BACKGROUND: Kaposis sarcoma-associated herpes virus is associated with primary effusion lymphoma and multicentric Castlemans disease. METHODS: Seropositivity to lytic and latent Kaposis sarcoma herpes virus (KSHV) antigens were examined in 2083 lymphomas and 2013 controls from six European countries. RESULTS: Antibodies against KSHV latent and lytic antigens were detectable in 4.5% and 3.4% of controls, respectively, and 3.6% of cases (P,0.05). The KSHV seropositivity was associated with splenic marginal zone lymphoma (SMZL) (odds ratio (OR)=4.11, 95% confidence interval (CI)=1.57-10.83) and multiple myeloma (OR=0.31, 95% CI=0.11-0.85). CONCLUSION: The KSHV is unlikely to contribute importantly to lymphomagenesis among immunocompetent subjects. However, the observed association with SMZL may underline a chronic antigen mechanism in its aetiology.. ...
TY - JOUR. T1 - Targeted inhibition of calcineurin signaling blocks calcium-dependent reactivation of Kaposi sarcoma-associated herpesvirus. AU - Zoeteweij, J. P.. AU - Moses, A. V.. AU - Rinderknecht, A. S.. AU - Davis, D. A.. AU - Overwijk, W. W.. AU - Yarchoan, R.. AU - Orenstein, J. M.. AU - Blauvelt, A.. PY - 2001/4/15. Y1 - 2001/4/15. N2 - Kaposi sarcoma-associated herpesvirus (KSHV) is associated with KS, primary effusion lymphoma (PEL), and multicentric Castleman disease. Reactivation of KSHV in latently infected cells and subsequent plasma viremia occur before the development of KS. Intracellular signaling pathways involved in KSHV reactivation were studied. In latently infected PEL cells (BCBL-1), KSHV reactivation in single cells was determined by quantitative flow cytometry. Viral particle production was determined by electron microscope analyses and detection of minor capsid protein in culture supernatants. Agents that mobilized intracellular calcium (ionomycin, thapsigargin) ...
Kaposis sarcoma-associated herpesvirus (KSHV; also referred to as human herpesvirus 8 [HHV-8]) belongs to the gammaherpesvirus family, which includes Epstein-Barr virus (EBV), herpesvirus saimiri (HSV), and murine gammaherpesvirus 68 (MHV-68) (1). KSHV infection is associated with Kaposis sarcoma (KS), the most common cancer in HIV-infected patients (1). KSHV is also linked to the development of several other lymphoproliferative malignancies, including primary effusion lymphoma (PEL) and a subset of multicentric Castlemans disease (2). Similar to other herpesviruses, the life cycle of KSHV consists of latent and lytic replication phases (3). Following acute infection, KSHV establishes latency in the immunocompetent hosts, where KSHV maintains its genome as an episome and expresses only a limited number of viral proteins or viral mRNAs. Thus, KSHV latency is an effective strategy for evading host immune detection (3). In KS lesions, most of the tumor cells are latently infected by KSHV, ...
Nuclear mRNA export is a highly complex and regulated process in cells. Cellular transcripts must undergo successful maturation processes, including splicing, 5-, and 3-end processing, which are essential for assembly of an export competent ribonucleoprotein particle. Many viruses replicate in the nucleus of the host cell and require cellular mRNA export factors to efficiently export viral transcripts. However, some viral mRNAs undergo aberrant mRNA processing, thus prompting the viruses to express their own specific mRNA export proteins to facilitate efficient export of viral transcripts and allowing translation in the cytoplasm. This review will focus on the Kaposis sarcoma-associated herpesvirus ORF57 protein, a multifunctional protein involved in all stages of viral mRNA processing and that is essential for virus replication. Using the example of ORF57, we will describe cellular bulk mRNA export pathways and highlight their distinct features, before exploring how the virus has evolved to exploit
Background Kaposi sarcoma-associated herpesvirus (KSHV) is the etiologic agent of primary effusion lymphomas (PEL). Herpesvirus Type 8 (HHV-8)) [1], is linked to all forms of Kaposi sarcoma, primary effusion lymphoma (PEL) [2C4], and some forms of multicentric Castelmans disease (MCD) [5,6]. PEL is a monoclonal/oligoclonal, rare, aggressive and body cavity-based B-cell lymphoma, accounting for approximately 3% of AIDS-related lymphomas [7,8]. This unusual lymphoproliferative disorder is divided into classical and solid variants. The classical PEL is characterized by malignant effusions in the serosal surfaces, mostly pleural, pericardial and peritoneal cavities and by the absence of an obvious tumor mass, lymphadenopathy or hepatosplenomegaly [9]. The solid PEL manifests with extracavitary tissue-based tumors that may precede PEL development [10], may follow malignant effusions [11], or may not at all be associated with PEL serous effusions [3,6,10,12C14]. The presence of KSHV genome in PEL ...
Kaposis sarcoma-associated herpesvirus (KSHV) has an etiologic role in Kaposis sarcoma, primary effusion lymphoma and multicentric Castlemans disease. These diseases are most common in immunocompromised individuals, especially those with AIDS. Similar to all herpesviruses, KSHV infection is lifelong. KSHV infection in tumor cells is primarily latent, with only a small subset of cells undergoing lytic infection. During latency, the KSHV genome persists as a multiple copy, extrachromosomal episome in the nucleus. In order to persist in proliferating tumor cells, the viral genome replicates once per cell cycle and then segregates to daughter cell nuclei. KSHV only expresses several genes during latent infection. Prominent among these genes, is the latency-associated nuclear antigen (LANA). LANA is responsible for KSHV genome persistence and also exerts transcriptional regulatory effects. LANA mediates KSHV DNA replication and in addition, is responsible for segregation of replicated genomes to daughter
Health,Kaposis sarcoma herpesvirus (KSHV) is a human tumor virus which cause...PELs are aggressive lymphomas with reported median survival time l...Researchers at the University of Helsinki have discovered that act...The findings by the research group of Dr. P?ivi Ojala (University ...The project involves scientists from two Academy of Finland Nation...,A,Novel,Treatment,for,KSHV-infected,Lymphomas,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
The novelty of our comprehensive study is the demonstration for the first time that a proinflammatory lipid metabolite, such as PGE2 and its receptors, plays a crucial role in herpes virus latency. Previous reports have indicated the role of Ca2+ in KSHV lytic cycle (17-20). In contrast, our studies showing the downregulation of LANA-1 expression by EP1 receptor antagonist, the blockage of supernatant-induced [Ca2+]i signal by EP1 antagonist, and the downregulation of PGE2-induced LANA-1 promoter activity by calcium chelators are the first demonstration of a role for [Ca2+]i in KSHV latency program. Unlike calcium, previous reports have shown the role of Src, PI3K, PKCζ/λ, and NF-κB in KSHV latency program (21-23). However, the novelty of our study is that the data linking PGE2/EP receptors with KSHV LANA-1 expression and LANA-1 promoter through PGE2 via Src, PI3K, PKCζ/λ, and NF-κB signal induction provides a new framework to understand the host mechanisms used by KSHV to induce these ...
5GTC: Crystal structure of complex between DMAP-SH conjugated with a Kaposis sarcoma herpesvirus LANA peptide (5-15) and nucleosome core particle
To determine the presence of Kaposi sarcoma-associated herpesvirus (KSHV) and other serologic markers, we tested serum specimens of 339 Amerindians, 181 rural non-Amerindians, and 1,133 urban blood donors (13 Amerindians) in the Brazilian Amazon. High KSHV seroprevalence in children and inverse association with herpes simplex virus type 2 indicates predominant nonsexual transmission among Amerindians.
The latency-associated nuclear antigen (LANA) of Kaposis sarcoma-associated herpesvirus functions as an origin-binding protein (OBP) and transcriptional regulator. LANA binds the terminal repeats via the C-terminal DNA-binding domain (DBD) to support latent DNA replication. To date, the structure of LANA has not been solved. Sequence alignments among OBPs of gammaherpesviruses have revealed that the C terminus of LANA is structurally related to EBNA1, the OBP of Epstein-Barr virus. Based on secondary structure predictions for LANA(DBD) and published structures of EBNA1(DBD), this study used bioinformatics tools to model a putative structure for LANA(DBD) bound to DNA. To validate the predicted model, 38 mutants targeting the most conserved motifs, namely three alpha-helices and a conserved proline loop, were constructed and functionally tested. In agreement with data for EBNA1, residues in helices 1 and 2 mainly contributed to sequence-specific DNA binding and replication activity, whilst ...
The life cycle of Kaposis sarcoma-associated herpesvirus (KSHV) consists of two phases, latent and lytic. The virus establishes latency as a strategy for avoiding host immune surveillance and fusing symbiotically with the host for lifetime persistent infection. However, latency can be disrupted and KSHV is reactivated for entry into the lytic replication. Viral lytic replication is crucial for efficient dissemination from its long-term reservoir to the sites of disease and for the spread of the virus to new hosts. The balance of these two phases in the KSHV life cycle is important for both the virus and the host and control of the switch between these two phases is extremely complex. Various environmental factors such as oxidative stress, hypoxia, and certain chemicals have been shown to switch KSHV from latency to lytic reactivation. Immunosuppression, unbalanced inflammatory cytokines and other viral coinfections also lead to the reactivation of KSHV. This review article summarizes the current
Kaposis sarcoma (KS) is a vascular tumor predominantly found in the immunosuppressed. Epidemiologic studies suggest that an infective agent is the etiologic culprit. Kaposis sarcoma-associated herpesvirus (KSHV), or human herpesvirus-8 (HHV-8), is a gamma human herpesvirus present in all epidemiol …
Epidemiology. Human herpesvirus 8 (HHV-8), also called Kaposi sarcoma (KS)-associated herpesvirus (KSHV), is a gamma human herpesvirus most closely related to Epstein-Barr virus. HHV-8 has been causally linked to all forms of KS (i.e., HIV-related, classic endemic, and iatrogenic) and with two rare neoplastic conditions usually associated with HIV infection: body cavity-based lymphoma, also known as primary effusion lymphoma (a B-cell lymphoma that typically arises in body cavities such as the pleural space), and multicentric Castleman disease (non-cancerous tumors that may develop in lymph nodes in a single site or in multiple sites throughout the body). The exact mechanism by which HHV-8 infection leads to neoplastic disease has not been fully elucidated, but seroconversion to HHV-8 antibody positivity virtually always precedes development of the tumors.1 The prevalence of antibodies to HHV-8 varies widely with age, geography, and certain risk factors. In the United States and Europe, 1% to 3% ...
Kaposis sarcoma-associated herpesvirus vOX2 protein: inhibits neutrophil function and can contribute to immune dysfunction and could have anti-inflammatory therapeutic potential
We have shown here that cultured primary human DMVEC cultures can be infected at different efficiencies by KSHV virions derived from several PEL cell lines. The infection causes a phenotype involving aligned and swirling bunches of elongated spindle-shaped cells that closely resembles that displayed by the pathogenic spindle cells of nodular KS lesions. Importantly, KSHV infection of the DMVEC cultures and the associated spindle cell conversion phenotype correlate almost completely with constitutive LANA1 protein expression in the same cells. Recent studies by Dupin et al. (10) have also confirmed that almost all spindle cells in late nodular KS lesions express LANA1. The similarity to the latent state found in both PEL cell lines and KS lesions is emphasized by the punctate nuclear character of the LANA1 signal (4), implying that the viral genomes also establish a multicopy episomal state in infected spindloid DMVEC. However, although the KSHV-infected spindle cells have high mitotic indices ...
Kaposis sarcoma-associated herpesvirus (KSHV) is a newly-identified human herpesvirus and an emerging pathogen. Increasing evidence indicate that this virus is the etiologic agent of Kaposis sarcoma (KS), primary effusion lymphoma (PEL) and multicentric Castlemans disease (MCD), leading neoplasia of AIDS patients. Unique among all DNA tumor viruses, KSHV lytic replication contributes significantly to the formation of KS lesions by either facilitating viral spread to the target site or releasing paracrine factors to support the growth of KS tumor cells. Therefore, KSHV reactivation from latency to lytic replication is not only important for viral propagation, but also critical for viral pathogenicity. My laboratory has been interested in the mechanisms used by KSHV to switch from latency to lytic life cycle. In the past a few years, several major accomplishments have been achieved. (1) Several KSHV immediate-early (IE) genes have been identified in our lab. Since the reactivation process is ...
Our laboratory investigates Kaposis sarcoma-associated herpesvirus (KSHV) or human herpesvirus 8 (HHV-8). KSHV has a causative role in Kaposis sarcoma, primary effusion lymphomas and multicentric Castlemans disease, an aggressive lymphoproliferative disorder. KSHV latently infects tumor cells and has evolved an intricate mechanism to efficiently persist in proliferating cells in the absence of chromosomal integration. KSHV persists in latently infected cells as an extrachromosomal, multiple copy plasmid (episome), from which it expresses several viral genes including the latency-associated nuclear antigen (LANA). LANA is essential for KSHV episome persistence in cells. LANA mediates viral DNA replication, which occurs in concert with cell DNA replication, and then tethers KSHV episomes to mitotic chromosomes to ensure their efficient segregation to progeny nuclei, thereby avoiding loss of the genome in the cytoplasm. LANA also exerts effects on cell growth and transcription. We are currently ...
Antibody titres against Kaposis sarcoma associated herpesvirus (KSHV or human herpesvirus 8 (HHV-8)) and Epstein-Barr virus (EBV) were examined in people who subsequently developed Kaposis sarcoma and non-Hodgkins lymphoma, within randomised controlled trials of antiretroviral therapy in adults infected with the human immunodeficiency virus-1 (HIV). For each case of Kaposis sarcoma (n=189) and each case of non-Hodgkins lymphoma (n=67), which developed after randomisation, one control was randomly selected from other trial participants, after matching for age, sex, ethnicity, mode of HIV transmission, type of treatment received and period of follow-up. Using sera taken an average of two and a half years before the diagnosis of cancer, titres of antibodies against KSHV latent (LANA) and lytic (K8.1) antigens and against EBV (VCA) antigens were investigated in relation to subsequent risks of cancer by calculating odds ratios (OR) using conditional logistic regression. Latent antibodies against KSHV
Kaposis sarcoma-associated herpesvirus (KSHV) bears four genes with homology to human being interferon regulatory factors (IRFs). PEL cell lines resulted in improved MHC II levels; overexpression of vIRF-3 in KSHV-negative B cells prospects to downmodulation of MHC II. This rules could be traced back to inhibition of class II transactivator (CIITA) transcription by vIRF-3. Reporter assays exposed the gamma interferon (IFN-γ)-sensitive CIITA promoters PIV and PIII were inhibited by vIRF-3. Consistently IFN-γ levels improved upon vIRF-3 knockdown in PEL cells. IFN-γ rules by vIRF-3 was confirmed in reporter assays as well as by upregulation of standard IFN-γ target genes upon knockdown of vIRF-3 in PEL cells. In summary we conclude that vIRF-3 contributes to the viral immunoevasion by downregulation of IFN-γ and CIITA and thus MHC II manifestation. Intro Kaposis sarcoma-associated herpesvirus (KSHV) also termed human being herpesvirus 8 (HHV-8) belongs to the gammaherpesvirus-2 subgroup ...
Researchers at the University of Pennsylvania School of Medicine have shed new light on how Kaposis Sarcoma-associated Herpes Virus (KSHV) subverts normal cell machinery to cause cancer. A KSHV protein called latency-associated nuclear antigen, LANA for short, helps the virus hide out from the immune system in infected cells. When LANA takes the place of other proteins that control cell growth, it can cause uncontrolled cell replication.
Speaker: Päivi Ojala Speaker Address: Faculty of Medicine, Department of Medicine, Imperial College London and Institute of Biotechnology, University of Helsinki Host: Teresa Frisan and Ingemar Ernberg
miR-155 is generally believed to be a multifunctional miRNA (9, 10). It is transcribed from a noncoding gene named BIC gene, which is highly conserved in many species and broadly expressed in various organs, tissues, and cell types, indicating its versatile functions in various biological processes. It has been demonstrated that miR-155 plays important roles in physiological conditions (e.g., circulation, hematopoiesis, immunity, and inflammation), as well as pathological conditions (e.g., neoplastic diseases and cardiovascular disorders). Up until now, there were only two reports about the roles of miR-155 in viral infection: one was about the miR-155 ortholog named miR-K12-11 encoded by Kaposis sarcoma-associated herpes virus (30); the other was the induced miR-155 expression during EBV infection (31). Both of the viruses belong to the herpesvirus family, DNA virus. The induced miR-155 and the viral ortholog miR-K12-11 were both found to participate in the biological process of the indicated ...
Science & Technology, Life Sciences & Biomedicine, Biochemistry & Molecular Biology, IRES, eIF4E, viruses, RNA structure, translation, CAP-INDEPENDENT TRANSLATION, RIBOSOME ENTRY SITE, HEPATITIS-C VIRUS, RNA SECONDARY STRUCTURE, MULTICENTRIC CASTLEMANS-DISEASE, SMALL-MOLECULE INHIBITION, PRIMARY EFFUSION LYMPHOMA, OPEN READING FRAME, GAG CODING REGION, KAPPA-B PATHWAY ...
In cells infected with the Kaposis sarcoma-associated herpesvirus (KSHV), CSL/CBF1 signaling is essential for viral replication and promotes the survival of KSHV-infected cells. CSL/CBF1 is a DNA adaptor molecule which recruits coactivator and corepressor complexes to regulate viral and cellular gene transcription and which is a major downstream effector molecule of activated Notch. The interaction of KSHV RTA and LANA with CSL/CBF1 has been shown to balance the lytic and latent viral life cycle. Here we report that a third KSHV protein, viral interferon regulatory factor 4 (vIRF4/K10), but none of the three other KSHV-encoded vIRFs, interacts with CSL/CBF1. Two regions of vIRF4 with dissimilar affinities contribute to CSL/CBF1 binding. Similar to Notch, vIRF4 targets the hydrophobic pocket in the beta trefoil domain of CSL/CBF1 through a short peptide motif which closely resembles a motif found in Notch but does not strictly follow the ΦWΦP consensus conserved in human and mouse Notch ...
KSHV is a herpesvirus, and is a large double-stranded DNA virus with a protein covering that packages its nucleic acids, called the capsid, which is then surrounded by an amorphous protein layer called the tegument, and finally enclosed in a lipid envelope derived in part from the cell membrane. KSHV has a genome which is approximately 165,000 nucleic acid bases in length. KSHV is a rhadinovirus, and is remarkable since it has stolen numerous genes from host cells including genes that encode for complement-binding protein, IL-6, BCL-2, cyclin-D, a G protein-coupled receptor, interferon regulatory factor and Flice inhibitory protein (FLIP), as well as DNA synthesis proteins including dihydrofolate reductase, thymidine kinase, thymidylate synthetase, DNA polymerase and many others. While no other human tumor virus possesses these same genes, other tumor viruses target the same cellular pathways illustrating that at a basic level, all tumor viruses appear to attack the same cellular control ...
The attachment entry and fusion of Kaposis sarcoma-associated herpesvirus (KSHV) with target cells are mediated TG101209 by complex equipment containing among others viral glycoprotein H (gH) and its alleged chaperone gL. They advertised KSHV illness and manifestation of gH/gL on target cells inhibited subsequent KSHV illness. Whereas gH only was able to bind to HS we observed that only the gH/gL complex TG101209 adhered to heparan sulfate-negative cells at lamellipodium-like constructions. The access of Kaposis sarcoma-associated herpesvirus (KSHV) also termed human being herpesvirus 8 (HHV-8) into target cells is only poorly understood. In general herpesviruses enter the cell through at least two consecutive methods including different viral glycoproteins and different cellular receptors. Attachment is the first step in this process. In KSHV this step is definitely mediated through engagement of heparan sulfate proteoglycans (HSPGs) within the cell surface (5 9 Attachment via binding to cell ...
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Author Summary The human gammaherpesviruses Epstein-Barr virus (EBV) and Kaposis sarcoma-associated herpesvirus (KSHV) are tightly associated with a number of different cancers. Unfortunately, due to their very narrow host tropism, characterizing the pathogenesis of these viruses has been difficult. Infection of laboratory mice with the rodent gammaherpesvirus, murine gammaherpesvirus 68 (MHV68), has proven to be an excellent approach for understanding how these viruses cause disease. One of the MHV68 encoded proteins, which is also found in KSHV, is called LANA and in the case of KSHV-associated diseases LANA expression is consistently detected in infected cells. Here we show that the MHV68 LANA shares a key function with the KSHV homolog-namely, modulating gene expression. Using a random mutagenesis protocol, we identified mLANA mutants that had lost transcriptional regulatory activity. We engineered these mutations back into the virus, used the viruses to infect mice, and find that this function is
Herpes Virus Type 8 / HHV8, 0.1 ml. Kaposis sarcoma-associated herpesvirus (KSHV) belongs to the gamma-(2)-herpesvirus subfamily and has been closely linked to the Kaposis sarcoma, primary effusion lymphoma (PEL) and multicentric Castlemans
Kaposi Sarcoma (KS) is the most prevalent neoplasm within HIV-infected patients and transplant recipients. Kaposis Sarcoma-Associated Herpesvirus (KSHV) causes the disease by using a novel mechanism that reprograms endothelial cells making them susceptible targets for viral infection and dissemination. We and others reported that KSHV induces lymphatic differentiation of blood vascular endothelial cells (BECs), by inducing PROX1 up-regulation. Importantly, KSHV G-protein coupled receptor (vGPCR) has been identified as the major viral gene responsible for cellular transformation and disease maintenance. Given that PROX1 is an important mediator of KSHV-induced cell reprogramming, we set out to determine if it had other functional implications in KS pathogenesis. In this study, we report that the regulator of G-protein signaling (RGS)-4 is selectively expressed in BECs and not in LECs, and acts as a cellular agonist against the transformation function of vGPCR. In effect, we found that RGS4 is ...
A UNC Lineberger study, led by Dirk Dittmer, PhD, reports the Kaposi sarcoma-associated herpes virus can commandeer a system involved in how host cells can affect changes in neighboring cells.
OBJECTIVES:. I. Determine the maximum tolerated dose of bryostatin 1 when administered with vincristine in patients with recurrent or refractory HIV-related B-cell lymphoma.. II. Determine the toxicity profile of this regimen in these patients. III. Determine the objective response and survival of these patients treated with this regimen.. IV. Determine the immunomodulatory effects of this regimen on interleukin-2 (IL-2), IL-2 receptor, and IL-6 cytokine levels in these patients.. V. Determine the effect of this regimen on CD4+ lymphocyte count and HIV load in these patients.. VI. Determine the effect of this regimen on the human herpes virus-8 load in these patients with body cavity-based lymphoma.. OUTLINE: This is a multicenter, dose-escalation study of bryostatin 1.. Patients receive bryostatin 1 IV continuously on days 1 and 15 and vincristine IV over 5 minutes on days 2 and 16. Treatment continues every 4 weeks for a minimum of 2 courses in the absence of disease progression or ...
As obligate intracellular pathogens, viruses depend on the host cell machinery to complete their life cycle. Kaposis sarcoma-associated herpesvirus (KSHV) is an oncogenic virus causally linked to the development of Kaposis sarcoma and several other lymphoproliferative malignancies. KSHV entry into cells is tightly regulated by diverse viral and cellular factors. In particular, KSHV actively engages cellular integrins and ubiquitination pathways for successful infection. Emerging evidence suggests that KSHV hijacks both actin and microtubule cytoskeletons at different phases during entry into cells. Here, we review recent findings on the early events during primary infection of KSHV and its closely related primate homolog rhesus rhadinovirus with highlights on the regulation of cellular cytoskeletons and signaling pathways that are important for this phase of virus life cycle.
Kaposis (KUH-po-shees) sarcoma (KS) is a tumor caused by Human herpesvirus 8 (HHV8), also known as Kaposis sarcoma-associated herpesvirus (KSHV). It was originally described by Moritz_Kaposi, a Hungarian dermatologist practicing at the University of Vienna in 1872. It became more widely known...
Why research says understanding the overlap between Kaposi sarcoma-associated herpesvirus (KSHV) and human herpesvirus 8 (HHV8)-positive large B-cell lymphomas and associated diseases may lead to better outcomes.. ...
The two human oncogenic -herpesviruses, Epstein Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV), are prototypic pathogens that are controlled by T cell responses. Despite their ubiquitous distribution, persistent infections and transforming potential, most carriers immune systems control them for life. Therefore, they serve as paradigms of how near-perfect cell-mediated immune control can be initiated and maintained for decades. Interestingly, EBV especially quite efficiently avoids dendritic cell (DC) activation, and little evidence exists that these most potent antigen-presenting cells of the human body are involved in the priming of immune control against this tumor virus. However, DCs can be harnessed therapeutically to expand virus-specific T cells for adoptive transfer therapy of patients with virus-associated malignancies and are also currently explored for vaccinations. Unfortunately, despite 55 and 25 years of research on EBV and KSHV, respectively, the priming of ...
The protein encoded by this gene is a signal transducer shared by many cytokines, including interleukin 6 (IL6), ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), and oncostatin M (OSM). This protein functions as a part of the cytokine receptor complex. The activation of this protein is dependent upon the binding of cytokines to their receptors. vIL6, a protein related to IL6 and encoded by the Kaposi sarcoma-associated herpesvirus, can bypass the interleukin 6 receptor (IL6R) and directly activate this protein. Knockout studies in mice suggest that this gene plays a critical role in regulating myocyte apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been described. A related pseudogene has been identified on chromosome 17 ...
Main description: This comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein-Barr virus, Kaposis Sarcoma-associated herpesvirus, cytomegalovirus, HHV6A, 6B and 7, and varicella-zoster virus. The viral diseases and cancers they cause are significant and often recurrent. Their prevalence in the developed world accounts for a major burden of disease, and as a result there is a great deal of research into the pathophysiology of infection and immunobiology. Another important area covered within this volume concerns antiviral therapy and the development of vaccines. All these aspects are covered in depth, both scientifically and in terms of clinical guidelines for patient care. The text is illustrated generously throughout and is fully referenced to the latest research and developments.. ...
Dr. Millers laboratory studies the mechanisms underlying the switch between latency and lytic replication of two oncogenic herpesviruses, Epstein-Barr virus and Kaposis sarcoma-associated herpesvirus. Current experiments explore how viral and cellular transcription factors that selectively bind to methylated DNA control expression of viral and cellular genes, how cellular gene expression is selectively inhibited while viral gene expression is enhanced, and how viral DNA replication is regulated by cellular proteins. Recent studies focus on a new class of anti-viral agents that inhibit reactivation of Epstein-Barr virus from latency into lytic infection.. ...
Dr. Millers laboratory studies the mechanisms underlying the switch between latency and lytic replication of two oncogenic herpesviruses, Epstein-Barr virus and Kaposis sarcoma-associated herpesvirus. Current experiments explore how viral and cellular transcription factors that selectively bind to methylated DNA control expression of viral and cellular genes, how cellular gene expression is selectively inhibited while viral gene expression is enhanced, and how viral DNA replication is regulated by cellular proteins. Recent studies focus on a new class of anti-viral agents that inhibit reactivation of Epstein-Barr virus from latency into lytic infection.. ...
Ornaghi S, Davis JN, Gorres KL, Miller G, Paidas MJ, van den Pol AN. 2016. Mood stabilizers inhibit cytomegalovirus infection. Virology. 499:121-135.. Gorres K, Daigle D, Mohanram S, McInerney GE, Lyons DE, Miller G. 2016. Valpromide inhibits lytic cycle reactivation of Epstein-Barr Virus. mBio. 7(2):e00113.. Gorres K, Daigle D, Mohanram S, Miller G. 2014. Activation and repression of Epstein-Barr Virus and Kaposis sarcoma-associated herpesvirus lytic cycles by short- and medium-chain fatty acids. J. Virol. 88:8028-8044. (Cover Photo ...
Misstear, K, Chanas, SA, Rezaee, SA, Colman, R, Quinn, LL, Long, HM, Goodyear, O, Lord, JM, Hislop, AD and Blackbourn, DJ (2012) Suppression of antigen-specific T cell responses by the Kaposis sarcoma-associated herpesvirus viral OX2 protein and its cellular orthologue, CD200. ...
Kaposis sarcoma associated herpesvirus (KSHV) or human herpesvirus 8 (HHV8) is a major etiological agent for multiple severe malignancies in immune-compromised patients. KSHV establishes lifetime persistence in the infected individuals and displays two distinct life cycles, generally a prolonged passive latent, and a short productive or lytic cycle. During latent phase, the viral episome is tethered to the host chromosome and replicates once during every cell division. Latency-associated nuclear antigen (LANA) is a predominant multifunctional nuclear protein expressed during latency, which plays a central role in episome tethering, replication and perpetual segregation of the episomes during cell division ...
Kaposis sarcoma‐associated herpesvirus (KSHV), a human gamma‐herpesvirus, is etiologically linked to the development of several malignancies, mainly Kaposis sarcoma
KSHV K8a Monoclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry applications. This antibody reacts with Virus samples. Clone: 8C12G10G1. Supplied as 100 µL unpurified antibody in ascites with 0.03% sodium azide.
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Viewed posteriorly the right kidney has its upper edge opposite the 11th dorsal spine and the lower edge of the 11th rib. Its lower edge is ...
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Expression and multiplicity of infection in moDCs of each of the KSHV-gene-encoding lentiviruses.(a) KSHV ORF expression by mature moDCs 6 days after transducti