Human herpesvirus 6A infects human embryonic fibroblasts and induces G2/M arrest and cell death

2012 ◽  
Vol 84 (4) ◽  
pp. 657-663 ◽  
Author(s):  
Lingyun Li ◽  
Bin Gu ◽  
Feng Zhou ◽  
Jing Chi ◽  
Fang Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Human Herpesvirus ◽  
Embryonic Fibroblasts ◽  
Human Embryonic Fibroblasts

scholarly journals Human Herpesvirus 6A Induces Dendritic Cell Death and HMGB1 Release without Virus Replication

Pathogens ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 57
Author(s):  
Rasmus Gustafsson
Keyword(s):  
Cell Death ◽  
Dendritic Cells ◽  
High Mobility ◽  
Human Herpesvirus ◽  
Human Monocyte ◽  
Hmgb1 Protein ◽  
Innate And Adaptive Immunity ◽  
Th2 Polarization ◽  
Dependent Cell ◽  
Ifn Γ

Human herpesvirus 6A (HHV-6A) is a common virus that has important immunomodulatory effects. Dendritic cells (DC) are key players in innate and adaptive immunity and are implicated in the pathogenesis of many human diseases, including infections. (1) Background: Previous studies have demonstrated suppressive effects of HHV-6A on key DC functions. (2) Methods: human monocyte derived dendritic cells were inoculated with HHV-6A and viral replication, cell viability, and release of high mobility group box 1 (HMGB1) protein from DC and of the cytokines IL-2, IL-4, IL-6, IL-10, TNF and IFN-γ after co-culture with allogenic CD4+ T cells were assessed. (3) Results: Nonproductive infection of HHV-6A in DC leads to titer-dependent cell death and the release of HMGB1 protein, and a Th2 polarization. (4) Conclusion: These immune responses aimed to clear the infection may also imply risks for inflammatory pathologies associated with HHV-6A such as multiple sclerosis.

scholarly journals Abortive Infection and Transformation of Human Embryonic Fibroblasts by Molluscum contagiosum Virus

1974 ◽  
Vol 24 (2) ◽  
pp. 237-246 ◽  
Author(s):  
G. Barbanti-Brodano ◽  
A. Mannini-Palenzona ◽  
O. Varoli ◽  
M. Portolani ◽  
M. La Placa
Keyword(s):  
Molluscum Contagiosum ◽  
Abortive Infection ◽  
Molluscum Contagiosum Virus ◽  
Embryonic Fibroblasts ◽  
Human Embryonic Fibroblasts

scholarly journals Human Herpesvirus and the Immune Checkpoint PD-1/PD-L1 Pathway: Disorders and Strategies for Survival

2021 ◽  
Vol 9 (4) ◽  
pp. 778
Author(s):  
Takayuki Murata
Keyword(s):  
Cell Death ◽  
Immune System ◽  
Programmed Cell Death ◽  
Immune Checkpoint ◽  
Human Herpesvirus ◽  
Barr Virus ◽  
Programmed Cell Death 1 ◽  
Epstein Barr ◽  
Simplex Virus ◽  
Human Herpesviruses

The immune system has evolved as a complex and efficient means of coping with extrinsic materials, such as pathogens and toxins, as well as intrinsic abnormalities, such as cancers. Although rapid and timely activation of the immune system is obviously important, regulated downregulation of the system is almost as significant as activation to prevent runaway immunity, such as allergies and hypercytokinemia. Therefore, the immune checkpoint programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is beneficial for the host. On the other hand, pathogens have evolved to evade host immunity by taking advantage of the PD-1/PD-L1 pathway. This review is focused on human herpesviruses, such as herpes simplex virus (HSV), cytomegalovirus (CMV), and Epstein–Barr virus (EBV), which cause various types of disorders, and their relationships with the PD-1/PD-L1 pathway. Understanding such relationships will be useful for developing preventative and therapeutic methods for disorders caused by herpesviruses.

Colchicine-like action of sevine on human embryonic fibroblasts in vitro

1972 ◽  
Vol 73 (6) ◽  
pp. 703-705
Author(s):  
A. F. Vasilos ◽  
V. D. Dmitrienko ◽  
I. G. Shroit
Keyword(s):  
Embryonic Fibroblasts ◽  
Human Embryonic Fibroblasts

scholarly journals Epigallocatechin gallate prevents senescence by alleviating oxidative stress and inflammation in WI-38 human embryonic fibroblasts

RSC Advances ◽  
2019 ◽  
Vol 9 (46) ◽  
pp. 26787-26798 ◽  
Author(s):  
Qiao Zhang ◽  
Yuqing Wu ◽  
Yue Guan ◽  
Fan Ling ◽  
Ying Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Epigallocatechin Gallate ◽  
Embryonic Fibroblasts ◽  
Age Related ◽  
Underlying Mechanisms ◽  
Human Embryonic Fibroblasts

Increased levels of oxidative stress and inflammation are the underlying mechanisms behind the aging process and age-related diseases.

scholarly journals Restoration of down-regulated PDGF receptors by TGF-β in human embryonic fibroblasts

FEBS Letters ◽  
1994 ◽  
Vol 339 (1-2) ◽  
pp. 84-88 ◽  
Author(s):  
Stelios Psarras ◽  
Dimitris Kletsas ◽  
Dimitri Stathakos
Keyword(s):  
Embryonic Fibroblasts ◽  
Human Embryonic Fibroblasts

scholarly journals The U95 Protein of Human Herpesvirus 6B Interacts with Human GRIM-19: Silencing of U95 Expression Reduces Viral Load and Abrogates Loss of Mitochondrial Membrane Potential

2007 ◽  
Vol 82 (2) ◽  
pp. 1011-1020 ◽  
Author(s):  
W. M. Yeo ◽  
Yuji Isegawa ◽  
Vincent T. K. Chow
Keyword(s):  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Human Herpesvirus ◽  
Ultrastructural Changes ◽  
Gene Encoding ◽  
Interacting Protein ◽  
Functional Aspects ◽  
Infected Cells

ABSTRACT To better understand the pathogenesis of human herpesvirus 6 (HHV-6), it is important to elucidate the functional aspects of immediate-early (IE) genes at the initial phase of the infection. To study the functional role of the HHV-6B IE gene encoding U95, we generated a U95-Myc fusion protein and screened a pretransformed bone marrow cDNA library for U95-interacting proteins, using yeast-two hybrid analysis. The most frequently appearing U95-interacting protein identified was GRIM-19, which belongs to the family of genes associated with retinoid-interferon mortality and serves as an essential component of the oxidative phosphorylation system. This interaction was verified by both coimmunoprecipitation and confocal microscopic coimmunolocalization. Short-term HHV-6B infection of MT-4 T-lymphocytic cells induced syncytial formation, resulted in decreased mitochondrial membrane potential, and led to progressively pronounced ultrastructural changes, such as mitochondrial swelling, myelin-like figures, and a loss of cristae. Compared to controls, RNA interference against U95 effectively reduced the U95 mRNA copy number and abrogated the loss of mitochondrial membrane potential. Our results indicate that the high affinity between U95 early viral protein and GRIM-19 may be closely linked to the detrimental effect of HHV-6B infection on mitochondria. These findings may explain the alternative cell death mechanism of expiration, as opposed to apoptosis, observed in certain productively HHV-6B-infected cells. The interaction between U95 and GRIM-19 is thus functionally and metabolically significant in HHV-6B-infected cells and may be a means through which HHV-6B modulates cell death signals by interferon and retinoic acid.

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