Cholesterol dependence of Newcastle Disease Virus entry

Martín, Juan José Aguilar; Holguera, Javier; Sánchez-Felipe, Lorena; Villar, Enrique; Muñoz-Barroso, Isabel

doi:10.1016/j.bbamem.2011.12.004

Cited by 34 publications

(28 citation statements)

References 66 publications

(92 reference statements)

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“…Similarly, the activity of PKC is essential for the entry of different non-enveloped [39] or enveloped viruses, such as influenza virus [38], alphavirus, rhabdovirus, poxvirus and herpes virus [40], which has been related to the entry through receptor-mediated endocytosis. Furthermore, we have previously suggested that caveolae/rafts could be a possible platform for NDV entry [28,41] and caveolae seem to be the major cell surface locations for PKC [42,43]. We also analyzed the effect of dynasore, a drug that inhibits the GTPase activity of dynamin 1, which has been implicated in clathrinand caveola-mediated endocytosis [44].…”

Section: Resultsmentioning

confidence: 99%

Entry of Newcastle Disease Virus into the host cell: Role of acidic pH and endocytosis

Sánchez-Felipe

Villar

Muñoz-Barroso

2014

Biochimica et Biophysica Acta (BBA) - Biomembranes

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Most paramyxoviruses enter the cell by direct fusion of the viral envelope with the plasma membrane. Our previous studies have shown the colocalization of Newcastle Disease Virus (NDV) with the early endosome marker EEA1 and the inhibition of NDV fusion by the caveolin-phosphorylating drug phorbol 12-myristate 13-acetate (PMA) prompted us to propose that NDV enters the cells via endocytosis. Here we show that the virus-cell fusion and cell-cell fusion promoted by NDV-F are increased by about 30% after brief exposure to low pH in HeLa and ELL-0 cells but not in NDV receptor- deficient cell lines such as GM95 or Lec1. After a brief low-pH exposure, the percentage of NDV fusion at 29 °C was similar to that at 37 °C without acid-pH stimulation, meaning that acid pH would decrease the energetic barrier to enhance fusion. Furthermore, preincubation of cells with the protein kinase C inhibitor bisindolylmaleimide led to the inhibition of about 30% of NDV infectivity, suggesting that a population of virus enters cells through receptor-mediated endocytosis. Moreover, the involvement of the GTPase dynamin in NDV entry is shown as its specific inhibitor, dynasore, also impaired NDV fusion and infectivity. Optimal infection of the host cells was significantly affected by drugs that inhibit endosomal acidification such as concanamycin A, monensin and chloroquine. These results support our hypothesis that entry of NDV into ELL-0 and HeLa cells occurs through the plasma membrane as well as by dynamin- low pH- and receptor- dependent endocytosis.

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Section: Resultsmentioning

confidence: 99%

Entry of Newcastle Disease Virus into the host cell: Role of acidic pH and endocytosis

Sánchez-Felipe

Villar

Muñoz-Barroso

2014

Biochimica et Biophysica Acta (BBA) - Biomembranes

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“…Cholesterol-enriched medium (CHEM) was prepared as described previously (37,38). Briefly, 10 mM cholesterol (CH) (Santa Cruz Biotechnology) stock was prepared in stirred and warmed DMSO at 80°C on a heating block.…”

Section: Methodsmentioning

confidence: 99%

Cholesterol Flux Is Required for Endosomal Progression of African Swine Fever Virions during the Initial Establishment of Infection

Cuesta-Geijo

Chiappi

Galindo

et al. 2016

J Virol

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African swine fever virus (ASFV) is a major threat for porcine production that has been slowly spreading in Eastern Europe since its first appearance in the Caucasus in 2007. ASFV enters the cell by endocytosis and gains access to the cytosol to start replication from late endosomes and multivesicular bodies. Cholesterol associated with low-density lipoproteins entering the cell by endocytosis also follows a trafficking pathway similar to that of ASFV. Here we show that cholesterol plays an essential role in the establishment of infection as the virus traffics through the endocytic pathway. In contrast to the case for other DNA viruses, such as vaccinia virus or adenovirus 5, cholesterol efflux from endosomes is required for ASFV release/entry to the cytosol. Accumulation of cholesterol in endosomes impairs fusion, resulting in retention of virions inside endosomes. ASFV also remodels intracellular cholesterol by increasing its cellular uptake and redistributes free cholesterol to viral replication sites. Our analysis reveals that ASFV manipulates cholesterol dynamics to ensure an appropriate lipid flux to establish productive infection. IMPORTANCESince its appearance in the Caucasus in 2007, African swine fever (ASF) has been spreading westwards to neighboring European countries, threatening porcine production. Due to the lack of an effective vaccine, ASF control relies on early diagnosis and widespread culling of infected animals. We investigated early stages of ASFV infection to identify potential cellular targets for therapeutic intervention against ASF. The virus enters the cell by endocytosis, and soon thereafter, viral decapsidation occurs in the acid pH of late endosomes. We found that ASFV infection requires and reorganizes the cellular lipid cholesterol. ASFV requires cholesterol to exit the endosome to gain access to the cytoplasm to establish productive replication. Our results indicate that there is a differential requirement for cholesterol efflux for vaccinia virus or adenovirus 5 compared to ASFV.

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“…Cantín et al [64] described the colocalization of NDV with caveolin and with the early endosome marker EEA1, leading to the suggestion that a certain percentage of the virus manages to penetrate the cell through caveolin-dependent endocytic pathways [67]. In that particular study, after 30 minutes of NDV infection, a strong colocalization of NDV HN protein and EEA1 was found, thus confirming that HN is targeted to early endosomes.…”

Section: Ndv-rac1 Interaction For Proliferation and Invasion Inhibmentioning

confidence: 76%

Newcastle Disease Virus Interaction in Targeted Therapy against Proliferation and Invasion Pathways of Glioblastoma Multiforme

Abdullah

Mustafa

Ideris

2014

BioMed Research International

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Glioblastoma multiforme (GBM), or grade IV glioma, is one of the most lethal forms of human brain cancer. Current bioscience has begun to depict more clearly the signalling pathways that are responsible for high-grade glioma initiation, migration, and invasion, opening the door for molecular-based targeted therapy. As such, the application of viruses such as Newcastle disease virus (NDV) as a novel biological bullet to specifically target aberrant signalling in GBM has brought new hope. The abnormal proliferation and aggressive invasion behaviour of GBM is reported to be associated with aberrant Rac1 protein signalling. NDV interacts with Rac1 upon viral entry, syncytium induction, and actin reorganization of the infected cell as part of the replication process. Ultimately, intracellular stress leads the infected glioma cell to undergo cell death. In this review, we describe the characteristics of malignant glioma and the aberrant genetics that drive its aggressive phenotype, and we focus on the use of oncolytic NDV in GBM-targeted therapy and the interaction of NDV in GBM signalling that leads to inhibition of GBM proliferation and invasion, and subsequently, cell death.

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Cholesterol dependence of Newcastle Disease Virus entry

Cited by 34 publications

References 66 publications

Entry of Newcastle Disease Virus into the host cell: Role of acidic pH and endocytosis

Entry of Newcastle Disease Virus into the host cell: Role of acidic pH and endocytosis

Cholesterol Flux Is Required for Endosomal Progression of African Swine Fever Virions during the Initial Establishment of Infection

Newcastle Disease Virus Interaction in Targeted Therapy against Proliferation and Invasion Pathways of Glioblastoma Multiforme

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