Integrative analyses reveal novel strategies in HPV11,-16 and -45 early infection

Kaczkowski, Bogumił; Rossing, Maria; Andersen, Ditte; Dreher, Anita; Morevati, Marya; Visser, Melissa A.; Winther, Ole; Nielsen, Finn Cilius; Norrild, Bodil

doi:10.1038/srep00515

Cited by 36 publications

(43 citation statements)

References 49 publications

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“…On a larger scale, several recent AP-MS studies have examined global host-virus protein interactions, generating comprehensive interaction networks that further highlight the benefit of applying proteomic approaches to investigating viral infection [120,124,125,129]. Moreover, the resulting large-scale protein interaction networks are useful in the development and optimization of statistical methods for characterizing protein associations, including the SAINT algorithm for determining specificity of protein interactions [130].…”

Section: Perspective: “Omic” Approaches In Characterizing Hdac Funmentioning

confidence: 99%

Histone Deacetylases in Herpesvirus Replication and Virus-Stimulated Host Defense

Guise

Budayeva

Diner

et al. 2013

Viruses

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Emerging evidence highlights a critical role for protein acetylation during herpesvirus infection. As prominent modulators of protein acetylation, histone deacetylases (HDACs) are essential transcriptional and epigenetic regulators. Not surprisingly, viruses have evolved a wide array of mechanisms to subvert HDAC functions. Here, we review the mechanisms underlying HDAC regulation during herpesvirus infection. We next discuss the roles of acetylation in host defense against herpesvirus infection. Finally, we provide a perspective on the contribution of current mass spectrometry-based “omic” technologies to infectious disease research, offering a systems biology view of infection.

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Section: Perspective: “Omic” Approaches In Characterizing Hdac Funmentioning

confidence: 99%

Histone Deacetylases in Herpesvirus Replication and Virus-Stimulated Host Defense

Guise

Budayeva

Diner

et al. 2013

Viruses

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“…IFI44 is differentially expressed in rhinovirus (RV) infected primary bronchial epithelial cells derived from humans with asthma vs. normal subjects [13]. Early stage human papillomavirus (HPV) infections also induce IFI44 expression in a human keratinocyte line [14], seemingly through the expression of HPV E7 oncoprotein [15]. However, HIV-1 infection seems to down-regulate expression of a set of ISGs in primary macrophages, including IFI44 [16].…”

Section: Introductionmentioning

confidence: 99%

IFI44 suppresses HIV-1 LTR promoter activity and facilitates its latency

et al. 2015

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IFI44 is an interferon-alfa inducible protein, and is associated with infection of several viruses. However, IFI44 elicits minimal antiviral effects on these viruses, and its exact role is still unknown. Here we show that IFI44 inhibits HIV-1 replication in vitro. Through depletion of endogenous IFI44 or overexpression of IFI44 we confirm that IFI44 suppresses HIV-1 LTR promoter activity and affects viral transcription. Furthermore, we find that IFI44 localizes to nuclei and binds to the HIV-1 LTR promoter in HIV-1 infected cells. Removing suppression of HIV-1 transcription benefits reactivation of HIV-1 proviruses for purging latent reservoirs. We demonstrate that depletion of endogenous IFI44 in J-LAT cells induces reactivation of latent HIV-1. Based on these results, we propose a model in which IFI44 is recruited to the HIV-1 LTR, which may suppress viral transcription and prevent reactivation of latent HIV-1. Our study suggests a previously unrecognized anti-HIV phenomenon for interferon-stimulated proteins.

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“…Other transcripts were potentiated by E6/E7 expression such as Cox-1 [27] . In a more recent study, E7 expression modified IFI44 , IFI44L and TP53INP2 - transcripts, which were also found to be downregulated in HPV16-positive HaCaT cells [28, 29]. The annotation of all genes discussed in the manuscript is included as Supplementary Table .…”

Section: Mrna Profilingmentioning

confidence: 99%

“…The most recent study where the HPV16 genome was transfected into HaCaT cells identified 338 differentially expressed genes (fold change between -3.8 and 3.5). The most upregulated genes were ANKRD1 , PSG s and HSPB8 and among the most downregulated genes were MMP s, SERPINB3 and SERPINB 4 [2, 29] (Fig. 1 ).…”

Section: Mrna Profilingmentioning

confidence: 99%

A Decade of Global mRNA and miRNA Profiling of HPV-Positive Cell Lines and Clinical Specimens

Kaczkowski

Morevati²,

Rossing³

et al. 2012

TOVJ

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For more than a decade, global gene expression profiling has been extensively used to elucidate the biology of human papillomaviruses (HPV) and their role in cervical- and head-and-neck cancers. Since 2008, the expression profiling of miRNAs has been reported in multiple HPV studies. Two major strategies have been employed in the gene and miRNA profiling studies: In the first approach, HPV positive tumors were compared to normal tissues or to HPV negative tumors. The second strategy relied on analysis of cell cultures transfected with single HPV oncogenes or with HPV genomes compared to untransfected cells considered as models for the development of premalignant and malignant transformations.In this review, we summarize what we have learned from a decade of global expression profiling studies. We performed comprehensive analysis of the overlap of the lists of differentially expressed genes and microRNAs, in both tissue samples and cell culture based studies. The review focuses mainly on HPV16, however reports from other HPV species are used as references. We discuss the low degree of consensus among different studies and the limitation of differential expression analysis as well as the fragmented miRNA-mRNA target correlation evidence. Furthermore, we propose an approach for future research to include more comprehensive miRNA-mRNA target correlation analysis and to apply systems biology/gene networks methodology.

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Integrative analyses reveal novel strategies in HPV11,-16 and -45 early infection

Cited by 36 publications

References 49 publications

Histone Deacetylases in Herpesvirus Replication and Virus-Stimulated Host Defense

Histone Deacetylases in Herpesvirus Replication and Virus-Stimulated Host Defense

IFI44 suppresses HIV-1 LTR promoter activity and facilitates its latency

A Decade of Global mRNA and miRNA Profiling of HPV-Positive Cell Lines and Clinical Specimens

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