Global protein profiling studies of chikungunya virus infection identify different proteins but common biological processes

Smith, Duncan R.

doi:10.1002/rmv.1802

Cited by 8 publications

(8 citation statements)

References 127 publications

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“…. This again supports a previous proposal that studies that investigate differentially expressed proteins are likely to identify different proteins but may highlight common biological processes .…”

Section: Studiessupporting

confidence: 90%

Analysis of protein profiling studies of β‐thalassemia/Hb E disease

Lithanatudom

Smith

2016

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A number of studies have used global protein profiling technologies on a range of patient samples to detect proteins that are differentially expressed in β-thalassemia/Hb E as an aid for understanding the physiopathology of this disease. Seven studies have identified a total of 111 unique, differentially expressed proteins. Seven proteins (prothrombin, alpha-1-antichymotrypsin, fibrinogen beta chain, hemoglobin beta, selenium-binding protein, microtubule-actin cross-linking factor and adenomatous polyposis coli protein 2) have been identified in two independent studies, whereas two proteins (carbonic anhydrase 1 and peroxiredoxin-2) have been identified in three independent studies. Both of these latter two proteins were consistently upregulated in the studies that identified them. Ontological analysis of all differentially regulated proteins identified "response to inorganic substances" as the most significant functional annotation cluster, which is consistent with iron overload being a major pathological consequence of this disease. Despite the range of samples investigated and the relatively small number of studies undertaken, a coherent picture of the mediators of the pathological consequences of β-thalassemia/Hb E disease is starting to emerge.

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Section: Studiessupporting

confidence: 90%

Analysis of protein profiling studies of β‐thalassemia/Hb E disease

Lithanatudom

Smith

2016

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“…Quantitative proteomics strategies have been used previously to study the effects of CHIKV infection in cell culture, mice, and patient serum (for a recent review see ). 2D‐DGE and 2D‐DIGE approaches identified between 15 and 51 differentially expressed proteins.…”

Section: Introductionmentioning

confidence: 99%

Temporal SILAC‐based quantitative proteomics identifies host factors involved in chikungunya virus replication

et al. 2015

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Chikungunya virus (CHIKV) is an arthropod-borne reemerging human pathogen that generally causes a severe persisting arthritis. Since 2005, the virus has infected millions of people during outbreaks in Africa, Indian Ocean Islands, Asia, and South/Central America. Many steps of the replication and expression of CHIKV's 12-kb RNA genome are highly dependent on cellular factors, which thus constitute potential therapeutic targets. SILAC and LC-MS/MS were used to define the temporal dynamics of the cellular response to infection. Using samples harvested at 8, 10, and 12 h postinfection, over 4700 proteins were identified and per time point 2800-3500 proteins could be quantified in both biological replicates. At 8, 10, and 12 h postinfection, 13, 38, and 106 proteins, respectively, were differentially expressed. The majority of these proteins showed decreased abundance. Most subunits of the RNA polymerase II complex were progressively degraded, which likely contributes to the transcriptional host shut-off observed during CHIKV infection. Overexpression of four proteins that were significantly downregulated (Rho family GTPase 3 (Rnd3), DEAD box helicase 56 (DDX56), polo-like kinase 1 (Plk1), and ubiquitin-conjugating enzyme E2C (UbcH10) reduced susceptibility of cells to CHIKV infection, suggesting that infection-induced downregulation of these proteins is beneficial for CHIKV replication. All MS data have been deposited in the ProteomeXchange with identifier PXD001330 (http://proteomecentral.proteomexchange.org/dataset/PXD001330).

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“…A number of proteomics studies have been carried out in CHIKV infection previously (Table 2), and the results were compared in a recent review by Smith [17]. All the four major pathways that we have identified in our study have been found to be modulated during CHIKV infection in one or more of these earlier studies.…”

Section: Common Set Of Pathways and Proteins Modulated In Chikv Infecmentioning

confidence: 69%

“…These include studies using cell lines like CHME-5, a microglial cell [9], WRL-68, a human hepatic fetal epithelial cell line [10] and SJCRH30, a human rhabdomyosarcoma cell line [11], and those in patient serum [12], in white blood cells isolated from Chikungunya fever patients [13] and in experimentally infected mice tissues such as the liver, brain and muscle [14][15][16]. A recent comparison of these studies [17] indicated that even though the results identified common pathways that are being modulated upon infection, there was less consistency in identifying individual proteins.…”

Section: Introductionmentioning

confidence: 99%

High throughput proteomic analysis and a comparative review identify the nuclear chaperone, Nucleophosmin among the common set of proteins modulated in Chikungunya virus infection

Abraham

Mudaliar

Jaleel

et al. 2015

Journal of Proteomics

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Chikungunya remained as a neglected tropical disease till its re-emergence in 2005 in the La RéUnion islands and subsequently, in India and many parts of South East Asia. These and the epidemics that followed in subsequent years ran an explosive course leading to extreme morbidity and attributed mortality to this originally benign virus infection. Apart from classical symptoms of acute fever and debilitating polyarthralgia lasting for several weeks, a number of complications were documented. These included aphthous-like ulcers and vesiculo-bullous eruptions on the skin, hepatic involvement, central nervous system complications such as encephalopathy and encephalitis, and transplacental transmission. The disease has recently spread to the Americas with its initial documentation in the Caribbean islands. The Asian genotype of this positive-stranded RNA virus of the Alphavirus genus has been attributed in these outbreaks. However, the disease ran a similar course as the one caused by the East, Central and South African (ECSA) genotype in the other parts of the world. Studies have documented a number of mutations in the re-emerging strains of the virus that enhances mosquito adaptability and modulates virus infectivity. This might support the occurrence of fiery outbreaks in the absence of herd immunity in affected population. Several research groups work to understand the pathogenesis of chikungunya and the mechanisms of complications using cellular and animal models. A few proteomics approaches have been employed earlier to understand the protein level changes in the infected cells. Our present study, which couples a high throughput proteomic analysis and a comparative review of these earlier studies, identifies a few critical molecules as hypothetical candidates that might be important in this infection and for future study.

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Global protein profiling studies of chikungunya virus infection identify different proteins but common biological processes

Cited by 8 publications

References 127 publications

Analysis of protein profiling studies of β‐thalassemia/Hb E disease

Analysis of protein profiling studies of β‐thalassemia/Hb E disease

Temporal SILAC‐based quantitative proteomics identifies host factors involved in chikungunya virus replication

High throughput proteomic analysis and a comparative review identify the nuclear chaperone, Nucleophosmin among the common set of proteins modulated in Chikungunya virus infection

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