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Dive into the research topics where Ossie F. Dyson is active.

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Featured researches published by Ossie F. Dyson.


Journal of Virology | 2004

Raf-Induced Vascular Endothelial Growth Factor Augments Kaposi's Sarcoma-Associated Herpesvirus Infection

Khalief E. Hamden; Patrick W. Ford; Audy G. Whitman; Ossie F. Dyson; Shi Yuan Cheng; James A. McCubrey; Shaw M. Akula

ABSTRACT Recombinant green fluorescent protein encoding Kaposis sarcoma-associated herpesvirus (rKSHV.152) infection of β-estradiol stimulated human foreskin fibroblasts (HFF) or HFF/ΔB-Raf[FF]:ER (expressing a weaker form of B-Raf) could be enhanced to levels comparable to that of HFF/ΔB-Raf[DD]:ER cells by pretreating cells with soluble vascular endothelial growth factor (VEGF). Conversely, VEGF expression and infection efficiency typically observed in β-estradiol stimulated HFF/ΔB-Raf[DD]:ER cells could be lowered significantly by treating with VEGF small interfering RNA. In addition, we observed enhancement of the KSHV infection in HFF cells transfected with human VEGF121. These results confirm the ability of Raf-induced VEGF to augment KSHV infection of cells.


Expert Opinion on Therapeutic Targets | 2007

Targeting the PI3K and MAPK pathways to treat Kaposi’s sarcoma-associated herpes virus infection and pathogenesis

Phelps J. Lambert; Aniqa Z Shahrier; Audy G. Whitman; Ossie F. Dyson; Adrian J. Reber; James A. McCubrey; Shaw M. Akula

Cells require the ability to appropriately respond to signals in their extracellular environment. To initiate, inhibit and control these processes, the cell has developed a complex network of signaling cascades. The phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways regulate several responses including mitosis, apoptosis, motility, proliferation, differentiation and many others. It is not surprising, therefore, that many viruses target the PI3K and MAPK pathways as a means to manipulate cellular function. Recently, Kaposi’s sarcoma-associated herpes virus (KSHV) has been added to the list. KSHV manipulates the PI3K and MAPK pathways to control such divergent processes as cell survival, cellular migration, immune responses, and to control its own reactivation and lytic replication. Manipulation of the PI3K and MAPK pathways also plays a role in malignant transformation. Here, the authors review the potential to target the PI3K and MAPK signaling pathways to inhibit KSHV infection and pathogenesis.


Journal of Biological Chemistry | 2010

Cell Membrane-bound Kaposi's Sarcoma-associated Herpesvirus-encoded Glycoprotein B Promotes Virus Latency by Regulating Expression of Cellular Egr-1

Ossie F. Dyson; Christopher M. Traylen; Shaw M. Akula

One of the important questions in the field of virus research is about the balance between latent and lytic cycles of replication. Kaposis sarcoma-associated herpesvirus (KSHV) remains predominantly in a latent state, with only 1–3% of cells supporting a lytic replication at any time. KSHV glycoprotein B (gB) is expressed not only on the virus envelope but also on the surfaces of the few cells supporting lytic replication. Using co-culture experiments, we determined that expression of KSHV gB on as few as 1–2% of human dermal microvascular endothelial cells resulted in a 10-fold inhibition of expression of ORF50, a viral gene critical for the onset of lytic replication. Also, we demonstrate that such a profound inhibitory effect of gB on the lytic cycle of virus replication is by repressing the ability of Egr-1 (early growth response-1) to bind and activate the ORF50 promoter. In general, virus-encoded late stage structural proteins, such as gB, are said to play major roles in virus entry and egress. The present report provides initial evidence supporting a role for membrane-associated gB expressed in a minimal number of cells to promote virus latency. These findings may have ramifications leading to a better understanding of the role of virus-encoded structural proteins not only in KSHV-related diseases but also in other viruses causing latent infections.


PLOS ONE | 2012

Resveratrol Inhibits KSHV Reactivation by Lowering the Levels of Cellular EGR-1

Ossie F. Dyson; Lia R. Walker; Adrian Whitehouse; Paul P. Cook; Shaw M. Akula

In the field of herpesvirus research, the exact molecular mechanism by which such viruses reactivate from latency remains elusive. Kaposis sarcoma-associated herpesvirus (KSHV) primarily exists in a latent state, while only 1–3% of cells support lytic infection at any specific time. KSHV reactivation from latency is an exceedingly intricate process mediated by the integration of viral and cellular factors. Previously, our lab has described early growth response-1 (Egr-1) as an essential component for the KSHV reactivation process via its ability to mediate transcription of KSHV ORF50, the gene encoding for replication and transcription activator (RTA), a viral component known to control the switch from latent to lytic infection. In here, electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) experiments revealed that Egr-1 binds KSHV ORF50 promoter (ORF50P) in at least two different GC-rich binding domains. Expression profiles of cellular egr-1 and KSHV-encoded ORF50 follow a similar pattern during de novo KSHV infection. Over-expressing Egr-1, a signaling component downstream of Raf>MEK>ERK1/2, in KSHV-infected cells activates KSHV lytic replication. Through performing more physiologically relevant experiments, we analyzed the effect of a dietary supplement containing resveratrol on KSHV-infected cells. Our results, for the first time, demonstrate resveratrol to act in lowering ERK1/2 activity and expression of Egr-1 in KSHV-infected cells, resulting in the suppression of virus reactivation from latency. Taken together, these findings will undoubtedly contribute to future studies on not only combating KSHV related disease conditions, but also on other herpesviruses-induced pathogenesis.


Cellular Microbiology | 2008

Differential regulation of the attachment of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected human B cells to extracellular matrix by KSHV-encoded gB and cellular αV integrins

Ossie F. Dyson; Telisha L. Oxendine; Khalief E. Hamden; Patrick W. Ford; Shaw M. Akula

Kaposis sarcoma‐associated herpesvirus (KSHV) has two modes of replications: latent and lytic replications. Reactivation from latency is dictated, in part, by the cell cycle. Herein, we have attempted to delineate the importance of cell cycle in KSHV pathogenesis by exploring the expression pattern of cell‐surface receptors during different phases of the cell cycle. αV integrin expression is augmented during S phase in fibroblasts, epithelial and KSHV‐infected cells. Using a Matrigel system, we pioneer the concept that KSHV‐infected primary effusion lymphoma cells can attach to extracellular matrix proteins. This attachment is mediated primarily via αV integrins or virally encoded gB, and occurs preferentially in cells from S phase or cells from S phase actively supporting a lytic infection respectively. Such an ability of infected B cells to attach to endothelial cells may also aid in the dissemination of infection. The keystone of this work is that for the first time, we describe the ability of KSHV‐infected B cells to preferentially use cellular (αV) or viral (gB) receptors to specifically bind cells, depending upon the stage of the cell cycle and infection.


Current HIV Research | 2005

AIDS related viruses, their association with leukemia, and Raf signaling.

Audy G. Whitman; Benjaman A. Bryan; Ossie F. Dyson; Dipali K. Patel; Dan Ramasamy; Senthilvelan Anantharaman; Adrian J. Reber; Shaw M. Akula

Leukemia is characterized by the production of an excessive number of abnormal white blood cells. Over time, this expanding population of poorly/non- functional white blood cells overwhelms the normal function of the bodys blood and immune systems. DNA translocations have been found common to leukemia, including Raf mutations. While the cause of leukemia is not known, several risk factors have been identified. In this review, we present an update on the role of AIDS related viruses as an etiology for leukemia. Human immunodeficiency virus-1 and -2 (HIV-1; -2) are the cause for the development of acquired immune deficiency syndrome (AIDS). Epstein-Barr virus (EBV), human cytomegalovirus (HCMV), Human papillomavirus (HPV), and Kaposis sarcoma-associated herpesvirus (KSHV) are specifically implicated in AIDS associated malignancies. However, there are other viruses that are associated to a lesser extent with the AIDS condition and they are Human T-cell leukemia virus-1 (HTLV-1), hepatitis B virus (HBV), hepatitis C virus (HCV), and human herpesvirus-6 (HHV-6). Of these viruses, HTLV-1 has been etiologically associated with leukemia. Recent evidence suggests that EBV, HBV, HCV, and KSHV may also play a role in the development of some types of leukemia. Raf signaling has been shown to aid in the infection and pathogenesis of many of these viruses, making Raf pathway components good potential targets for the treatment of leukemia induced by AIDS related viruses.


Intervirology | 2007

β1 Integrins Mediate Tubule Formation Induced by Supernatants Derived from KSHV-Infected Cells

Ossie F. Dyson; Benjaman A. Bryan; Phelps J. Lambert; Patrick W. Ford; Shaw M. Akula

Objective: Angiogenesis is defined as the formation of new blood vessels. In a recently concluded study, we identified Kaposi’s sarcoma-associated herpesvirus (KSHV)-infected cells derived from primary effusion lymphoma (PEL) to overexpress vascular endothelial growth factor (VEGF) that had the propensity to mediate tubule formation on a Matrigel, an indicator of angiogenesis. The objective of this study was to determine the receptor molecules that mediate the tubule formation induced by the supernatant derived from KSHV-infected PEL cells. Methods: The identity of receptor(s) that play a role in mediating tubule formation driven by PEL supernatant was determined by the classical in vitro angiogenesis assay conducted on a Matrigel. Results: RGD peptides, antibodies, and siRNA specific to β1 integrins significantly lowered the ability of the PEL supernatants to induce tubule formation by endothelial cells. β1 Integrins mediated tubule formation to comparable levels in endothelial cells that were incubated with supernatants derived from uninduced or TPA-induced PEL cells. Interestingly, the β1 integrins did not seem to have a major role in cellular attachment. Conclusion: We report for the first time a critical role for β1 integrins in angiogenesis supported by the supernatant from KSHV-infected PEL cells.


Journal of Investigative Dermatology | 2012

Cloning a Human Saliva-Derived Peptide for Preventing KSHV Transmission

Philippe A. Grange; L. Gressier; John F. Williams; Ossie F. Dyson; Shaw M. Akula; Nicolas Dupin

Abbreviations: GFP, green fluorescent protein; HFF, primary human foreskin fibroblast; hLf, human lactoferrin; hPI, hours post infection; KSHV, Kaposi sarcoma herpesvirus; qPCR, quantitative PCR


Journal of Cellular and Molecular Medicine | 2009

Raman tweezers provide the fingerprint of cells supporting the late stages of KSHV reactivation

Ossie F. Dyson; Patrick W. Ford; De Chen; Yong-qing Li; Shaw M. Akula

Kaposi’s sarcoma‐associated herpesvirus (KSHV) has both latent and lytic phases of replication. The molecular switch that triggers a reactivation is still unclear. Cells from the S phase of the cell cycle provide apt conditions for an active reactivation. In order to specifically delineate the Raman spectra of cells supporting KSHV reactivation, we followed a novel approach where cells were sorted based on the state of infection (latent versus lytic) by a flow cytometer and then analysed by the Raman tweezers. The Raman bands at 785, 813, 830, 1095 and 1128 cm−1 are specifically altered in cells supporting KSHV reactivation. These five peaks make up the Raman fingerprint of cells supporting KSHV reactivation. The physiological relevance of the changes in these peaks with respect to KSHV reactivation is discussed in the following report.


Journal of General Virology | 2006

Raf/MEK/ERK signalling triggers reactivation of Kaposi's sarcoma-associated herpesvirus latency

Patrick W. Ford; Benjaman A. Bryan; Ossie F. Dyson; Douglas A. Weidner; Vishnu Chintalgattu; Shaw M. Akula

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Shaw M. Akula

East Carolina University

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