Microarray study reveals that HIV-1 induces rapid type-I interferon-dependent p53 mRNA up-regulation in human primary CD4+T cells

Imbeault, Michaël; Ouellet, Michel; Tremblay, Michel J.

doi:10.1186/1742-4690-6-5

Cited by 51 publications

(56 citation statements)

References 71 publications

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“…The temporal effects on the host cellular protein profile were in accord with the transcriptomic profile reported recently by Imbeault et al (23). The observation that the proapoptotic factor p53 was upregulated in HIV-1-infected primary CD4 cells would be in line with the prelude to apoptosis seemingly evident in our present study at 24 h p.i.…”

Section: Vol 83 2009 Proteomic Analysis Of Hiv-infected Primary Cd4supporting

confidence: 80%

“…Earlier work done with HIV-infected CD4 T-cell lines has implicated cellular functions, including cholesterol biosynthesis, cell cycle arrest, apoptosis, and cell signaling, based on transcriptomic changes in the presence of HIV replication (8,10,19,51,54). Changes associated with apoptosis induction have recently been reported to occur early during ex vivo HIV infection of primary CD4 T cells (23), which is accompanied by notable induction of p53 transcription.…”

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confidence: 99%

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Dynamic Host Energetics and Cytoskeletal Proteomes in Human Immunodeficiency Virus Type 1-Infected Human Primary CD4 Cells: Analysis by Multiplexed Label-Free Mass Spectrometry

Chan¹,

Sutton

Jacobs

et al. 2009

J Virol

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We report on a proteomic analysis of ex vivo human immunodeficiency virus (HIV) type 1 infection in human primary CD4 cells by shotgun liquid chromatography-tandem mass spectrometry analysis, revealing two distinct proteomic profiles at two phases of virus replication. Relative to mock-infected cells, 168 signature proteins exhibited abundance changes at the first sign of Gag p24 production (8 h postinfection [p.i.]) or the peak of virus replication (24 h p.i.); interestingly, most of the changes were exclusive to only one phase of virus replication. Based on characterization by functional ontology and known human-HIV protein interactions, we observed the enrichment for protein abundance increases pertaining to protein synthesis and nucleasomal reorganization amid an otherwise placid cellular proteome at the first sign of HIV replication. In contrast, we observed indications of decreased protein turnover, concomitant with heightened DNA repair activities and preludes to apoptosis, in the presence of robust virus replication. We also observed hints of disruptions in protein and small molecule trafficking. Our label-free proteomic strategy allowed us to perform multiplexed comparisons-we buttressed our detection specificity with the use of a reverse transcriptase inhibitor as a counterscreen, enabling highlighting of cellular protein abundance changes unique to robust virus replication as opposed to viral entry. In conjunction with complementary high-throughput screens for cellular partners of HIV, we put forth a model pinpointing specific rerouting of cellular biosynthetic, energetic, and trafficking pathways as HIV replication accelerates in human primary CD4 cells.

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Section: Vol 83 2009 Proteomic Analysis Of Hiv-infected Primary Cd4supporting

confidence: 80%

mentioning

confidence: 99%

Dynamic Host Energetics and Cytoskeletal Proteomes in Human Immunodeficiency Virus Type 1-Infected Human Primary CD4 Cells: Analysis by Multiplexed Label-Free Mass Spectrometry

Chan¹,

Sutton

Jacobs

et al. 2009

J Virol

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“…This result is not entirely surprising: in vitro HIV infection rapidly activated the expression of proapoptotic genes in CD4 ϩ T cells (30 ); programmed cell death upon HIV infection and bystander activation were the major cause of CD4 ϩ T cell destruction (9 ); and CD4 ϩ T cells from long-term nonprogressors are significantly protected from spontaneous apoptosis (31 ). Our study indicates that, in addition to CD4 ϩ T cells, the whole PBMC population has been reprogrammed to accelerate the loss of cells in RPs.…”

Section: Discussionmentioning

confidence: 92%

Transcriptomic Analysis of Peripheral Blood Mononuclear Cells in Rapid Progressors in Early HIV Infection Identifies a Signature Closely Correlated with Disease Progression

Zhang

et al. 2013

Clinical Chemistry

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BACKGROUND:A substantial percentage (10%-15%) of HIV-infected individuals experience a sharp decline in CD4 ϩ T-cell counts and progress to AIDS quickly after primary infection. Identification of biomarkers distinguishing rapid progressors (RPs) vs chronic progressors (CPs) is critical for early clinical intervention and could provide novel strategies to facilitate vaccine design and immune therapy.

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“…31,32 Viral infections have also been shown to affect TRP53 activity by inducing type 1 IFN-mediated Trp53 mRNA upregulation. [33][34][35] On the other hand, TRP53 activation enhances IFN signaling. 36 During Salmonella infection, we observed both an increase in type 1 IFN expression and enhanced Trp53 transcription.…”

Section: Discussionmentioning

confidence: 99%

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

et al. 2011

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Typhoid fever, which is caused by Salmonella typhi and paratyphi, is a severe systemic disease that remains a major public health issue in several areas of the world. We can model the human disease using mice infected with a related bacterium, Salmonella typhimurium. This model recapitulates several clinical aspects of the human disease and allows for the study of the host response to Salmonella typhimurium infection in vivo. Previous work in our laboratory has identified three Immunity to typhimurium loci (Ity, Ity2 and Ity3) in the wild-derived MOLF/Ei mice, influencing survival after infection with Salmonella typhimurium. The MOLF/Ei alleles at Ity and Ity2 are protective, while the MOLF/Ei allele at Ity3 confers susceptibility. In this paper, we have generated a novel cross combination between the highly susceptible strain, MOLF/Ei, and the resistant strain, 129S6, to better define the genetic architecture of susceptibility to infection in MOLF/Ei. Using this cross, we have replicated the locus on chr 11 (Ity2) and identified a novel locus on chr 13 (Ity13). Using microarrays and transcriptional profiling, we examined the response of uninfected and infected Ity2 congenic mice. These analyses demonstrate a role for both type-1-interferon (IFN) and TRP53 signaling in the pathogenesis of Salmonella infection.

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Microarray study reveals that HIV-1 induces rapid type-I interferon-dependent p53 mRNA up-regulation in human primary CD4+T cells

Cited by 51 publications

References 71 publications

Dynamic Host Energetics and Cytoskeletal Proteomes in Human Immunodeficiency Virus Type 1-Infected Human Primary CD4 Cells: Analysis by Multiplexed Label-Free Mass Spectrometry

Dynamic Host Energetics and Cytoskeletal Proteomes in Human Immunodeficiency Virus Type 1-Infected Human Primary CD4 Cells: Analysis by Multiplexed Label-Free Mass Spectrometry

Transcriptomic Analysis of Peripheral Blood Mononuclear Cells in Rapid Progressors in Early HIV Infection Identifies a Signature Closely Correlated with Disease Progression

Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2

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