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Article ; Online: Complement Inhibitors Vitronectin and Clusterin Are Recruited from Human Serum to the Surface of Coronavirus OC43-Infected Lung Cells through Antibody-Dependent Mechanisms.

Fox, Candace R / Parks, Griffith D

2021 Volume 14, Issue 1

Abstract: Little is known about the role of complement (C') in infections with highly prevalent circulating human coronaviruses such as OC43, a group of viruses of major public health concern. Treatment of OC43-infected human lung cells with human serum resulted ... ...

Abstract	Little is known about the role of complement (C') in infections with highly prevalent circulating human coronaviruses such as OC43, a group of viruses of major public health concern. Treatment of OC43-infected human lung cells with human serum resulted in C3 deposition on their surfaces and generation of C5a, indicating robust C' activation. Real-time cell viability assays showed that in vitro C'-mediated lysis of OC43 infected cells requires C3, C5 and C6 but not C7, and was substantially delayed as compared to rapid C'-mediated killing of parainfluenza virus type 5 (PIV5)-infected cells. In cells co-infected with OC43 and PIV5, C'-mediated lysis was delayed, similar to OC43 infected cells alone, suggesting that OC43 infection induced dominant inhibitory signals. When OC43-infected cells were treated with human serum, their cell surfaces contained both Vitronectin (VN) and Clusterin (CLU), two host cell C' inhibitors that can alter membrane attack complex (MAC) formation and C'-mediated killing. VN and CLU were not bound to OC43-infected cells after treatment with antibody-depleted serum. Reconstitution experiments with purified IgG and VN showed that human antibodies are both necessary and sufficient for VN recruitment to OC43-infected lung cells-novel findings with implications for CoV pathogenesis.
MeSH term(s)	Antibodies/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cell Survival/immunology ; Clusterin/metabolism ; Complement Activation ; Complement Inactivator Proteins/metabolism ; Complement Membrane Attack Complex/metabolism ; Complement System Proteins/metabolism ; Coronavirus OC43, Human/immunology ; Coronavirus OC43, Human/pathogenicity ; Humans ; Lung/metabolism ; Lung/virology ; Parainfluenza Virus 5/immunology ; Vitronectin/metabolism
Chemical Substances	Antibodies ; CLU protein, human ; Clusterin ; Complement Inactivator Proteins ; Complement Membrane Attack Complex ; Vitronectin ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2021-12-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14010029
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Broad-Spectrum, Potent, and Durable Ceria Nanoparticles Inactivate RNA Virus Infectivity by Targeting Virion Surfaces and Disrupting Virus-Receptor Interactions.

Fox, Candace R / Kedarinath, Kritika / Neal, Craig J / Sheiber, Jeremy / Kolanthai, Elayaraja / Kumar, Udit / Drake, Christina / Seal, Sudipta / Parks, Griffith D

Molecules (Basel, Switzerland)

2023 Volume 28, Issue 13

Abstract: There is intense interest in developing long-lasting, potent, and broad-spectrum antiviral disinfectants. Ceria nanoparticles (CNPs) can undergo surface redox reactions ( ... ...

Abstract	There is intense interest in developing long-lasting, potent, and broad-spectrum antiviral disinfectants. Ceria nanoparticles (CNPs) can undergo surface redox reactions (Ce
MeSH term(s)	Animals ; Cats ; Humans ; COVID-19 ; SARS-CoV-2/genetics ; Disinfectants ; Antiviral Agents/pharmacology ; Nanoparticles ; Virion ; RNA ; Calicivirus, Feline/genetics
Chemical Substances	Disinfectants ; Antiviral Agents ; RNA (63231-63-0)
Language	English
Publishing date	2023-07-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules28135190
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Article ; Online: Histone Deacetylase Inhibitors Enhance Cell Killing and Block Interferon-Beta Synthesis Elicited by Infection with an Oncolytic Parainfluenza Virus.

Fox, Candace R / Parks, Griffith D

Viruses

2019 Volume 11, Issue 5

Abstract: Previous results have shown that infection with the cytoplasmic-replicating parainfluenza virus 5 mutant P/V-CPI- sensitizes cells to DNA damaging agents, resulting in the enhanced killing of airway cancer cells. Here, we have tested the hypothesis that ... ...

Abstract	Previous results have shown that infection with the cytoplasmic-replicating parainfluenza virus 5 mutant P/V-CPI- sensitizes cells to DNA damaging agents, resulting in the enhanced killing of airway cancer cells. Here, we have tested the hypothesis that histone deacetylase (HDAC) inhibitors can also act with P/V-CPI- infection to enhance cancer cell killing. Using human small cell lung cancer and laryngeal cancer cell lines, 10 HDAC inhibitors were tested for their effect on viability of P/V-CPI- infected cells. HDAC inhibitors such as scriptaid enhanced caspase-3/7, -8 and -9 activity induced by P/V-CPI- and overall cell toxicity. Scriptaid-mediated enhanced killing was eliminated in lung cancer cells that were engineered to express a protein which sequesters double stranded RNA. Scriptaid also enhanced cancer cell killing by two other negative strand RNA viruses - the La Crosse virus and vesicular stomatitis virus. Scriptaid treatment enhanced the spread of the P/V-CPI- virus through a population of cancer cells, and suppressed interferon-beta induction through blocking phosphorylation and nuclear translocation of Interferon Regulatory Factor 3 (IRF-3). Taken together, these data support a role for combinations of a cytoplasmic-replicating RNA virus such as the P/V-CPI- mutant along with chemotherapeutic agents.
MeSH term(s)	Caspases/genetics ; Caspases/metabolism ; Cell Line, Tumor ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Hydroxylamines/pharmacology ; Interferon Regulatory Factor-3/genetics ; Interferon Regulatory Factor-3/metabolism ; Interferon-beta/biosynthesis ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Neoplasms/virology ; Oncolytic Viruses/genetics ; Oncolytic Viruses/physiology ; Parainfluenza Virus 5/genetics ; Parainfluenza Virus 5/physiology ; Quinolines/pharmacology
Chemical Substances	Histone Deacetylase Inhibitors ; Hydroxylamines ; IRF3 protein, human ; Interferon Regulatory Factor-3 ; Quinolines ; scriptaid ; Interferon-beta (77238-31-4) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2019-05-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v11050431
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Complement Inhibitors Vitronectin and Clusterin Are Recruited from Human Serum to the Surface of Coronavirus OC43-Infected Lung Cells through Antibody-Dependent Mechanisms

Fox, Candace R. / Parks, Griffith D.

Viruses. 2021 Dec. 24, v. 14, no. 1

2021

Abstract: Little is known about the role of complement (C’) in infections with highly prevalent circulating human coronaviruses such as OC43, a group of viruses of major public health concern. Treatment of OC43-infected human lung cells with human serum resulted ... ...

Abstract	Little is known about the role of complement (C’) in infections with highly prevalent circulating human coronaviruses such as OC43, a group of viruses of major public health concern. Treatment of OC43-infected human lung cells with human serum resulted in C3 deposition on their surfaces and generation of C5a, indicating robust C’ activation. Real-time cell viability assays showed that in vitro C’-mediated lysis of OC43 infected cells requires C3, C5 and C6 but not C7, and was substantially delayed as compared to rapid C’-mediated killing of parainfluenza virus type 5 (PIV5)-infected cells. In cells co-infected with OC43 and PIV5, C’-mediated lysis was delayed, similar to OC43 infected cells alone, suggesting that OC43 infection induced dominant inhibitory signals. When OC43-infected cells were treated with human serum, their cell surfaces contained both Vitronectin (VN) and Clusterin (CLU), two host cell C’ inhibitors that can alter membrane attack complex (MAC) formation and C’-mediated killing. VN and CLU were not bound to OC43-infected cells after treatment with antibody-depleted serum. Reconstitution experiments with purified IgG and VN showed that human antibodies are both necessary and sufficient for VN recruitment to OC43-infected lung cells–novel findings with implications for CoV pathogenesis.
Keywords	Mammalian orthorubulavirus 5 ; Orthocoronavirinae ; blood serum ; cell viability ; complement ; humans ; lungs ; mixed infection ; pathogenesis ; public health
Language	English
Dates of publication	2021-1224
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v14010029
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Parainfluenza Virus Infection Sensitizes Cancer Cells to DNA-Damaging Agents: Implications for Oncolytic Virus Therapy.

Fox, Candace R / Parks, Griffith D

Journal of virology

2018 Volume 92, Issue 7

Abstract: A parainfluenza virus 5 (PIV5) with mutations in the P/V gene (P/V- ... ...

Abstract	A parainfluenza virus 5 (PIV5) with mutations in the P/V gene (P/V-CPI
MeSH term(s)	Animals ; Cercopithecus aethiops ; DNA Damage ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Humans ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/metabolism ; Mice ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Oncolytic Virotherapy/methods ; Oncolytic Viruses/genetics ; Oncolytic Viruses/metabolism ; Parainfluenza Virus 2, Human/genetics ; Parainfluenza Virus 2, Human/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Vero Cells ; X-Linked Inhibitor of Apoptosis Protein/genetics ; X-Linked Inhibitor of Apoptosis Protein/metabolism
Chemical Substances	BIRC5 protein, human ; DDB1 protein, human ; DNA-Binding Proteins ; Inhibitor of Apoptosis Proteins ; Neoplasm Proteins ; TP53 protein, human ; Tumor Suppressor Protein p53 ; X-Linked Inhibitor of Apoptosis Protein ; XIAP protein, human
Language	English
Publishing date	2018-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01948-17
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: CD24 Expression Dampens the Basal Antiviral State in Human Neuroblastoma Cells and Enhances Permissivity to Zika Virus Infection.

Kedarinath, Kritika / Fox, Candace R / Crowgey, Erin / Mazar, Joseph / Phelan, Peter / Westmoreland, Tamarah J / Alexander, Kenneth A / Parks, Griffith D

Viruses

2022 Volume 14, Issue 8

Abstract: Zika virus (ZIKV) exhibits distinct selectivity for infection of various cells and tissues, but how host cellular factors modulate varying permissivity remains largely unknown. Previous studies showed that the neuroblastoma cell line SK-N-AS (expressing ... ...

Abstract	Zika virus (ZIKV) exhibits distinct selectivity for infection of various cells and tissues, but how host cellular factors modulate varying permissivity remains largely unknown. Previous studies showed that the neuroblastoma cell line SK-N-AS (expressing low levels of cellular protein CD24) was highly restricted for ZIKV infection, and that this restriction was relieved by ectopic expression of CD24. We tested the hypothesis that CD24 expression allowed ZIKV replication by suppression of the antiviral response. SK-N-AS cells expressing an empty vector (termed CD24-low cells) showed elevated basal levels of phosphorylated STAT1, IRF-1, IKKE, and NFκB. In response to exogenously added type I interferon (IFN-I), CD24-low cells had higher-level induction of antiviral genes and activity against two IFN-I-sensitive viruses (VSV and PIV5-P/V) compared to SK-N-AS cells with ectopic CD24 expression (termed CD24-high cells). Media-transfer experiments showed that the inherent antiviral state of CD24-low cells was not dependent on a secreted factor such as IFN-I. Transcriptomics analysis revealed that CD24 expression decreased expression of genes involved in intracellular antiviral pathways, including IFN-I, NFκB, and Ras. Our findings that CD24 expression in neuroblastoma cells represses intracellular antiviral pathways support the proposal that CD24 may represent a novel biomarker in cancer cells for susceptibility to oncolytic viruses.
MeSH term(s)	Antiviral Agents/pharmacology ; CD24 Antigen ; Humans ; Interferon Type I ; Neuroblastoma ; Zika Virus/physiology ; Zika Virus Infection
Chemical Substances	Antiviral Agents ; CD24 Antigen ; CD24 protein, human ; Interferon Type I
Language	English
Publishing date	2022-08-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14081735
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Histone Deacetylase Inhibitors Enhance Cell Killing and Block Interferon-Beta Synthesis Elicited by Infection with an Oncolytic Parainfluenza Virus

Fox, Candace R / Parks, Griffith D

Viruses. 2019 May 10, v. 11, no. 5

2019

Abstract	Previous results have shown that infection with the cytoplasmic-replicating parainfluenza virus 5 mutant P/V-CPI- sensitizes cells to DNA damaging agents, resulting in the enhanced killing of airway cancer cells. Here, we have tested the hypothesis that histone deacetylase (HDAC) inhibitors can also act with P/V-CPI- infection to enhance cancer cell killing. Using human small cell lung cancer and laryngeal cancer cell lines, 10 HDAC inhibitors were tested for their effect on viability of P/V-CPI- infected cells. HDAC inhibitors such as scriptaid enhanced caspase-3/7, -8 and -9 activity induced by P/V-CPI- and overall cell toxicity. Scriptaid-mediated enhanced killing was eliminated in lung cancer cells that were engineered to express a protein which sequesters double stranded RNA. Scriptaid also enhanced cancer cell killing by two other negative strand RNA viruses – the La Crosse virus and vesicular stomatitis virus. Scriptaid treatment enhanced the spread of the P/V-CPI- virus through a population of cancer cells, and suppressed interferon-beta induction through blocking phosphorylation and nuclear translocation of Interferon Regulatory Factor 3 (IRF-3). Taken together, these data support a role for combinations of a cytoplasmic-replicating RNA virus such as the P/V-CPI- mutant along with chemotherapeutic agents.
Keywords	California encephalitis orthobunyavirus ; DNA damage ; Mammalian orthorubulavirus 5 ; RNA ; Vesiculovirus ; caspase-3 ; cell lines ; cytotoxicity ; drug therapy ; enzyme inhibitors ; histone deacetylase ; humans ; interferon regulatory factor-3 ; interferon-beta ; laryngeal neoplasms ; lung neoplasms ; mutants ; neoplasm cells ; phosphorylation ; viability ; viruses
Language	English
Dates of publication	2019-0510
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v11050431
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Broad-Spectrum, Potent, and Durable Ceria Nanoparticles Inactivate RNA Virus Infectivity by Targeting Virion Surfaces and Disrupting Virus–Receptor Interactions

Candace R. Fox / Kritika Kedarinath / Craig J. Neal / Jeremy Sheiber / Elayaraja Kolanthai / Udit Kumar / Christina Drake / Sudipta Seal / Griffith D. Parks

Molecules, Vol 28, Iss 5190, p

2023 Volume 5190

Abstract: There is intense interest in developing long-lasting, potent, and broad-spectrum antiviral disinfectants. Ceria nanoparticles (CNPs) can undergo surface redox reactions (Ce 3+ ↔ Ce 4+ ) to generate ROS without requiring an external driving force. Here, ... ...

Abstract	There is intense interest in developing long-lasting, potent, and broad-spectrum antiviral disinfectants. Ceria nanoparticles (CNPs) can undergo surface redox reactions (Ce 3+ ↔ Ce 4+ ) to generate ROS without requiring an external driving force. Here, we tested the mechanism behind our prior finding of potent inactivation of enveloped and non-enveloped RNA viruses by silver-modified CNPs, AgCNP1 and AgCNP2. Treatment of human respiratory viruses, coronavirus OC43 and parainfluenza virus type 5 (PIV5) with AgCNP1 and 2, respectively, prevented virus interactions with host cell receptors and resulted in virion aggregation. Rhinovirus 14 (RV14) mutants were selected to be resistant to inactivation by AgCNP2. Sequence analysis of the resistant virus genomes predicted two amino acid changes in surface-located residues D91V and F177L within capsid protein VP1. Consistent with the regenerative properties of CNPs, surface-applied AgCNP1 and 2 inactivated a wide range of structurally diverse viruses, including enveloped (OC43, SARS-CoV-2, and PIV5) and non-enveloped RNA viruses (RV14 and feline calicivirus; FCV). Remarkably, a single application of AgCNP1 and 2 potently inactivated up to four sequential rounds of virus challenge. Our results show broad-spectrum and long-lasting anti-viral activity of AgCNP nanoparticles, due to targeting of viral surface proteins to disrupt interactions with cellular receptors.
Keywords	anti-viral ; virucidal ; nanoparticles ; disinfectant ; rhinovirus ; coronavirus ; Organic chemistry ; QD241-441
Language	English
Publishing date	2023-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Metal-Mediated Nanoscale Cerium Oxide Inactivates Human Coronavirus and Rhinovirus by Surface Disruption.

Neal, Craig J / Fox, Candace R / Sakthivel, Tamil Selvan / Kumar, Udit / Fu, Yifei / Drake, Christina / Parks, Griffith D / Seal, Sudipta

ACS nano

2021 Volume 15, Issue 9, Page(s) 14544–14556

Abstract: The COVID19 pandemic has brought global attention to the threat of emerging viruses and to antiviral therapies, in general. In particular, the high transmissibility and infectivity of respiratory viruses have been brought to the general public's ... ...

Abstract	The COVID19 pandemic has brought global attention to the threat of emerging viruses and to antiviral therapies, in general. In particular, the high transmissibility and infectivity of respiratory viruses have been brought to the general public's attention, along with the need for highly effective antiviral and disinfectant materials/products. This study has developed two distinct silver-modified formulations of redox-active nanoscale cerium oxide (AgCNP1 and AgCNP2). The formulations show specific antiviral activities toward tested OC43 coronavirus and RV14 rhinovirus pathogens, with materials characterization demonstrating a chemically stable character for silver nanophases on ceria particles and significant differences in Ce
MeSH term(s)	COVID-19 ; Cerium ; Humans ; Rhinovirus ; SARS-CoV-2
Chemical Substances	Cerium (30K4522N6T) ; ceric oxide (619G5K328Y)
Language	English
Publishing date	2021-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1936-086X
ISSN (online)	1936-086X
DOI	10.1021/acsnano.1c04142
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Potent Inactivation of Human Respiratory Viruses Including SARS-CoV-2 by a Photoactivated Self-Cleaning Regenerative Antiviral Coating.

Kumar, Udit / Fox, Candace R / Kolanthai, Elayaraja / Neal, Craig J / Kedarinath, Kritika / Fu, Yifei / Marcelo, Erik / Babu, Balaashwin / Parks, Griffith D / Seal, Sudipta

ACS applied materials & interfaces

2022 Volume 14, Issue 36, Page(s) 40659–40673

Abstract: The COVID-19 pandemic marks an inflection point in the perception and treatment of human health. Substantial resources have been reallocated to address the direct medical effects of COVID-19 and to curtail the spread of the virus. Thereby, shortcomings ... ...

Abstract	The COVID-19 pandemic marks an inflection point in the perception and treatment of human health. Substantial resources have been reallocated to address the direct medical effects of COVID-19 and to curtail the spread of the virus. Thereby, shortcomings of traditional disinfectants, especially their requirement for regular reapplication and the related complications (e.g., dedicated personnel and short-term activity), have become issues at the forefront of public health concerns. This issue became especially pressing when infection-mitigating supplies dwindled early in the progression of the pandemic. In consideration of the constant threat posed by emerging novel viruses, we report a platform technology for persistent surface disinfection to combat virus transmission through nanomaterial-mediated, localized UV radiation emission. In this work, two formulations of Y
MeSH term(s)	Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; COVID-19 ; Disinfectants ; Humans ; Pandemics ; SARS-CoV-2 ; Viruses ; Zika Virus ; Zika Virus Infection/drug therapy
Chemical Substances	Antiviral Agents ; Disinfectants
Language	English
Publishing date	2022-08-25
Publishing country	United States
Document type	Journal Article
ISSN	1944-8252
ISSN (online)	1944-8252
DOI	10.1021/acsami.2c11653
Database	MEDical Literature Analysis and Retrieval System OnLINE

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