Microarray analysis of A549 cells infected with rabbitpox virus (RPV): a comparison of wild-type RPV and RPV deleted for the host range gene, SPI-1

Brum, Lauren M; Lopez, Maria-Cecilia; Varela, Juan Carlos; Baker, Henry V.; Moyer, Richard W.

doi:10.1016/s0042-6822(03)00532-4

Cited by 44 publications

(52 citation statements)

References 33 publications

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“…Interestingly, 90% of the total significant gene changes in Mt1/2 (ϩ/ϩ) and Mt1/2 (Ϫ/Ϫ) mice at 3 h were mRNA decreases. This largescale decrease in mRNA levels as an early response to stress is similar to that observed previously with viral infection of lung cells in vitro (47). Furthermore, twice as many decreases in different transcripts were observed in Mt1/2 (Ϫ/Ϫ) mice as compared with Mt1/2 (ϩ/ϩ) mice at 3 h, suggesting that, in the absence of Mt, this early injury involves factors responsible for normal transcriptional processing.…”

Section: Expression Differences In Genes Involved In the Inflammatorysupporting

confidence: 87%

The Role of Metallothionein in the Pathogenesis of Acute Lung Injury

Wesselkamper

McDowell²,

Medvedovic³

et al. 2006

Am J Respir Cell Mol Biol

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Often fatal, acute lung injury has a complicated etiology. Previous studies from our laboratory in mice have demonstrated that survival during acute lung injury is a complex trait governed by multiple loci. We also found that the increase in metallothionein (MT) is one of the greatest noted in transcriptome-wide analyses of gene expression. To assess the role of MT in nickel-induced acute lung injury, the survival of Mt-transgenic, Mt1/2 (ϩ/ϩ) , and Mt1/2 (Ϫ/Ϫ) mice was compared. Pulmonary inflammation and global gene expression were compared in Mt1/2 (ϩ/ϩ) and Mt1/2 (Ϫ/Ϫ) mice. Genetargeted Mt1/2 (Ϫ/Ϫ) mice were more susceptible than Mt1/2 (ϩ/ϩ) mice to nickel-induced inflammation, surfactant-associated protein B transcript loss, and lethality. Similarly, Mt-transgenic mice exhibited increased survival. MAPPFinder analyses also noted significant decreases in genes involved in protein processing (e.g., ubiquitination, folding), which were greater in Mt1/2 (Ϫ/Ϫ) mice as compared with Mt1/2 (ϩ/ϩ) mice early in the progression of acute lung injury, possibly due to a zinc-mediated transcript destabilization. In contrast, transcript levels of genes associated with the inflammatory response, extracellular matrix regulation, and coagulation/fibrinolysis were increased more in Mt1/2 (Ϫ/Ϫ) mice as compared with Mt1/2 (ϩ/ϩ) mice late in the development of acute lung injury. Thus, MT ultimately improves survival in the progression of acute lung injury in mice. Transcriptome-wide analysis suggests that this survival may be mediated through changes in the destabilization of transcripts associated with protein processing, the subsequent augmentation of transcripts controlling inflammation, extracellular matrix regulation, coagulation/fibrinolysis, and disruption of surfactant homeostasis.

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Section: Expression Differences In Genes Involved In the Inflammatorysupporting

confidence: 87%

The Role of Metallothionein in the Pathogenesis of Acute Lung Injury

Wesselkamper

McDowell²,

Medvedovic³

et al. 2006

Am J Respir Cell Mol Biol

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“…It is well established that poxviruses can interfere with cellular transcripts, leading to reductions in host proteins (35,36,40,41). Therefore, we compared the rate of Clr-b protein loss to the amount of mRNA.…”

Section: Clr-b Transcript Is Reduced During Infectionmentioning

confidence: 99%

“…Given the potential for the NKR-P1 and Clr system of receptors and ligands to be involved in the response to poxvirus infection and the ability of poxviruses to interfere with protein expression through destabilization of cellular transcripts (35)(36)(37), we tested the hypothesis that Clr-b is modulated during poxvirus infection. We found that infection of mouse cells with either VV or ECTV reduces Clr-b on the cell surface.…”

mentioning

confidence: 99%

Poxvirus Infection-Associated Downregulation of C-Type Lectin-Related-b Prevents NK Cell Inhibition by NK Receptor Protein-1B

Williams

Wilson

Davidson

et al. 2012

The Journal of Immunology

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Innate immune recognition of virus-infected cells includes NK cell detection of changes to endogenous cell-surface proteins through inhibitory receptors. One such receptor system is the NK cell receptor protein-1B (NKR-P1B) and its ligand C-type lectin-related-b (Clr-b). NKR-P1B and Clr-b are encoded within the NK cell gene complex, a locus that has been linked to strain-dependent differences in susceptibility to infection by poxviruses. In this study, we report the impact of vaccinia virus (VV) and ectromelia virus infection on expression of Clr-b and Clr-b–mediated protection from NK cells. We observed a loss of Clr-b cell-surface protein upon VV and ectromelia virus infection of murine cell lines and bone marrow-derived macrophages. The reduction of Clr-b is more rapid than MHC class I, the prototypic ligand of NK cell inhibitory receptors. Reduction of Clr-b requires active viral infection but not expression of late viral genes, and loss of mRNA appears to lag behind loss of Clr-b surface protein. Clr-b–mediated protection from NK cells is lost following VV infection. Together, these results provide the second example of Clr-b modulation during viral infection and suggest reductions of Clr-b may be involved in sensitizing poxvirus-infected cells to NK cells.

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“…Scaling factors after normalization to the spike-in controls ranged between 0.42 and 1.44, with a median of 0.70 and a standard deviation of 0.27. A similar normalization strategy was used for microarray analysis of rabbitpox virus infection of human cells (14).…”

Section: Arrest Of Viral Intermediate Transcription and Lack Of Viralmentioning

confidence: 99%

Role of Viral Factor E3L in Modified Vaccinia Virus Ankara Infection of Human HeLa Cells: Regulation of the Virus Life Cycle and Identification of Differentially Expressed Host Genes

Ludwig

Mages

Staib

et al. 2005

J Virol

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Modified vaccinia virus Ankara (MVA) is a highly attenuated virus strain being developed as a vaccine for delivery of viral and recombinant antigens. The MVA genome lacks functional copies of numerous genes interfering with host response to infection. The interferon resistance gene E3L encodes one important viral immune defense factor still made by MVA. Here we demonstrate an essential role of E3L to allow for completion of the MVA molecular life cycle upon infection of human HeLa cells. A deletion mutant virus, MVA-ΔE3L, was found defective in late protein synthesis, viral late transcription, and viral DNA replication in infected HeLa cells. Moreover, we detected viral early and continuing intermediate transcription associated with degradation of rRNA, indicating rapid activation of 2′-5′-oligoadenylate synthetase/RNase L in the absence of E3L. Further molecular monitoring of E3L function by microarray analysis of host cell transcription in MVA- or MVA-ΔE3L-infected HeLa cells revealed an overall significant down regulation of more than 50% of cellular transcripts expressed under mock conditions already at 5 h after infection, with a more prominent shutoff following MVA-ΔE3L infection. Interestingly, a cluster of genes up regulated exclusively in MVA-ΔE3L-infected cells could be identified, including transcripts for interleukin 6, growth arrest and DNA damage-inducible protein β, and dual-specificity protein phosphatases. Our data indicate that lack of E3L inhibits MVA antigen production in human HeLa cells at the level of viral late gene expression and suggest that E3L can prevent activation of additional host factors possibly affecting the MVA molecular life cycle

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Microarray analysis of A549 cells infected with rabbitpox virus (RPV): a comparison of wild-type RPV and RPV deleted for the host range gene, SPI-1

Cited by 44 publications

References 33 publications

The Role of Metallothionein in the Pathogenesis of Acute Lung Injury

The Role of Metallothionein in the Pathogenesis of Acute Lung Injury

Poxvirus Infection-Associated Downregulation of C-Type Lectin-Related-b Prevents NK Cell Inhibition by NK Receptor Protein-1B

Role of Viral Factor E3L in Modified Vaccinia Virus Ankara Infection of Human HeLa Cells: Regulation of the Virus Life Cycle and Identification of Differentially Expressed Host Genes

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