• Antivirals
• EBV infection
• Fungal immunomodulatory proteins
• Fusion
• Glycoprotein B
• HSV-1 infection

• Herpesvirus 1, Human/drug effects
• Herpesvirus 1, Human/physiology
• Humans
• Herpesvirus 4, Human/drug effects
• Herpesvirus 4, Human/physiology
• Antiviral Agents/pharmacology
• Antiviral Agents/chemistry
• Ganoderma/chemistry
• Virus Internalization/drug effects
• Viral Envelope Proteins/metabolism
• Viral Envelope Proteins/chemistry
• Fungal Proteins/pharmacology
• Fungal Proteins/chemistry
• Epstein-Barr Virus Infections/drug therapy
• Epstein-Barr Virus Infections/virology
• Animals
• Herpes Simplex/drug therapy
• Herpes Simplex/virology
• Cell Line

• Innate immunity
• RIG-I and PKR
• Vault RNAs

• Immunity, Innate/genetics
• Interferons
• Apoptosis
• Autophagy

• Consejo Nacional de Humanidades, Ciencias y Tecnologías (Conahcyt)

• CRISPR-Cas9
• Shiga toxins
• bacterial toxin
• cholera toxin
• genetic screen
• glycosphingolipids
• large clostridial toxins
• membrane vesicle trafficking
• protein glycosylation
• ricin

• R01NS080833, R01NS117626, R01AI132387, R21NS106159, R01AI139087, and R01AI158503 NIH HHS

Pulmonary lymphomatoid granulomatosis (PLG) is a lymphoproliferative disease associated with Epstein-Barr viral infection occurring mainly in adults and rarely in children. It is characterized by multiple pulmonary nodules. Its diagnosis depends on lung biopsy findings. Most patients are immunodeficient, and it commonly presents in children undergoing chemotherapy for leukemia. We report the case of a child with PLG caused by a mutation in the macrophage-expressed gene 1 (MPEG1), suggesting possible PLG occurrence in children undergoing treatment for pulmonary nodular lesions.

This study reports a case of PLG without apparent immunodeficiency, suggesting the possibility of this disease occurrence during the treatment of pulmonary nodular lesions in children. Initially, the cause was assumed to be an atypical pathogen. Following conventional anti-infective treatment, chest computed tomography findings revealed that there were still multiple nodules in the lungs. Additionally, the patient was found to be infected with the Epstein-Barr virus. Histopathological examination of the resected lung revealed lymphoproliferative lesions with necrosis. Small lymphocytes, plasma cells, and histiocytes were observed in the background, although Reed-Sternberg cells were absent. Immunohistochemical staining [CD20(+), CD30(+), and CD3(+)] and EBV-encoded small RNA1/2 in situ hybridization of small lymphocytes revealed approximately 200 cells/high-power field. Whole exon sequencing of the patient revealed a mutation in the MPEG1. The patient was eventually diagnosed with PLG and transferred to the Department of Pediatric Oncology for bone marrow transplantation.

As PLG is rare and fatal, it should be suspected in clinical settings when treatment of initial diagnosis is ineffective.

• Pulmonary lymphomatoid granulomatosis
• Child
• Epstein-Barr virus
• Lymphoproliferative disease
• Leukemia
• Case report

Epstein-Bar virus (EBV) can directly cause lymphoproliferative disease (LPD), including AIDS-defining lymphomas such as Burkitt’s lymphoma and other non-Hodgkin lymphomas (NHL), as well as human immunodeficiency virus (HIV)-related Hodgkin lymphoma (HL). The prevalence of EBV in HL and NHL is elevated in HIV-positive individuals compared with the general population. Rates of incidence of AIDS-defining cancers have been declining in HIV-infected individuals since initiation of combination anti-retroviral therapy (cART) use in 1996. However, HIV-infected persons remain at an increased risk of cancers related to infections with oncogenic viruses. Proposed pathogenic mechanisms of HIV-related cancers include decreased immune surveillance, decreased ability to suppress infection-related oncogenic processes and a state of chronic inflammation marked by alteration of the cytokine profile and expanded numbers of cytotoxic T lymphocytes with down-regulated co-stimulatory molecules and increased expression of markers of senescence in the setting of treated HIV infection. Here we discuss the cooperation of EBV-infected B cell- and environment-associated factors that may contribute to EBV-related lymphomagenesis in HIV-infected individuals. Environment-derived lymphomagenic factors include impaired host adaptive and innate immune surveillance, cytokine dysregulation and a pro-inflammatory state observed in the setting of chronic, cART-treated HIV infection. B cell factors include distinctive EBV latency patterns and host protein expression in HIV-associated LPD, as well as B cell-stimulating factors derived from HIV infection. We review the future directions for expanding therapeutic approaches in targeting the viral and immune components of EBV LPD pathogenesis.

• Epstein-Barr virus
• HIV
• Immunology
• immunodeficiency
• lymphoproliferative disease

Equine herpesvirus type 5 (EHV5) is a ubiquitous, yet obscure pathogen in the horse population and is commonly associated with fatal equine multinodular pulmonary fibrosis (EMPF). To date, little is known about the precise pathogenesis of EHV5. Here, we evaluated the dynamics of EHV5 infection in representative ex vivo and in vitro equine models, using immunofluorescence staining and virus titration. EHV5 was unable to infect epithelial cells lining the mucosa of nasal and tracheal explants. Similarly, primary equine respiratory epithelial cells (EREC) were not susceptible to EHV5 following inoculation at the apical or basolateral surfaces. Upon direct delivery of EHV5 particles to lung explants, few EHV5-positive cell clusters were observed at 72 hours post-inoculation (hpi). These EHV5-positive cells were identified as cytokeratin-positive alveolar cells. Next, we examined the potential of EHV5 to infect three distinct equine PBMC populations (CD172a⁺ monocytes, CD3⁺ T lymphocytes and Ig light chain⁺ B lymphocytes). Monocytes did not support EHV5 replication. In contrast, up to 10% of inoculated equine T and B lymphocytes synthetized intracellular viral antigens 24 hpi and 72 hpi, respectively. Still, the production of mature virus particles was hampered, as we did not observe an increase in extracellular virus titer. After reaching a peak, the percentage of infected T and B lymphocytes decayed, which was partly due to the onset of apoptosis, but not necrosis. Based on these findings, we propose a model for EHV5 pathogenesis in the horse. Uncovering EHV5 pathogenesis is the corner step to finally contain or even eradicate the virus.

Fabry disease (FD) is a disorder caused by mutations in the gene encoding for lysosomal enzyme α-galactosidase A (α-GAL). Reduced α-GAL activity leads to progressive accumulation of globotriaosylceramide (Gb3), also known as CD77. The recent report of increased expression of CD77 in blood cells of patients with FD indicated that this molecule can be used as a potential marker for monitoring enzyme replacement therapy (ERT).

The purpose of this study was to evaluate the CD77 levels throughout ERT in FD patients (V269M mutation).

We evaluated the fluctuations in PBMC (peripheral blood mononuclear cell) membrane CD77 expression in FD patients undergoing ERT and correlated these levels with those observed in different cell types.

A greater CD77 expression was found in phagocytes of patients compared to controls at baseline. Interestingly, the variability in CD77 levels is larger in patients at baseline (340 - 1619 MIF) and after 12 months of ERT (240 - 530 MIF) compared with the control group (131 - 331 MFI). Furthermore, by analyzing the levels of CD77 in phagocytes from patients throughout ERT, we found a constant decrease in CD77 levels.

The increased CD77 levels in the phagocytes of Fabry carriers together with the decrease in CD77 levels throughout ERT suggest that measuring CD77 levels in phagocytes is a promising tool for monitoring the response to ERT in FD.

• Apoptosis/genetics
• Apoptosis Regulatory Proteins/antagonists & inhibitors
• Apoptosis Regulatory Proteins/metabolism
• Bcl-2-Like Protein 11/antagonists & inhibitors
• Bcl-2-Like Protein 11/metabolism
• Burkitt Lymphoma/metabolism
• Burkitt Lymphoma/pathology
• Cell Line
• Herpesvirus 4, Human/genetics
• Herpesvirus 4, Human/growth & development
• Herpesvirus 4, Human/metabolism
• Humans
• Proto-Oncogene Proteins/antagonists & inhibitors
• Proto-Oncogene Proteins/metabolism

• 15032 Cancer Research UK
• C5575/A15032 Cancer Research UK

• BCL-2 family
• EBV
• apoptosis
• genetic cooperation
• growth transformation
• latency
• p53
• virus cancers

• Apoptosis
• Burkitt Lymphoma/virology
• Cell Transformation, Viral/genetics
• Cell Transformation, Viral/physiology
• DNA Damage/genetics
• Gene Expression Regulation, Viral
• Herpesvirus 4, Human/genetics
• Herpesvirus 4, Human/pathogenicity
• Herpesvirus 4, Human/physiology
• Host-Pathogen Interactions
• Humans
• RNA, Viral
• Viral Proteins
• Virus Latency/genetics
• Virus Latency/physiology

• 15032 Cancer Research UK
• C5575/A15032 Cancer Research UK

Epstein–Barr virus (EBV) is known to be associated with the development of malignant lymphoma and lymphoproliferative disorders (LPDs) in immunocompromised patients. EBV, a B-lymphotropic gamma-herpesvirus, causes infectious mononucleosis and oral hairy leukoplakia, as well as various pathological types of lymphoid malignancy. Furthermore, EBV is associated with epithelial malignancies such as nasopharyngeal carcinoma (NPC), salivary gland tumor, gastric carcinoma and breast carcinoma. In terms of oral disease, there have been several reports of EBV-related oral squamous cell carcinoma (OSCC) worldwide. However, the role of EBV in tumorigenesis of human oral epithelial or lymphoid tissue is unclear. This review summarizes EBV-related epithelial and non-epithelial tumors or tumor-like lesions of the oral cavity. In addition, we describe EBV latent genes and their expression in normal epithelium, inflamed gingiva, epithelial dysplasia and SCC, as well as considering LPDs (MTX- and age-related) and DLBCLs of the oral cavity.

• Activation-induced cytidine deaminase (AID)
• Early growth transcription response-1 (Egr-1)
• Epstein–Barr virus (EBV)
• MTX- and age-related EBV + B-cell LPD
• Oral squamous cell carcinoma (OSCC)

• Adrenal Cortex Hormones/administration & dosage
• Adrenal Cortex Hormones/therapeutic use
• Adult
• Antibodies, Viral/blood
• Asian People
• Autoantigens/immunology
• DNA, Viral/blood
• Deoxyribonucleases/immunology
• Dose-Response Relationship, Drug
• Epstein-Barr Virus Infections/complications
• Epstein-Barr Virus Nuclear Antigens/immunology
• Genome, Viral
• Herpesvirus 4, Human/enzymology
• Herpesvirus 4, Human/genetics
• Humans
• Immunoglobulin A/blood
• Immunoglobulin G/blood
• Lupus Erythematosus, Systemic/blood
• Lupus Erythematosus, Systemic/drug therapy
• Lupus Erythematosus, Systemic/immunology
• Lupus Erythematosus, Systemic/virology
• Middle Aged
• Ribonucleoproteins, Small Nuclear/immunology
• Taiwan
• Viral Load
• snRNP Core Proteins

Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancies

• EBV
• Epithelial tumors
• Latency
• Lymphoid tumors
• Oncogenes
• Oncogenesis

Despite much work, safe and effective approaches to attack and deplete the long-lived reservoir of cells latently infected with HIV-1 remain an elusive goal. Patients infected with HIV-1 treated with cytotoxic agents or bone marrow transplantation can experience decreases in the reservoir of HIV-1 latently infected cells. Other viruses capable of long-term latency, such as herpesviruses, can sense host cell apoptosis and respond by initiating replication. These observations suggest that other viruses capable of long-term latency, like HIV-1, might also sense when its host cell is about to undergo apoptosis and respond by initiating replication.

Pro-monocytic (U1) and lymphoid (ACH-2) HIV-1 persistently infected cell lines were treated with cytotoxic drugs – doxorubicin, etoposide, fludarabine phosphate, or vincristine – and activation of latent HIV-1 was evaluated using assays for HIV-1 RNA and p24 production. Both cell lines showed dose-dependent increases in apoptosis and associated HIV-1 activation following exposure to the cytotoxic agents. Pretreatment of the cells with the pan-caspase inhibitor Z-VAD-FMK prior to exposure to the cytotoxic agents inhibited apoptosis and viral activation. Direct exposure of the latently infected cell lines to activated caspases also induced viral replication. HIV-1 virions produced in association with host cell apoptosis were infectious.

The results indicate that latent HIV-1 can sense when its host cell is undergoing apoptosis and responds by completing its replication cycle. The results may help explain why patients treated with cytotoxic regimens for bone marrow transplantation showed reductions in the reservoir of latently infected cells. The results also suggest that the mechanisms that HIV-1 uses to sense and respond to host cell apoptosis signals may represent helpful new targets for approaches to attack and deplete the long-lived reservoir of cells latently infected with HIV-1.

Cells undergoing apoptosis are known to modulate their tissue microenvironments. By acting on phagocytes, notably macrophages, apoptotic cells inhibit immunological and inflammatory responses and promote trophic signaling pathways. Paradoxically, because of their potential to cause death of tumor cells and thereby militate against malignant disease progression, both apoptosis and tumor-associated macrophages (TAMs) are often associated with poor prognosis in cancer. We hypothesized that, in progression of malignant disease, constitutive loss of a fraction of the tumor cell population through apoptosis could yield tumor-promoting effects.

Here, we demonstrate that apoptotic tumor cells promote coordinated tumor growth, angiogenesis, and accumulation of TAMs in aggressive B cell lymphomas. Through unbiased “in situ transcriptomics” analysis—gene expression profiling of laser-captured TAMs to establish their activation signature in situ—we show that these cells are activated to signal via multiple tumor-promoting reparatory, trophic, angiogenic, tissue remodeling, and anti-inflammatory pathways. Our results also suggest that apoptotic lymphoma cells help drive this signature. Furthermore, we demonstrate that, upon induction of apoptosis, lymphoma cells not only activate expression of the tumor-promoting matrix metalloproteinases MMP2 and MMP12 in macrophages but also express and process these MMPs directly. Finally, using a model of malignant melanoma, we show that the oncogenic potential of apoptotic tumor cells extends beyond lymphoma.

In addition to its profound tumor-suppressive role, apoptosis can potentiate cancer progression. These results have important implications for understanding the fundamental biology of cell death, its roles in malignant disease, and the broader consequences of apoptosis-inducing anti-cancer therapy.

•

Apoptotic lymphoma cells promote tumor growth, angiogenesis, and TAM accumulation

• sudan
• epstein barr virus (ebv)
• breast cancer
• dna methylation

The resinous metabolites commonly known as frankincense or olibanum are produced by trees of the genus Boswellia and have attracted increasing popularity in Western countries in the last decade for their various pharmacological activities. This review described the pharmacological specific details mainly on anti-inflammatory, anti-carcinogenic, anti-bacterial and apoptosis-regulating activities of individual triterpenoid together with the relevant mechanism. In addition, species-characterizing triterpenic markers with the methods for their detection, bioavailability, safety and other significant properties were reviewed for further research.

• Adult
• Aged
• Aged, 80 and over
• Antigens, CD/immunology
• Antigens, CD7/immunology
• CD2 Antigens/immunology
• Female
• Flow Cytometry
• Humans
• Immunoglobulin Light Chains/immunology
• Immunohistochemistry
• Japan/epidemiology
• Lymphoma, Large B-Cell, Diffuse/immunology
• Lymphoma, Large B-Cell, Diffuse/mortality
• Lymphoma, Large B-Cell, Diffuse/pathology
• Male
• Middle Aged
• Retrospective Studies
• T-Lymphocytes/immunology

• Epstein-Barr virus (EBV)
• post-transplant lymphoproliferative disorder (PTLD)
• survivin

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy, which commonly occurs in Southern China, Taiwan, North Africa and Southeast Asia. Nasopharyngeal carcinoma is strongly associated with Epstein-Barr virus infection. The p53 tumour suppressor protein is rarely mutated in NPC suggesting that the inactivation of p53 pathway in NPC could be due to the presence of EBV proteins. The aim of this work was to determine the effects of EBV proteins namely LMP1 and LMP2A on the expression levels of p53 protein.

In this work we found that LMP1, but not LMP2A, decreased p53 protein levels. Overexpression of LMP1 resulted in increased ubiquitination of p53 suggesting that the decreased p53 protein levels by LMP1 was due to increased degradation of the protein. The reduction of p53 protein levels was independent of the PI3K-Akt pathway.

LMP1, but not LMP2A, reduced p53 protein levels through the increase in the polyubiquitination of p53 protein and was independent of the PI3K-Akt pathway.

• Apoptosis/drug effects
• B-Lymphocytes/drug effects
• B-Lymphocytes/pathology
• B-Lymphocytes/virology
• Cell Line
• Drug Resistance, Viral/drug effects
• Etoposide/pharmacology
• Gene Deletion
• Gene Expression Regulation, Viral/drug effects
• Gene Knockout Techniques
• Genetic Loci/genetics
• Herpesvirus 4, Human/drug effects
• Herpesvirus 4, Human/genetics
• Herpesvirus 4, Human/physiology
• Humans
• Ionomycin/pharmacology
• Proto-Oncogene Proteins c-bcl-2/metabolism
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• RNA, Small Interfering/metabolism
• Reproducibility of Results
• Signal Transduction/drug effects
• Staurosporine/pharmacology
• Viral Proteins/metabolism
• Virus Latency

• Wellcome Trust
• 077489 Wellcome Trust
• 077489 British Heart Foundation

Epstein-Barr virus (EBV) is implicated in the pathogenesis of multiple human tumours of lymphoid and epithelial origin. The virus infects and immortalizes B cells establishing a persistent latent infection characterized by varying patterns of EBV latent gene expression (latency 0, I, II and III). The CDK1 activator, Response Gene to Complement-32 (RGC-32, C13ORF15), is overexpressed in colon, breast and ovarian cancer tissues and we have detected selective high-level RGC-32 protein expression in EBV-immortalized latency III cells. Significantly, we show that overexpression of RGC-32 in B cells is sufficient to disrupt G2 cell-cycle arrest consistent with activation of CDK1, implicating RGC-32 in the EBV transformation process. Surprisingly, RGC-32 mRNA is expressed at high levels in latency I Burkitt's lymphoma (BL) cells and in some EBV-negative BL cell-lines, although RGC-32 protein expression is not detectable. We show that RGC-32 mRNA expression is elevated in latency I cells due to transcriptional activation by high levels of the differentially expressed RUNX1c transcription factor. We found that proteosomal degradation or blocked cytoplasmic export of the RGC-32 message were not responsible for the lack of RGC-32 protein expression in latency I cells. Significantly, analysis of the ribosomal association of the RGC-32 mRNA in latency I and latency III cells revealed that RGC-32 transcripts were associated with multiple ribosomes in both cell-types implicating post-initiation translational repression mechanisms in the block to RGC-32 protein production in latency I cells. In summary, our results are the first to demonstrate RGC-32 protein upregulation in cells transformed by a human tumour virus and to identify post-initiation translational mechanisms as an expression control point for this key cell-cycle regulator.

Molecular adjuvants are a promising method to enhance virus-specific immune responses and protect against HIV-1 infection. Immune activation by ligands for receptors such as CD40 can induce dendritic cell activation and maturation. Here we explore the incorporation of two CD40 mimics, Epstein Barr Virus gene LMP1 or an LMP1-CD40 chimera, into a strain of SIV that was engineered to be limited to a single cycle of infection.

Full length LMP1 or the chimeric protein LMP1-CD40 was cloned into the nef-locus of single-cycle SIV. Human and Macaque monocyte derived macrophages and DC were infected with these viruses. Infected cells were analyzed for activation surface markers by flow cytometry. Cells were also analyzed for secretion of pro-inflammatory cytokines IL-1β, IL-6, IL-8, IL-12p70 and TNF by cytometric bead array.

Overall, single-cycle SIV expressing LMP1 and LMP1-CD40 produced a broad and potent T_H1-biased immune response in human as well as rhesus macaque macrophages and DC when compared with control virus. Single-cycle SIV-LMP1 also enhanced antigen presentation by lentiviral vector vaccines, suggesting that LMP1-mediated immune activation may enhance lentiviral vector vaccines against HIV-1.

• ebv
• vdr
• transcription regulation
• ebna
• vitamin d3

• Animals
• Calcifediol/metabolism
• Cell Line
• Cell Line, Tumor
• Epstein-Barr Virus Nuclear Antigens/genetics
• Epstein-Barr Virus Nuclear Antigens/metabolism
• Gene Expression Regulation
• Herpesvirus 4, Human/genetics
• Herpesvirus 4, Human/metabolism
• Humans
• Lymphocytes/cytology
• Lymphocytes/physiology
• Mass Spectrometry
• Receptors, Calcitriol/genetics
• Receptors, Calcitriol/metabolism

• Cell Adhesion Molecules/metabolism
• Cells, Cultured
• Chromatography, High Pressure Liquid
• Detergents/pharmacology
• Endothelial Cells/drug effects
• Endothelial Cells/metabolism
• Erythrocytes/drug effects
• Erythrocytes/metabolism
• Flow Cytometry
• Fluorescent Antibody Technique
• Gene Expression Regulation, Enzymologic/drug effects
• Globosides/chemistry
• Globosides/metabolism
• Glycosyltransferases/genetics
• Glycosyltransferases/metabolism
• Humans
• Kinetics
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Solubility/drug effects
• Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
• Tumor Necrosis Factor-alpha/pharmacology
• Umbilical Veins/cytology

• epstein-barr virus
• burkitt's lymphoma
• cancer pathogenesis
• c-myc
• apoptosis

• Animals
• Burkitt Lymphoma/virology
• Epstein-Barr Virus Infections/virology
• Herpesvirus 4, Human/pathogenicity
• Humans

• Wellcome Trust
• Cancer Research UK
• Medical Research Council

• ppargamma
• b cell lymphoma
• proliferation
• sirna
• overexpression

• Burkitt Lymphoma/genetics
• Burkitt Lymphoma/pathology
• Cell Line, Tumor
• Cell Proliferation
• Cell Survival
• Gene Knockdown Techniques
• Genetic Vectors/metabolism
• Humans
• Ligands
• NF-kappa B/metabolism
• PAX5 Transcription Factor/metabolism
• PPAR gamma/genetics
• PPAR gamma/metabolism
• Positive Regulatory Domain I-Binding Factor 1
• Proto-Oncogene Proteins c-bcl-2/metabolism
• RNA Interference
• Repressor Proteins/metabolism

• ES01247 NIEHS NIH HHS
• P30 ES001247 NIEHS NIH HHS
• T32HL007152 NHLBI NIH HHS
• DE11390 NIDCR NIH HHS
• T32 HL007152 NHLBI NIH HHS
• R01 DE011390 NIDCR NIH HHS

• Animals
• B-Lymphocytes/metabolism
• Burkitt Lymphoma/complications
• Burkitt Lymphoma/genetics
• Burkitt Lymphoma/pathology
• Burkitt Lymphoma/virology
• Epstein-Barr Virus Infections/complications
• Epstein-Barr Virus Infections/diagnosis
• Epstein-Barr Virus Nuclear Antigens/genetics
• Genes, myc
• Herpesvirus 4, Human/metabolism
• Humans
• Immunologic Memory
• Malaria/complications
• MicroRNAs/metabolism
• Models, Biological
• Translocation, Genetic

• Apoptosis
• Arachidonate 12-Lipoxygenase/metabolism
• Arachidonate 5-Lipoxygenase/genetics
• Arachidonate 5-Lipoxygenase/metabolism
• Burkitt Lymphoma/enzymology
• Burkitt Lymphoma/genetics
• Burkitt Lymphoma/pathology
• Burkitt Lymphoma/virology
• Cell Line, Tumor
• Cell Survival
• Disease Progression
• Herpesvirus 4, Human/physiology
• Humans
• Lipid Peroxidation
• RNA, Neoplasm/genetics
• Reactive Oxygen Species/metabolism
• Reverse Transcriptase Polymerase Chain Reaction

• Animals
• Apoptosis
• Hematopoiesis
• Humans
• Leukemia/blood
• Leukemia/drug therapy
• Leukemia/metabolism
• Lymphoma/blood
• Lymphoma/drug therapy
• Lymphoma/metabolism
• Multiple Myeloma/blood
• Multiple Myeloma/drug therapy
• Multiple Myeloma/metabolism
• Myelodysplastic Syndromes/blood
• Myelodysplastic Syndromes/drug therapy
• Myelodysplastic Syndromes/metabolism
• Receptors, Transforming Growth Factor beta/blood
• Receptors, Transforming Growth Factor beta/metabolism
• Signal Transduction
• Transforming Growth Factor beta/biosynthesis
• Transforming Growth Factor beta/blood
• Transforming Growth Factor beta/metabolism

• R01 HL082946 NHLBI NIH HHS

• Epstein-Barr Virus Infections/complications
• Epstein-Barr Virus Infections/prevention & control
• Herpesvirus 4, Human/immunology
• Herpesvirus 4, Human/pathogenicity
• Herpesvirus 4, Human/physiology
• Humans
• Immunocompromised Host
• Immunotherapy/methods
• Lymphoma, B-Cell/immunology
• Lymphoma, B-Cell/prevention & control
• Lymphoma, B-Cell/virology
• Lymphoproliferative Disorders/immunology
• Lymphoproliferative Disorders/prevention & control
• Lymphoproliferative Disorders/virology
• Organ Transplantation/adverse effects
• Postoperative Complications/prevention & control
• Postoperative Complications/virology

• Animals
• Gene Expression Profiling
• Herpesvirus 4, Human/physiology
• Humans
• Immunotherapy, Active/methods
• Neoplasms/genetics
• Neoplasms/immunology
• Neoplasms/virology

• Antineoplastic Agents/pharmacology
• Cisplatin/pharmacology
• Drug Resistance, Neoplasm
• Female
• Humans
• Immunoenzyme Techniques
• Lipids/analysis
• Ovarian Neoplasms/metabolism
• Ovarian Neoplasms/pathology
• Paclitaxel/pharmacology
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• RNA, Neoplasm/genetics
• RNA, Neoplasm/metabolism
• Receptors, Cell Surface/metabolism
• Reverse Transcriptase Polymerase Chain Reaction
• Trihexosylceramides/metabolism
• Tumor Cells, Cultured

• Apoptosis
• Apoptosis Regulatory Proteins/metabolism
• Caspases/metabolism
• Cell Line
• Chimerin Proteins/genetics
• Chimerin Proteins/metabolism
• Enzyme Activation
• Fas Ligand Protein
• Herpesvirus 4, Human/physiology
• Humans
• Lymphoma, B-Cell/metabolism
• Lymphoma, B-Cell/pathology
• Membrane Glycoproteins/metabolism
• NF-kappa B/metabolism
• Signal Transduction
• TNF-Related Apoptosis-Inducing Ligand
• Tumor Necrosis Factor-alpha/metabolism
• Tumor Necrosis Factors/metabolism
• Viral Matrix Proteins/genetics
• Viral Matrix Proteins/metabolism

• CA105157 NCI NIH HHS
• R01 AI41769 NIAID NIH HHS

• AIDS-Related Opportunistic Infections/complications
• HIV Infections/complications
• Humans
• Monoclonal Gammopathy of Undetermined Significance/complications

• Animals
• Apoptosis/physiology
• Cattle
• Cells, Cultured
• Cytopathogenic Effect, Viral/physiology
• Diarrhea Viruses, Bovine Viral/genetics
• Diarrhea Viruses, Bovine Viral/pathogenicity
• Gene Expression Regulation, Viral
• Muscle, Skeletal/cytology
• RNA, Double-Stranded/metabolism
• RNA, Messenger/metabolism
• RNA, Viral/metabolism

• Apoptosis
• Burkitt Lymphoma/metabolism
• Burkitt Lymphoma/pathology
• Cell Line, Tumor
• Child
• Clone Cells
• Epstein-Barr Virus Nuclear Antigens/genetics
• Epstein-Barr Virus Nuclear Antigens/metabolism
• Female
• Gene Expression Regulation, Viral
• Genome, Viral/genetics
• Herpesvirus 4, Human/physiology
• Humans
• Proto-Oncogene Proteins c-myc/metabolism
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Transcription, Genetic
• Tumor Cells, Cultured
• Viral Matrix Proteins/metabolism
• Viral Proteins/metabolism
• Virus Latency/physiology

• Antigens, Viral/genetics
• Apoptosis/genetics
• B-Lymphocytes/virology
• Base Sequence
• Binding Sites
• Cells, Cultured
• Epstein-Barr Virus Nuclear Antigens/genetics
• Epstein-Barr Virus Nuclear Antigens/metabolism
• Herpesvirus 4, Human/growth & development
• Humans
• Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism
• Minor Histocompatibility Antigens
• Molecular Sequence Data
• Promoter Regions, Genetic
• Proto-Oncogene Proteins c-bcl-2/genetics
• RNA, Messenger/analysis
• RNA, Messenger/metabolism
• Receptors, Notch/metabolism
• Repressor Proteins/metabolism
• Transcriptional Activation
• Viral Matrix Proteins/genetics
• Viral Matrix Proteins/metabolism
• Viral Proteins

• R01 CA083937 NCI NIH HHS
• T32 GM008360 NIGMS NIH HHS
• CA83937 NCI NIH HHS
• GM08360 NIGMS NIH HHS

• Animals
• Cell Survival
• Cell Transformation, Neoplastic
• Cell Transformation, Viral/physiology
• Gammaherpesvirinae/chemistry
• Gammaherpesvirinae/metabolism
• Gammaherpesvirinae/physiology
• Herpesviridae Infections/metabolism
• Herpesviridae Infections/virology
• Humans
• Membrane Proteins/metabolism
• Rhadinovirus/chemistry
• Signal Transduction
• Terminal Repeat Sequences
• Tumor Virus Infections/metabolism
• Tumor Virus Infections/virology
• Viral Matrix Proteins/physiology
• Viral Proteins/physiology
• Virus Latency