Human Cytomegalovirus IE1 Protein Enhances Herpes Simplex Virus Type 1-induced Syncytial Formation in U373MG Cells

Shin, Kyusoon; Park, Chung Gyu; Hwang, Eung Soo; Chen, Yong

doi:10.3346/jkms.2008.23.6.1046

Cited by 8 publications

(4 citation statements)

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“…U373MG transfected with empty LNCX vector, were used as control cells. 17 Jurkat cells (ATCC TIB-152: male) were used as control T cell source. The cells were cultured in Dulbecco's modified Eagles medium (DMEM; GIBCO, Grand Island, NY, USA) with 10% fetal bovine serum (FBS; GIBCO), 100 U/mL penicillin and 100 U/mL streptomycin (Life Technologies, Carlsbad, CA, USA) in a 37°C incubator with 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Human Cytomegalovirus (HCMV)-infected Astrocytoma Cells Impair the Function of HCMV-specific Cytotoxic T Cells

2020

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Background Human cytomegalovirus (HCMV) infection in glioblastoma multiforme (GBM) is associated with a poor prognosis and may affect the pathogenesis of GBM. In this study, we investigated the role of HCMV-infected astrocytoma cells in impairing the activity of cytotoxic T lymphocytes (CTLs) specific to the HCMV protein. Methods CTLs specific to HCMV immediate early (IE)-1 were expanded from peripheral blood mononuclear cells of healthy donors by stimulating CD8+ T lymphocytes with U373MG cells (ATCC HTB-17: male) expressing HCMV IE-1. The death rate of the target and the effector cells was determined by the total count of the remaining respective cells after the interaction of them. Results The death rate of the target cells by CTLs increased depending on HLA restriction and the effector:target (E:T) ratio. The death rate of effector cells in the HCMV-infected U373MG cell culture was 37.1% on day 4 post-infection. The removal of the culture supernatant from HCMV-infected U373MG cells prior to adding the effector cells increased target cell death from 8.4% to 40.8% at E:T = 1:1, but not at E:T = 3:1. The transfer of cells from a 24-hour co-culture of the HCMV-infected U373MG cells and CTLs to HCMV IE-1-expressing target cells resulted in decreasing the cell death rate of the target cells from 31.1% to 13.0% at E:T = 1:1, but not at E:T = 3:1. HCMV infection of U373MG cells decreases the activity of CTLs specific to HCMV when the number of CTLs is low. Conclusion These results suggest that HCMV could impair CTL activity and facilitate glioblastoma growth unchecked by CTLs.

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Section: Methodsmentioning

confidence: 99%

Human Cytomegalovirus (HCMV)-infected Astrocytoma Cells Impair the Function of HCMV-specific Cytotoxic T Cells

2020

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“…In another clinical study, DNMT inhibitor azacytidine ( Table 1) initiated viral gene re-expression in EBV linked tumors (Chan et al, 2004). While these inhibitors are promising candidates as the therapeutics to control of herpesviral infections (Figure 1), the possibilities of reactivation and status of co-infection with other (Schang et al, 2002;Kudoh et al, 2004;Taylor et al, 2004;Shin et al, 2008) Purvalanol A HSV, VZV and EBV (Schang et al, 2002;Kudoh et al, 2004;Moffat et al, 2004) Olomoucine II HSV and HCMV (Moffat et al, 2004) Indirubin-3'-monoxime HCMV GSK3b (Hertel et al, 2007 VEGFR tyrosine kinase (Aoki and Tosato, 2004) viruses must be meticulously examined (Ritchie et al, 2009). For example, the usage of suberoylanilide hydroxamic acid (SAHA) or trichostatin A (TSA) ( Table 1) provoked myocarditis through Coxsackievirus B3-induced myocardial apoptosis (Zhou et al, 2015).…”

Section: Epigenetic Targeted Therapymentioning

confidence: 99%

Targeting Host Cellular Factors as a Strategy of Therapeutic Intervention for Herpesvirus Infections

Asha

Sharma-Walia

2021

Front. Cell. Infect. Microbiol.

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Herpesviruses utilize various host factors to establish latent infection, survival, and spread disease in the host. These factors include host cellular machinery, host proteins, gene expression, multiple transcription factors, cellular signal pathways, immune cell activation, transcription factors, cytokines, angiogenesis, invasion, and factors promoting metastasis. The knowledge and understanding of host genes, protein products, and biochemical pathways lead to discovering safe and effective antivirals to prevent viral reactivation and spread infection. Here, we focus on the contribution of pro-inflammatory, anti-inflammatory, and resolution lipid metabolites of the arachidonic acid (AA) pathway in the lifecycle of herpesvirus infections. We discuss how various herpesviruses utilize these lipid pathways to their advantage and how we target them to combat herpesvirus infection. We also summarize recent development in anti-herpesvirus therapeutics and new strategies proposed or under clinical trials. These anti-herpesvirus therapeutics include inhibitors blocking viral life cycle events, engineered anticancer agents, epigenome influencing factors, immunomodulators, and therapeutic compounds from natural extracts.

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“…HSV-1 infects 60-80% of people worldwide and causes infectious corneal blindness, the common cold sore and potentially fatal encephalitis [1,2]. HSV is one of the leading infectious viral pathogens found in immunocompromised hosts, such as transplant recipients [3]. HSV induces tissue damage including cell infiltration, perivascular inflammation and syncytial formation [3].…”

mentioning

confidence: 99%

“…HSV is one of the leading infectious viral pathogens found in immunocompromised hosts, such as transplant recipients [3]. HSV induces tissue damage including cell infiltration, perivascular inflammation and syncytial formation [3]. HSV initially infects the epithelial cells and then enters the sensory nerve terminals.…”

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confidence: 99%

Herpes Simplex Virus Linked to AlzheimerÂ’s Disease

Cheng¹

2013

J Trop Dis

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Herpes simplex virus (HSV) is a neurotropic double-stranded DNA virus which includes the HSV-1 and HSV-2 subtypes. HSV is composed of an inner DNA core, a capsid (e.g. VP22), the tegument, and an outer envelope, which is a lipid membrane containing glycoproteins. HSV-1 infects 60-80% of people worldwide and causes infectious corneal blindness, the common cold sore and potentially fatal encephalitis [1,2]. HSV is one of the leading infectious viral pathogens found in immunocompromised hosts, such as transplant recipients [3]. HSV induces tissue damage including cell infiltration, perivascular inflammation and syncytial formation [3]. HSV initially infects the epithelial cells and then enters the sensory nerve terminals. During its life cycle in the sensory nervous system, HSV travels by retrograde transport to the neuronal cell bodies in the trigeminal ganglia, and then either enters latency or replicates. Replicated or reactivated HSV travels by anterograde transport out of the cell body to the central nervous system in addition to the peripheral mucosal membrane.Alzheimer's disease (AD) is a progressive neurodegenerative disease leading to the irreversible loss of neurons and the loss of intellectual abilities, including memory and cognition. According to the National Institute on Aging, AD afflicts 2.5-4.5 millions Americans and 18 million people worldwide. AD is pathologically characterized by intracellular neurofibrillary tangles and extracellular senile plaques. While the pathogenesis of AD is still elusive, it is widely recognized that APP plays a central role in the pathogenesis of AD based on the following evidence: i) APP is the precursor to beta-amyloid peptide (Abeta), a main constituent of senile plaques which causes cell death, synaptic defects and memory impairment [4][5][6][7][8][9]; ii) Disruption of APP-mediated axonal transport contributes to the neurodegeneration associated with AD [10]; iii) Aberrant APP phosphorylation results in Abeta production, cell stress and degeneration [10][11][12].RT-PCR studies reveal the existence of HSV-1 DNA in plaques of frontal and temporal cortices in post-mortem brains of both sporadic and familial Alzheimer's disease [13][14][15][16]. The presence of HSV-1 in the brain is considered to be a risk factor for AD in elderly people who carry the apolipoprotein E ε4 allele [17]. Viral proteins of HSV-1 interact with many AD susceptibility genes or proteins [18]. In addition, epidemiological study demonstrates that HSV-1 reactivation, as measured by seropositive IgM, is a high risk factor for AD and that HSV-1 chronic infection contributes to the progressive brain damage characteristic of AD [19]. A more recent similar study shows that anti-HSV IgG antibody avidity is higher in AD patients and much higher in subjects with amnestic mild cognitive impairment (a prodromal stage of AD) than in controls, suggesting that seropositve IgG could be adopted as a biomarker for early diagnosis of amnestic mild cognitive impairment as well as AD [20]. These data suggest a link ...

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Human Cytomegalovirus IE1 Protein Enhances Herpes Simplex Virus Type 1-induced Syncytial Formation in U373MG Cells

Cited by 8 publications

References 54 publications

Human Cytomegalovirus (HCMV)-infected Astrocytoma Cells Impair the Function of HCMV-specific Cytotoxic T Cells

Human Cytomegalovirus (HCMV)-infected Astrocytoma Cells Impair the Function of HCMV-specific Cytotoxic T Cells

Targeting Host Cellular Factors as a Strategy of Therapeutic Intervention for Herpesvirus Infections

Herpes Simplex Virus Linked to AlzheimerÂ’s Disease

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