Cell Fusion by Canine Distemper Virus-Infecied Cells and their Plasma Membranes

Intervirology ◽  
1977 ◽  
Vol 8 (4) ◽  
pp. 218-225 ◽  
Author(s):  
Linda E. Fisher ◽  
Robert H. Bussell
Keyword(s):  
Cell Fusion ◽  
Canine Distemper Virus ◽  
Plasma Membranes ◽  
Canine Distemper

scholarly journals Mink SLAM V-Region V74I Substitutions Contribute to the Formation of Syncytia Induced by Canine Distemper Virus

2021 ◽  
Vol 7 ◽  
Author(s):  
Yawen Wang ◽  
Jie Chen ◽  
Bo Hu ◽  
Chengyan Gong ◽  
Ning Shi ◽  
...  
Keyword(s):  
Amino Acid ◽  
Cell Fusion ◽  
Canine Distemper Virus ◽  
Molecular Data ◽  
Site Directed Mutagenesis ◽  
Raccoon Dog ◽  
Canine Distemper ◽  
Ligand Interaction ◽  
V Region ◽  
Fusion Efficiency

The Signal lymphatic activation molecule (SLAM, also known as CD150) as the cellular receptor of canine distemper virus (CDV) plays an important role in the virus-host interaction. However, it is still unknown whether amino acid differences in the SLAM variable (V) region affect the formation of syncytia. Here, using raccoon dog SLAM (rSLAM) and mink SLAM (mSLAM), we performed SLAM-V homologous modeling, site-directed mutagenesis, and surface expression analysis, as well as a cell fusion assay, to study the interaction between SLAM and CDV. More specifically, our investigation focused on two amino acid residues (74 and 129) of SLAM, previously predicted to play a relevant role in receptor-ligand interaction. Our results indicated that only residues at position 60, 74, and 129 were different between rSLAM and mSLAM among the 29 amino acids that might interact with CDV H, and residues 74 and 129 were located in the interface region interacting with CDV H. The amino acid substitution at the positions of 74 have a significant effect on the expression of mSLAM. The SLAM-V74I mutation in mink significantly improved the cell fusion efficiency of CDV. In contrast, the SLAM-I74V mutation in the raccoon dog significantly decreased cell fusion efficiency. We conclude that residue 74 of SLAM plays an important role during the the formation of syncytia. Only when implementing CDV infection analysis, the rSLAM-Q129R can significantly decreased the mean number of syncytia, but the mSLAM-R129Q can't. Additionally, residue 60 show variability between rSLAM and mSLAM. We believe that our study makes a significant contribution to the literature because we provide molecular data, partially accounting for the differences in host membrane and virus interaction laying the foundation for further molecular work.

scholarly journals Antibodies to CD9, a Tetraspan Transmembrane Protein, Inhibit Canine Distemper Virus-Induced Cell-Cell Fusion but Not Virus-Cell Fusion

2000 ◽  
Vol 74 (16) ◽  
pp. 7554-7561 ◽  
Author(s):  
Erik Schmid ◽  
Andreas Zurbriggen ◽  
Uta Gassen ◽  
Bert Rima ◽  
Volker ter Meulen ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Canine Distemper Virus ◽  
Transmembrane Protein ◽  
Single Step ◽  
Canine Distemper ◽  
Culture Cells ◽  
Life Threatening ◽  
Step Growth ◽  
Growth Experiments ◽  
Cell Cell

ABSTRACT Canine distemper virus (CDV) causes a life-threatening disease in several carnivores including domestic dogs. Recently, we identified a molecule, CD9, a member of the tetraspan transmembrane protein family, which facilitates, and antibodies to which inhibit, the infection of tissue culture cells with CDV (strain Onderstepoort). Here we describe that an anti-CD9 monoclonal antibody (MAb K41) did not interfere with binding of CDV to cells and uptake of virus. In addition, in single-step growth experiments, MAb K41 did not induce differences in the levels of viral mRNA and proteins. However, the virus release of syncytium-forming strains of CDV, the virus-induced cell-cell fusion in lytically infected cultures, and the cell-cell fusion of uninfected with persistently CDV-infected HeLa cells were strongly inhibited by MAb K41. These data indicate that anti-CD9 antibodies selectively block virus-induced cell-cell fusion, whereas virus-cell fusion is not affected.

scholarly journals Mechanism of reduction of virus release and cell-cell fusion in persistent canine distemper virus infection

2003 ◽  
Vol 106 (4) ◽  
pp. 303-310 ◽  
Author(s):  
Nadine Meertens ◽  
Michael H. Stoffel ◽  
Pascal Cherpillod ◽  
Riccardo Wittek ◽  
Marc Vandevelde ◽  
...  
Keyword(s):  
Virus Infection ◽  
Cell Fusion ◽  
Canine Distemper Virus ◽  
Virus Release ◽  
Canine Distemper ◽  
Cell Cell

Synergistic inhibition in cell–cell fusion mediated by the matrix and nucleocapsid protein of canine distemper virus

2007 ◽  
Vol 129 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Dominique Wiener ◽  
Philippe Plattet ◽  
Pascal Cherpillod ◽  
Ljerka Zipperle ◽  
Marcus G. Doherr ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Nucleocapsid Protein ◽  
Canine Distemper Virus ◽  
Canine Distemper ◽  
Synergistic Inhibition ◽  
The Matrix ◽  
Cell Cell

scholarly journals Cell Fusion by Canine Distemper Virus-Infected Cells

1972 ◽  
Vol 10 (6) ◽  
pp. 1179-1183 ◽  
Author(s):  
Anne M. Rankin ◽  
Linda E. Fisher ◽  
Robert H. Bussell
Keyword(s):  
Cell Fusion ◽  
Canine Distemper Virus ◽  
Canine Distemper ◽  
Infected Cells

scholarly journals CD9-dependent regulation of Canine distemper virus-induced cell–cell fusion segregates with the extracellular domain of the haemagglutinin

2006 ◽  
Vol 87 (6) ◽  
pp. 1635-1642 ◽  
Author(s):  
K. Singethan ◽  
E. Topfstedt ◽  
S. Schubert ◽  
W. P. Duprex ◽  
B. K. Rima ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Measles Virus ◽  
Canine Distemper Virus ◽  
Transmembrane Protein ◽  
Extracellular Domain ◽  
Canine Distemper ◽  
Viral Glycoprotein ◽  
F Protein ◽  
H Protein ◽  
Cell Cell

Antibodies to CD9, a member of the tetraspan transmembrane-protein family, selectively inhibit Canine distemper virus (CDV)-induced cell–cell fusion. Neither CDV-induced virus–cell fusion nor cell–cell fusion induced by the closely related morbillivirus Measles virus (MV) is affected by anti-CD9 antibodies. As CDV does not bind CD9, an unknown, indirect mechanism is responsible for the observed inhibition of cell–cell fusion. It was investigated whether this effect was restricted to only one viral glycoprotein, either the haemagglutinin (H) or the fusion (F) protein, which form a fusion complex on the surface of virions and infected cells, or whether it is dependent on both in transient co-transfection assays. The susceptibility to CD9 antibodies segregates with the H protein of CDV. By exchanging portions of the H proteins of CDV and MV, it was determined that the complete extracellular domain, including the predicted stem structure (stem 1, barrel strand 1 and stem 2) and globular head domain, of the CDV-H protein mediates the effect. This suggests that interaction of the CDV-H protein with an unknown cellular receptor(s) is regulated by CD9, rather than F protein-mediated membrane fusion.

scholarly journals Intratumoral Canine Distemper Virus Infection Inhibits Tumor Growth by Modulation of the Tumor Microenvironment in a Murine Xenograft Model of Canine Histiocytic Sarcoma

2021 ◽  
Vol 22 (7) ◽  
pp. 3578
Author(s):  
Federico Armando ◽  
Adnan Fayyad ◽  
Stefanie Arms ◽  
Yvonne Barthel ◽  
Dirk Schaudien ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Virus Infection ◽  
Tumor Growth ◽  
Canine Distemper Virus ◽  
Xenograft Model ◽  
Histiocytic Sarcoma ◽  
Oncolytic Viruses ◽  
Canine Distemper ◽  
Murine Xenograft Model ◽  
The Impact

Histiocytic sarcomas refer to highly aggressive tumors with a poor prognosis that respond poorly to conventional treatment approaches. Oncolytic viruses, which have gained significant traction as a cancer therapy in recent decades, represent a promising option for treating histiocytic sarcomas through their replication and/or by modulating the tumor microenvironment. The live attenuated canine distemper virus (CDV) vaccine strain Onderstepoort represents an attractive candidate for oncolytic viral therapy. In the present study, oncolytic virotherapy with CDV was used to investigate the impact of this virus infection on tumor cell growth through direct oncolytic effects or by virus-mediated modulation of the tumor microenvironment with special emphasis on angiogenesis, expression of selected MMPs and TIMP-1 and tumor-associated macrophages in a murine xenograft model of canine histiocytic sarcoma. Treatment of mice with xenotransplanted canine histiocytic sarcomas using CDV induced overt retardation in tumor progression accompanied by necrosis of neoplastic cells, increased numbers of intratumoral macrophages, reduced angiogenesis and modulation of the expression of MMPs and TIMP-1. The present data suggest that CDV inhibits tumor growth in a multifactorial way, including direct cell lysis and reduction of angiogenesis and modulation of MMPs and their inhibitor TIMP-1, providing further support for the concept of its role in oncolytic therapies.

scholarly journals Drivers of canine distemper virus exposure in dogs at a wildlife interface in Janos, Mexico

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Rocío Almuna ◽  
Andrés M. López‐Pérez ◽  
Rosa E. Sarmiento ◽  
Gerardo Suzán
Keyword(s):  
Canine Distemper Virus ◽  
Canine Distemper ◽  
Virus Exposure

scholarly journals Antiviral Screen against Canine Distemper Virus-Induced Membrane Fusion Activity

Viruses ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 128
Author(s):  
Neeta Shrestha ◽  
Flavio M. Gall ◽  
Jonathan Vesin ◽  
Marc Chambon ◽  
Gerardo Turcatti ◽  
...  
Keyword(s):  
Membrane Fusion ◽  
Small Molecule ◽  
High Throughput Screening ◽  
Measles Virus ◽  
Canine Distemper Virus ◽  
Rna Virus ◽  
Preventive Measure ◽  
Close Relative ◽  
Fusion Activity ◽  
Canine Distemper

Canine distemper virus (CDV), a close relative of the human pathogen measles virus (MeV), is an enveloped, negative sense RNA virus that belongs to the genus Morbillivirus and causes severe diseases in dogs and other carnivores. Although the vaccination is available as a preventive measure against the disease, the occasional vaccination failure highlights the importance of therapeutic alternatives such as antivirals against CDV. The morbilliviral cell entry system relies on two interacting envelope glycoproteins: the attachment (H) and fusion (F) proteins. Here, to potentially discover novel entry inhibitors targeting CDV H, F and/or the cognate receptor: signaling lymphocyte activation molecule (SLAM) proteins, we designed a quantitative cell-based fusion assay that matched high-throughput screening (HTS) settings. By screening two libraries of small molecule compounds, we successfully identified two membrane fusion inhibitors (F2736-3056 and F2261-0043). Although both inhibitors exhibited similarities in structure and potency with the small molecule compound 3G (an AS-48 class morbilliviral F-protein inhibitor), F2736-3056 displayed improved efficacy in blocking fusion activity when a 3G-escape variant was employed. Altogether, we present a cell-based fusion assay that can be utilized not only to discover antiviral agents against CDV but also to dissect the mechanism of morbilliviral-mediated cell-binding and cell-to-cell fusion activity.

scholarly journals Seroprevalence and risk factors of canine distemper virus in the pet and stray dogs in Haa, western Bhutan

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Tshering Dorji ◽  
Tenzin Tenzin ◽  
Kuenga Tenzin ◽  
Dawa Tshering ◽  
Karma Rinzin ◽  
...  
Keyword(s):  
Risk Factors ◽  
Canine Distemper Virus ◽  
Canine Distemper ◽  
Stray Dogs
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