scholarly journals Human Herpesvirus 8 and Host-Cell Interaction: Long-Lasting Physiological Modifications, Inflammation and Related Chronic Diseases

2020 ◽  
Vol 8 (3) ◽  
pp. 388
Author(s):  
Fabrizio Angius ◽  
Angela Ingianni ◽  
Raffaello Pompei
Keyword(s):  
Cholesterol Metabolism ◽  
Neutral Lipids ◽  
Human Herpesvirus ◽  
Insulin Receptors ◽  
Cell Interaction ◽  
Human Herpesvirus 8 ◽  
Herpesvirus 8 ◽  
Dna And Rna ◽  
Persistent Viruses ◽  
Hhv8 Infection

Oncogenic and latent-persistent viruses belonging to both DNA and RNA groups are known to cause serious metabolism alterations. Among these, the Human Herpesvirus 8 (HHV8) infection induces stable modifications in biochemistry and cellular metabolism, which in turn affect its own pathological properties. HHV8 enhances the expression of insulin receptors, supports the accumulation of neutral lipids in cytoplasmic lipid droplets and induces alterations in both triglycerides and cholesterol metabolism in endothelial cells. In addition, HHV8 is also known to modify immune response and cytokine production with implications for cell oxidative status (i.e., reactive oxygen species activation). This review underlines the recent findings regarding the role of latent and persistent HHV8 viral infection in host physiology and pathogenesis.

scholarly journals Human Herpesvirus 8 (HHV8) Infection and Related Diseases in Italian Transplant Cohorts

2013 ◽  
Vol 13 (6) ◽  
pp. 1619-1620 ◽  
Author(s):  
G. Riva ◽  
P. Barozzi ◽  
C. Quadrelli ◽  
D. Vallerini ◽  
E. Zanetti ◽  
...  
Keyword(s):  
Human Herpesvirus ◽  
Human Herpesvirus 8 ◽  
Herpesvirus 8 ◽  
Hhv8 Infection

scholarly journals Anti-Human Herpesvirus 8 antibodies affect both insulin and glucose uptake by virus-infected human endothelial cells

2018 ◽  
Vol 12 (06) ◽  
pp. 485-491 ◽  
Author(s):  
Fabrizio Angius ◽  
Enrica Piras ◽  
Stefano Spolitu ◽  
Luisa Marras ◽  
Sara Federica Armas ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Glucose Uptake ◽  
Cell Metabolism ◽  
Human Herpesvirus ◽  
Insulin Binding ◽  
Human Herpesvirus 8 ◽  
Oncogenic Viruses ◽  
Human Endothelial Cells ◽  
Herpesvirus 8 ◽  
Hhv8 Infection

Introduction: Human Herpesvirus 8 (HHV8) is known to be the cause of the malignant tumour named Kaposi’s sarcoma. It is believed to induce an intense modification of cell metabolism in endothelial cells. In this work we analysed the role of anti-HHV8 antibodies in both the insulin and glucose uptake of HHV8-infected primary human endothelial cells (HUVEC). Methodology: Western blotting, immunofluorescence and radiolabelled glucose were employed to assess the pPI3K expression, insulin binding and glucose-uptake by HUVEC cells, respectively. Results: We confirmed that HHV8-infection is able to enhance both insulin binding and glucose-uptake in HHV8-infected primary endothelial cells; in addition, we found that anti-HHV8 specific antibodies are able to further increase both insulin and glucose uptake during the late latent phase of HHV8-infection in vitro. Conclusions: These findings suggest that a specific immune response to HHV8-infection may cooperate in boosting the cell metabolism, further enhancing the already increased insulin binding and glucose-uptake in HHV8-infected cells, which is a peculiar property of several oncogenic viruses.

scholarly journals Long-Term Infection and Transformation of Dermal Microvascular Endothelial Cells by Human Herpesvirus 8

1999 ◽  
Vol 73 (8) ◽  
pp. 6892-6902 ◽  
Author(s):  
Ashlee V. Moses ◽  
Kenneth N. Fish ◽  
Rebecca Ruhl ◽  
Patricia P. Smith ◽  
Joanne G. Strussenberg ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Herpesvirus ◽  
Lytic Replication ◽  
Human Herpesvirus 8 ◽  
Microvascular Endothelial Cells ◽  
Herpesvirus 8 ◽  
Spindle Cells ◽  
Hhv8 Infection ◽  
Microvascular Endothelial

ABSTRACT Human herpesvirus 8 (HHV8) infects Kaposi’s sarcoma (KS) spindle cells in situ, as well as the lesional endothelial cells considered to be spindle cell precursors. The HHV8 genome contains several oncogenes, suggesting that infection of endothelial and spindle cells could induce cellular transformation and tumorigenesis and promote the formation of KS lesions. To investigate the potential of HHV8 infection of endothelial cells to contribute to the development of KS, we have developed an in vitro model utilizing dermal microvascular endothelial cells that support significant HHV8 infection. In contrast to existing in vitro systems used to study HHV8 pathogenesis, the majority of dermal endothelial cells are infected with HHV8 and the viral genome is maintained indefinitely. Infection is predominantly latent, with a small percentage of cells supporting lytic replication, and latency is responsive to lytic induction stimuli. Infected endothelial cells develop a spindle shape resembling that of KS lesional cells and show characteristics of a transformed phenotype, including loss of contact inhibition and acquisition of anchorage-independent growth. These results describe a relevant model system in which to study virus-host interactions in vitro and demonstrate the ability of HHV8 to induce phenotypic changes in infected endothelial cells that resemble characteristics of KS spindle cells in vivo. Thus, our results are consistent with a direct role for HHV8 in the pathogenesis of KS.

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