details about this article) |
9/104. Protean manifestations of human papillomavirus type 60 infection on the extremities.BACKGROUND: Human papillomavirus type 60 (HPV-60) induces a ridged wart or an epidermal cyst on the sole of the foot, exhibiting identical pathological changes, with a single refractile eosinophilic intracytoplasmic inclusion body in infected cells. However, there is no information on the role of HPV-60 in the development of cutaneous lesions on other anatomical sites. OBJECTIVES: To perform the clinicopathological analysis of various cutaneous lesions of a patient in relation to HPV genotype. PATIENT: A 50-year-old male patient developed multiple papules, plaques and nodules on his hand, arm and legs. RESULTS: Clinicopathologically, the lesions were classified into three categories. A common wart on the finger showed papillomatosis and acanthosis characterized by numerous keratohyalin granules. Plane warts on the arm showed perinuclear vacuolization of the cells in the upper Malpighian layer. On the other hand, a pigmented papillomatous nodule on the finger, and the other lesions on the hands and legs exhibited similar histological features with a unique cytoplasmic eosinophilic inclusion body. All the three categorized lesions were equally positive for HPV capsid antigen by immunohistochemistry. By blot hybridization analysis for HPV sequences, it was revealed that a common wart on the finger and plane warts on the arm harboured HPV-27 and HPV-3, respectively, while all the other lesions harboured HPV-60. The histological localization of each viral DNA was confirmed in the corresponding lesions by in situ hybridization. CONCLUSIONS: HPV-60 is able to induce papular and nodular lesions on the extremities.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
10/104. BK polyomavirus interstitial nephritis in a renal transplant patient with no previous acute rejection episodes.A renal transplant patient treated with tacrolimus and mycophenolate-mofetil (MMF) developed progressive graft function deterioration 10 months after transplantation. biopsy of the graft showed severe, focally accentuated interstitial inflammation with focal tubulitis and tubular necrosis, and medium-severe interstitial fibrosis with focal tubular atrophy. Glomerular and vascular structures were preserved. On careful examination, in some sections, tubular epithelial cells showed a definite increase with deformation of the nuclear shape, chromatin irregularities with peripheral dislocation and inclusion bodies. These cytopathic changes suggested polyoma virus infection ("decoy cells"). Subsequent screening of the urinary sediment confirmed the presence of many "decoy cells". Immunohistochemical analysis of the biopsy showed many tubular cells were strongly positive for the SV 40 antigen, specific for BK polyoma virus. A diagnosis of interstitial nephritis due to BK polyoma virus was made, though the coexistence of cellular rejection could not be excluded. At variance with previous reports, our patient had not had repeated episodes of rejection before biopsy or heavy immunosuppressive treatment, such as ALG, OKT3, after transplantation. This case shows that even in the absence of vigorous anti-rejection therapy an immunosuppressive regimen based on tacrolimus and MMF may involve the risk of BK polyoma virus- associated interstitial nephritis.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
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