Role of Actin Microfilaments in Canine Distemper Virus Replication in Vero Cells

Katayama, Hirofumi; Hori, Masaru; Sato, Koichi; Kajita, Masatoshi; Ozaki, Hiroshi; Karaki, Hideaki; Ohashi, Kousaburo; Kai, Chieko

doi:10.1292/jvms.66.409

Cited by 12 publications

(10 citation statements)

References 22 publications

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“…Afadin connects the cytoplasmic tail of nectin to the actin cytoskeleton, which may help the cell contract while fusion pores form (see movie S4 in the supplemental material). Interestingly, F-actin contributes to particle assembly by several paramyxoviruses, including SeV, RSV, and Newcastle disease virus (35)(36)(37)(38)(39). F-actin, which contributes to the release of MV particles from HeLa cells (40), also accumulates at the cellular junc- tions during MV transmission from dendritic cells to lymphocytes (41).…”

Section: Discussionmentioning

confidence: 99%

The Nectin-4/Afadin Protein Complex and Intercellular Membrane Pores Contribute to Rapid Spread of Measles Virus in Primary Human Airway Epithelia

Singh

Hornick

Krishnamurthy

et al. 2015

J Virol

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The discovery that measles virus (MV) uses the adherens junction protein nectin-4 as its epithelial receptor provides a new vantage point from which to characterize its rapid spread in the airway epithelium. We show here that in well-differentiated primary cultures of airway epithelial cells from human donors (HAE), MV infectious centers form rapidly and become larger than those of other respiratory pathogens: human respiratory syncytial virus, parainfluenza virus 5, and Sendai virus. While visible syncytia do not form after MV infection of HAE, the cytoplasm of an infected cell suddenly flows into an adjacent cell, as visualized through wild-type MV-expressed cytoplasmic green fluorescent protein (GFP). High-resolution video microscopy documents that GFP flows through openings that form on the lateral surfaces between columnar epithelial cells. To assess the relevance of the protein afadin, which connects nectin-4 to the actin cytoskeleton, we knocked down its mRNA. This resulted in more-limited infectious-center formation. We also generated a nectin-4 mutant without the afadin-binding site in its cytoplasmic tail. This mutant was less effective than wild-type human nectin-4 at promoting MV infection in primary cultures of porcine airway epithelia. Thus, in airway epithelial cells, MV spread requires the nectin-4/afadin complex and is based on cytoplasm transfer between columnar cells. Since the viral membrane fusion apparatus may open the passages that allow cytoplasm transfer, we refer to them as intercellular membrane pores. Virus-induced intercellular pores may contribute to extremely efficient measles contagion by promoting the rapid spread of the virus through the upper respiratory epithelium. IMPORTANCE Measles virus (MV

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Section: Discussionmentioning

confidence: 99%

The Nectin-4/Afadin Protein Complex and Intercellular Membrane Pores Contribute to Rapid Spread of Measles Virus in Primary Human Airway Epithelia

Singh

Hornick

Krishnamurthy

et al. 2015

J Virol

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“…This is the first report of cytochalasin D inhibiting the replication of a nonenveloped RNA virus. There are examples of the importance of an intact actin network in the transcription/ replication of human parainfluenza virus type 3, canine distemper virus, respiratory syncytial virus, and Newcastle disease virus (8,12,13,14,23,24,29,30). Early ultrastructural studies of FCV infection noted the formation of filaments in infected cells and the association of virions with these filaments (33).…”

Section: Discussionmentioning

confidence: 99%

Entry of Feline Calicivirus Is Dependent on Clathrin-Mediated Endocytosis and Acidification in Endosomes

Stuart

Brown

2006

J Virol

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Feline calicivirus is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of Caliciviridae. We have examined the entry process of feline calicivirus (FCV). An earlier study demonstrated that acidification in endosomes may be required. We have confirmed this observation and expanded upon it, demonstrating, using drugs to inhibit the various endocytic pathways and dominant-negative mutants, that FCV infects cells via clathrin-mediated endocytosis. We have also observed that FCV permeabilizes cell membranes early during infection to allow the coentry of toxins such as ␣-sarcin. Inhibitors of endosome acidification such as chloroquine and bafilomycin A1 blocked this permeabilization event, demonstrating that acidification is required for uncoating of the genome and access to the cytoplasm.

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“…Total RNA extraction, semi-quantitative RT-PCR, agarose electrophoresis, and quantification of bands were performed as described previously (Katayama et al, 2004).…”

Section: Semiquantitative Reverse Transcription-polymerase Chain Reacmentioning

confidence: 99%

Canine Distemper Virus Induces Apoptosis Through Caspase‐3 and ‐8 Activation in Vero Cells

Kajita

Katayama

Murata

et al. 2006

Journal of Veterinary Medicine, Series B

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We investigated the signal-transduction pathway of canine distemper virus-Onderstepoort (CDV-Ond) vaccine strain-mediated apoptosis in Vero cells. Canine distemper virus-Onderstepoort at a multiplicity of infection (MOI) of 0.1 induced DNA fragmentation 48 h after infection. Immunofluorescence staining revealed that 57% +/- 4% of the CDV-N-protein-positive cells were terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive, and all TUNEL-positive cells were CDV-N-protein-positive, indicating that CDV-Ond induced apoptosis only in the infected cells. We also found that CDV-Ond infection induced activation of caspase-3 and caspase-8. In the semi-quantitative reverse transcription-polymerase chain reaction assay for apoptosis-related genes, the expression of mRNA of the death receptor, Fas, was also increased in CDV-Ond-infected cells. In contrast, the expressions of Bcl-2 and Bax, regulators for intrinsic apoptotic signaling through the mitochondria, did not change. These results suggest that CDV-Ond induced apoptosis by activating caspase-3, possibly through caspase-8 signaling rather than through p53/Bax-mediated, mitochondrial signaling in the infected cells.

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Role of Actin Microfilaments in Canine Distemper Virus Replication in Vero Cells

Cited by 12 publications

References 22 publications

The Nectin-4/Afadin Protein Complex and Intercellular Membrane Pores Contribute to Rapid Spread of Measles Virus in Primary Human Airway Epithelia

The Nectin-4/Afadin Protein Complex and Intercellular Membrane Pores Contribute to Rapid Spread of Measles Virus in Primary Human Airway Epithelia

Entry of Feline Calicivirus Is Dependent on Clathrin-Mediated Endocytosis and Acidification in Endosomes

Canine Distemper Virus Induces Apoptosis Through Caspase‐3 and ‐8 Activation in Vero Cells

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