Identification of cellular proteins modified in response to African swine fever virus infection by proteomics

Alfonso, Patricia; Rivera, José; Hernáez, Bruno; Alonso, Covadonga; Escribano, José M.

doi:10.1002/pmic.200300742

Cited by 67 publications

(70 citation statements)

References 62 publications

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“…Moreover, the proteomic profiling of virus-infected cells has led mostly to the identification of proteins whose altered expression results from the cytopathic consequences of viral replication. These include modifications in heat shock proteins or markers of apoptosis and/or neurodegeneration, as illustrated in studies using West Nile virus-infected neurons or cells lines infected with Nipah virus, respiratory syncytial virus, or African swine fever virus (2,9,11,17). A striking feature is that our study using BDV-infected neurons did not reveal any change in proteins falling into the above-mentioned categories, further stressing the exquisite noncytolytic adaptation of BDV to its neuronal target cell.…”

Section: Discussionmentioning

confidence: 53%

Proteomic Analysis Reveals Selective Impediment of Neuronal Remodeling upon Borna Disease Virus Infection

Suberbielle

Stella

Pont

et al. 2008

J Virol

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The neurotropic virus Borna disease virus (BDV) persists in the central nervous systems of a wide variety of vertebrates and causes behavioral disorders. BDV represents an intriguing example of a virus whose persistence in neurons leads to altered brain function in the absence of overt cytolysis and inflammation. The bases of BDV-induced behavioral impairment remain largely unknown. To better characterize the neuronal response to BDV infection, we compared the proteomes of primary cultures of cortical neurons with and without BDV infection. We used two-dimensional liquid chromatography fractionation, followed by protein identification by nanoliquid chromatography-tandem mass spectrometry. This analysis revealed distinct changes in proteins implicated in neurotransmission, neurogenesis, cytoskeleton dynamics, and the regulation of gene expression and chromatin remodeling. We also demonstrated the selective interference of BDV with processes related to the adaptative response of neurons, i.e., defects in proteins regulating synaptic function, global rigidification of the cytoskeleton network, and altered expression of transcriptional and translational repressors. Thus, this work provides a global view of the neuronal changes induced by BDV infection together with new clues to understand the mechanisms underlying the selective interference with neuronal plasticity and remodeling that characterizes BDV persistence.The analysis of the response of a host cell to a pathogenic microorganism represents a daunting task, as it often results in complex and numerous changes in gene expression (37). Generally, these changes strongly depend on the nature of the pathogen interaction with its host. In the case of the central nervous system (CNS), the deleterious consequences of viral infection are often due to the cytopathic nature of viral replication (25, 38), or, alternatively, they can result from the immune response to the virus (31). However, some viruses can also persist in the CNS and cause diseases without an overt cytopathic effect or inflammation (1). These viral models provide a unique opportunity to unravel the molecular mechanisms underlying virus-induced neuronal dysfunction. A better understanding of the pathological consequences of viral persistence in the CNS may help to shed light on the pathogenesis of many neurological diseases of unclear etiology where viruses are thought to play a role (34, 47).Infection with Borna disease virus (BDV) represents an ideal paradigm for the investigation of the neuronal consequences due to the persistence of a noncytolytic virus. BDV is an enveloped virus with a nonsegmented, negative-strand RNA genome (13, 44). BDV infects a wide variety of mammals (35), possibly including humans (6, 29). Infected hosts develop a large spectrum of neurological disorders, ranging from immune-mediated diseases to behavioral alterations without inflammation (35, 41), reminiscent of symptoms observed in certain human neuropsychiatric diseases (28). These neurobehavioral manifestations reflect th...

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Section: Discussionmentioning

confidence: 53%

Proteomic Analysis Reveals Selective Impediment of Neuronal Remodeling upon Borna Disease Virus Infection

Suberbielle

Stella

Pont

et al. 2008

J Virol

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“…2). Up-regulated HSPB1 has been found in cells infected with African swine fever virus (19), enterovirus 71 (20), or FHV (23). Interestingly one HSPB1 protein spot presented an increase, whereas another HSPB1 protein spot presented a decrease, demonstrating that the up-regulated HSPB1 may not be specific to IBDV infection and that different isoforms or modifications of HSPB1 may play different roles during IBDV infection.…”

Section: Ibdv Infection Hijacking Of the Host Translation Appara-mentioning

confidence: 99%

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Zheng

Ling

Shi

et al. 2008

Molecular & Cellular Proteomics

109

127

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“…WSL-R line 379 is a macrophage cell line from wild swine origin that was kindly provided by Günther Kiel (FriedrichLoeffler Institut, Greifswald, Germany) and grown in Iscove's medium (Gibco) plus F-12 nutrient mixture (Gibco) plus 10% FBS. The BA71V (adapted to grow in Vero cells) and 608 VR13 (with a low number of passages in Vero cells [3]) ASFV isolates were used in infection experiments carried out at 37°C with 5% CO 2 . In most cases, ASFV stocks from culture supernatants were clarified and semipurified from vesicles by ultracentrifugation at 40,000 ϫ g through a 40% (wt/vol) sucrose cushion in phosphate-buffered saline (PBS) for 1 h at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Dynamin- and Clathrin-Dependent Endocytosis in African Swine Fever Virus Entry

Hernáez

Alonso

2010

J Virol

Self Cite

132

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African swine fever virus (ASFV) is a large DNA virus that enters host cells after receptor-mediated endocytosis and depends on acidic cellular compartments for productive infection. The exact cellular mechanism, however, is largely unknown. In order to dissect ASFV entry, we have analyzed the major endocytic routes using specific inhibitors and dominant negative mutants and analyzed the consequences for ASFV entry into host cells. Our results indicate that ASFV entry into host cells takes place by clathrin-mediated endocytosis which requires dynamin GTPase activity. Also, the clathrin-coated pit component Eps15 was identified as a relevant cellular factor during infection. The presence of cholesterol in cellular membranes, but not lipid rafts or caveolae, was found to be essential for a productive ASFV infection. In contrast, inhibitors of the Na ؉ /H ؉ ion channels and actin polymerization inhibition did not significantly modify ASFV infection, suggesting that macropinocytosis does not represent the main entry route for ASFV. These results suggest a dynamin-dependent and clathrin-mediated endocytic pathway of ASFV entry for the cell types and viral strains analyzed.

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Identification of cellular proteins modified in response to African swine fever virus infection by proteomics

Cited by 67 publications

References 62 publications

Proteomic Analysis Reveals Selective Impediment of Neuronal Remodeling upon Borna Disease Virus Infection

Proteomic Analysis Reveals Selective Impediment of Neuronal Remodeling upon Borna Disease Virus Infection

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Dynamin- and Clathrin-Dependent Endocytosis in African Swine Fever Virus Entry

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