Persistent infections with Sendai virus and Newcastle disease viruses

Lawton, Philippe; Karimi, Zeinab; Mancinelli, Luca; Seto, J. T.

doi:10.1007/bf01309891

Cited by 9 publications

(5 citation statements)

References 18 publications

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“…Because membrane fusion is a key step for the entry of intact virus into the host cells ( Knipe and Howley, 2013 ), we also investigated the role of villin in viral infection. Productive infection in the case of fusogenic enveloped viruses such as Sendai is reflected by syncytia formation and production of progeny viruses ( Famulari and Fleissner, 1976 ; Lawton et al. , 1986 ).…”

Section: Resultsmentioning

confidence: 99%

Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes

Chandra

Kalaivani

Kumar

et al. 2017

MBoC

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MBoC | ARTICLE Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes ABSTRACT Reconstituted Sendai viral envelopes (virosomes) are well recognized for their promising potential in membrane fusion-mediated delivery of bioactive molecules to liver cells. Despite the known function of viral envelope glycoproteins in catalyzing fusion with cellular membrane, the role of host cell proteins remains elusive. Here, we used two-dimensional differential in-gel electrophoresis to analyze hepatic cells in early response to virosomeinduced membrane fusion. Quantitative mass spectrometry together with biochemical analysis revealed that villin, an actin-modifying protein, is differentially up-regulated and phosphorylated at threonine 206-an early molecular event during membrane fusion. We found that villin influences actin dynamics and that this influence, in turn, promotes membrane mixing through active participation of Sendai viral envelope glycoproteins. Modulation of villin in host cells also resulted in a discernible effect on the entry and egress of progeny Sendai virus. Taken together, these results suggest a novel mechanism of regulated viral entry in animal cells mediated by host factor villin.

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Section: Resultsmentioning

confidence: 99%

Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes

Chandra

Kalaivani

Kumar

et al. 2017

MBoC

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“…Similar to other RNA viruses such as measles virus (14), Sendai virus (SeV) (15), mumps virus (16), vesicular stomatitis virus (17,18), parainfluenza virus type 3 (PIV3) (19), and respiratory syncytial virus (RSV) (20), NDV can establish persistent infection under some circumstances, as reported previously (15,21,22). For establishment of persistent infection in vitro, there is normally a fine dynamic equilibrium between virus infection and viral clearance by host innate immune responses.…”

mentioning

confidence: 75%

Newcastle Disease Virus Establishes Persistent Infection in Tumor Cells In Vitro : Contribution of the Cleavage Site of Fusion Protein and Second Sialic Acid Binding Site of Hemagglutinin-Neuraminidase

Rangaswamy

Wang

Cheng

et al. 2017

J Virol

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Newcastle disease virus (NDV) is an oncolytic virus being developed for the treatment of cancer. Following infection of a human ovarian cancer cell line (OVCAR3) with a recombinant low-pathogenic NDV, persistent infection was established in a subset of tumor cells. Persistently infected (PI) cells exhibited resistance to superinfection with NDV and established an antiviral state, as demonstrated by upregulation of interferon and interferon-induced genes such as myxoma resistance gene 1 (Mx1) and retinoic acid-inducing gene-I (RIG-I). Viruses released from PI cells induced higher cell-to-cell fusion than the parental virus following infection in two tumor cell lines tested, HT1080 and HeLa, and remained attenuated in chickens. Two mutations, one in the fusion (F) protein cleavage site, F117S (F 117S ), and another in hemagglutinin-neuraminidase (HN), G169R (HN 169R ), located in the second sialic acid binding region, were responsible for the hyperfusogenic phenotype. F 117S improves F protein cleavage efficiency, facilitating cell-to-cell fusion, while HN 169R possesses a multifaceted role in contributing to higher fusion, reduced receptor binding, and lower neuraminidase activity, which together result in increased fusion and reduced viral replication. Thus, establishment of persistent infection in vitro involves viral genetic changes that facilitate efficient viral spread from cell to cell as a potential mechanism to escape host antiviral responses. The results of our study also demonstrate a critical role in the viral life cycle for the second receptor binding region of the HN protein, which is conserved in several paramyxoviruses.IMPORTANCE Oncolytic Newcastle disease virus (NDV) could establish persistent infection in a tumor cell line, resulting in a steady antiviral state reflected by constitutively expressed interferon. Viruses isolated from persistently infected cells are highly fusogenic, and this phenotype has been mapped to two mutations, one each in the fusion (F) and hemagglutinin-neuraminidase (HN) proteins. The F 117S mutation in the F protein cleavage site improved F protein cleavage efficiency while the HN 169R mutation located at the second receptor binding site of the HN protein contributed to a complex phenotype consisting of a modest increase in fusion and cell killing, lower neuraminidase activity, and reduced viral growth. This study highlights the intricate nature of these two mutations in the glycoproteins of NDV in the establishment of persistent infection. The data also shed light on the critical balance between the F and HN proteins required for efficient NDV infection and their role in avian pathogenicity.KEYWORDS NDV, Newcastle disease virus, fusion, paramyxovirus, persistent infection

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“…Virus. The Z strain of Sendai virus and host range mutants ts-fl and F1-R were propagated and assayed as before (18,38).…”

Section: Methodsmentioning

confidence: 99%

Organ tropism of Sendai virus in mice: proteolytic activation of the fusion glycoprotein in mouse organs and budding site at the bronchial epithelium

Tashiro

Yamakawa

Tobita

et al. 1990

J Virol

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Persistent infections with Sendai virus and Newcastle disease viruses

Cited by 9 publications

References 18 publications

Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes

Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes

Newcastle Disease Virus Establishes Persistent Infection in Tumor Cells In Vitro : Contribution of the Cleavage Site of Fusion Protein and Second Sialic Acid Binding Site of Hemagglutinin-Neuraminidase

Organ tropism of Sendai virus in mice: proteolytic activation of the fusion glycoprotein in mouse organs and budding site at the bronchial epithelium

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