Mass Spectrometry Reveals Specific and Global Molecular Transformations during Viral Infection

Go, Eden P.; Wikoff, William R.; Shen, Zhouxin; O’Maille, Grace; Morita, Hirotoshi; Conrads, Thomas P.; Nordström, Anders; Trauger, Sunia A.; Uritboonthai, Wilasinee; Lucas, David A.; Chan, King C.; Veenstra, Timothy D.; Lewicki, Hanna; Oldstone, Michael B. A.; Schneemann, Anette; Siuzdak, Gary

doi:10.1021/pr060215t

Cited by 41 publications

(34 citation statements)

References 58 publications

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“…This hypothesis is supported by evidence that shows that the IBDV VP1 protein interacts with the carboxyl-terminal domain of EIF4A2 (40) and by data that demonstrate that the families of RNA viruses hijack the host translation apparatus to successfully complete viral mRNAs translation (41). Moreover RPSA and ARPP0 up-regulation was also found in cells infected with rice yellow mottle virus (17), FHV (23), and SARS-CoV (25), suggesting that the two proteins may not be specific to IBDV infectionassociated cells and tissues.…”

Section: Discussionmentioning

confidence: 79%

“…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%

“…The comparative proteomics approaches coupling 2-DE and MS (2-DE/MS) effectively help the study of the molecular profiles of virus-infected cells (16). In plant viruses, 2-DE/MS has been used to study the cellular changes in rice yellow mottle virus-infected cells in susceptible and partially resistant rice cultivars (17) and in tobacco mosaic virus-infected tomato (18 (23)(24)(25). Therefore, the proteomics strategies provide an overall understanding of the cellular factors involved in various stages of infection and give an insight into the alteration of signaling pathways to further understand viral pathogenesis.…”

mentioning

confidence: 99%

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Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Zheng

Ling

Shi

et al. 2008

Molecular & Cellular Proteomics

108

127

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Section: Discussionmentioning

confidence: 79%

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

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Zheng

Ling

Shi

et al. 2008

Molecular & Cellular Proteomics

108

127

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“…For instance, crq is expressed in D. melanogaster haemocytes/macrophages and it plays a specific role in the recognition and phagocytosis of apoptotic cells and Staphylococcus aureus (Franc et al, 1996(Franc et al, , 1999Sears et al, 2003;Stuart et al, 2005). Its expression is also upregulated after a viral infection (Go et al, 2006). Our results show that crq is upregulated in the gastric caeca, midgut and garland cells, with these tissues being the primary barrier against the ingested microbes and inhaled fungal spores.…”

Section: Fig 5 Temporal Regulation Of the Sr-bis In Non Esteroidogementioning

confidence: 70%

Expression of the Scavenger Receptor Class B type I (SR-BI) family in Drosophila melanogaster

Herboso¹,

Talamillo²,

Pérez³

et al. 2011

Int. J. Dev. Biol.

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In mammals, cholesterol is transformed into steroid hormones in the adrenal gland, the ovaries or the testes. The Scavenger Receptors Class B Type I (SR-BI) are membrane proteins that belong to the CD36 family and participate in the selective uptake of high density lipoprotein cholesteryl ester in the mammalian steroidogenic tissues. Fourteen members of the CD36 family have been identified in Diptera, although their expression patterns remain uncharacterized. Using in situ hybridization we have characterized the expression patterns of the fourteen SR-BIs in Drosophila melanogaster. We analyzed three different developmental larval stages prior to and during the peak of the insect steroid hormone ecdysone, which triggers the larval to pupal transition. We focused on the steroidogenic tissues, such as the prothoracic gland, the ovaries and the testes, and extended our analysis to non-steroidogenic tissues, such as the fat body, salivary glands, the gut, the gastric caeca or the central nervous system. Our results show highly regulated expression patterns, with three genes crq, pes and Snmp being upregulated in steroidogenic tissues at the onset of pupariation when steroidogenesis is crucial. This study underlines the importance of the transport of cholesterol and steroids in the process of ecdysone synthesis.

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“…Previous investigations have shown that this is due in part to RNA2 competing more effectively for the translational apparatus, but it is likely that additional aspects underlie this differential regulation (14). Not surprisingly, the synthesis of RdRp and coat protein is also controlled temporally, with RdRp being generated early in infection and coat protein much later (13,15,16). This leads to a situation in which progeny RNA is packaged into particles with a significant delay following synthesis, raising the question of where in the cell this RNA is located and how it is stabilized during that time.…”

mentioning

confidence: 99%

Cytoplasmic Granule Formation and Translational Inhibition of Nodaviral RNAs in the Absence of the Double-Stranded RNA Binding Protein B2

Petrillo

Venter

Short

et al. 2013

J Virol

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bFlock House virus (FHV) is a positive-sense RNA insect virus with a bipartite genome. RNA1 encodes the RNA-dependent RNA polymerase, and RNA2 encodes the capsid protein. A third protein, B2, is translated from a subgenomic RNA3 derived from the 3= end of RNA1. B2 is a double-stranded RNA (dsRNA) binding protein that inhibits RNA silencing, a major antiviral defense pathway in insects. FHV is conveniently propagated in Drosophila melanogaster cells but can also be grown in mammalian cells. It was previously reported that B2 is dispensable for FHV RNA replication in BHK21 cells; therefore, we chose this cell line to generate a viral mutant that lacked the ability to produce B2. Consistent with published results, we found that RNA replication was indeed vigorous but the yield of progeny virus was negligible. Closer inspection revealed that infected cells contained very small amounts of coat protein despite an abundance of RNA2. B2 mutants that had reduced affinity for dsRNA produced analogous results, suggesting that the dsRNA binding capacity of B2 somehow played a role in coat protein synthesis. Using fluorescence in situ hybridization of FHV RNAs, we discovered that RNA2 is recruited into large cytoplasmic granules in the absence of B2, whereas the distribution of RNA1 remains largely unaffected. We conclude that B2, by binding to double-stranded regions in progeny RNA2, prevents recruitment of RNA2 into cellular structures, where it is translationally silenced. This represents a novel function of B2 that further contributes to successful completion of the nodaviral life cycle.T he nodaviruses are a family of positive-strand RNA viruses that naturally infect insects and fish. They have a bipartite genome that contains approximately 4,500 bases and encodes three proteins. The most thoroughly studied nodavirus is the insect virus Flock House virus (FHV), which has served as an important model system to investigate the structural and molecular basis of RNA replication, virus assembly, and inhibition of antiviral host responses (1). The larger of the two genomic RNAs, RNA1 (3.1 kb), encodes the RNAdependent RNA polymerase (RdRp; 112 kDa), which is located on the outer membrane of mitochondria in infected cells (2, 3). Viral RNA synthesis induces so-called spherules (4), i.e., membrane invaginations, which are thought to sequester the replication complexes and double-stranded RNA (dsRNA) intermediates to protect them from RNA silencing, a major antiviral pathway activated in insects upon infection with RNA viruses (5). Further protection from RNA silencing is afforded by FHV protein B2 (11.6 kDa), a dsRNA binding protein that is translated from RNA3 (387 nucleotides), a subgenomic RNA derived from the 3= end of RNA1 (6-8). The capsid protein, protein alpha (43 kDa), is translated from RNA2 (1.4 kb), the second genomic RNA segment.Although a seemingly simple virus, FHV uses a sophisticated regulatory system to control its gene expression. This regulation occurs at several levels and is currently incompletely understo...

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Mass Spectrometry Reveals Specific and Global Molecular Transformations during Viral Infection

Cited by 41 publications

References 58 publications

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Expression of the Scavenger Receptor Class B type I (SR-BI) family in Drosophila melanogaster

Cytoplasmic Granule Formation and Translational Inhibition of Nodaviral RNAs in the Absence of the Double-Stranded RNA Binding Protein B2

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