Epigenetic reprogramming of host genes in viral and microbial pathogenesis

Paschos, Konstantinos; Allday, Martin J.

doi:10.1016/j.tim.2010.07.003

Cited by 203 publications

(160 citation statements)

References 91 publications

(83 reference statements)

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“…Recent studies highlight the ways in which bacterial and viral pathogens affect host epigenetic status by influencing DNA methylation and histone modification 17,29) . The most well documented example is infection with Helicobacter pylori, which induces aberrant DNA methylation and deacetylation of Histone H3…”

Section: Special Issue (Mini Review) Gut Microbiota and Epigeneticsmentioning

confidence: 99%

Commensal microbiota-derived signals regulate host immune system through epigenetic modifications

Takahashi

Hase

2015

Inflammation and Regeneration

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Commensal microbiota colonizing the digestive tract is a symbiotic partner of its host, as it plays a critical role in nutrient metabolism as well as the development and maturation of the host immune system. Although it is clear that regulation of the host-commensal relationship is crucial to mammalian health, the underlying mechanisms regulating gut homeostasis are yet to be elucidated. Epigenetic modifications, including DNA methylation and histone methylation/acetylation, alter the structure of chromatin to regulate the transcriptional program of eukaryotic cells. At the whole genome level, these modifications possibly play a key role in regulating the mutually beneficial relationship between the host and the gut microbiota. In this review, we describe how the commensal microbiota and its metabolic by-products modify the epigenome of host cells, and in turn, change their development and functional behavior.Rec.2/24/2015, Acc.3/1/2015, pp129-136

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Section: Special Issue (Mini Review) Gut Microbiota and Epigeneticsmentioning

confidence: 99%

Commensal microbiota-derived signals regulate host immune system through epigenetic modifications

Takahashi

Hase

2015

Inflammation and Regeneration

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“…This analysis may be especially useful when a pathogen is not detected or the pathogenic role of a detected microbial agent is in question. Circulating blood leukocytes react to pathogens by recognizing pathogen-specific molecular patterns through pattern recognition receptors leading to up-or down-regulation of the expression of host genes associated with immune functions (2,3), with differential activation of host transcriptional programs with different pathogens (4). Thus, host blood transcriptional profiles and representative biomarkers may be powerful tools for categorizing infection (5).…”

mentioning

confidence: 99%

Gene expression profiles in febrile children with defined viral and bacterial infection

Hu¹,

Crosby

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

116

119

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Viral infections are common causes of fever without an apparent source in young children. Despite absence of bacterial infection, many febrile children are treated with antibiotics. Virus and bacteria interact with different pattern recognition receptors in circulating blood leukocytes, triggering specific host transcriptional programs mediating immune response. Therefore, unique transcriptional signatures may be defined that discriminate viral from bacterial causes of fever without an apparent source. Gene expression microarray analyses were conducted on blood samples from 30 febrile children positive for adenovirus, human herpesvirus 6, or enterovirus infection or with acute bacterial infection and 22 afebrile controls. Blood leukocyte transcriptional profiles clearly distinguished virus-positive febrile children from both virus-negative afebrile controls and afebrile children with the same viruses present in the febrile children. Virus-specific gene expression profiles could be defined. The IFN signaling pathway was uniquely activated in febrile children with viral infection, whereas the integrin signaling pathway was uniquely activated in children with bacterial infection. Transcriptional profiles classified febrile children with viral or bacterial infection with better accuracy than white blood cell count in the blood. Similarly accurate classification was shown with data from an independent study using different microarray platforms. Our results support the paradigm of using host response to define the etiology of childhood infections. This approach could be an important supplement to highly sensitive tests that detect the presence of a possible pathogen but do not address its pathogenic role in the patient being evaluated.

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“…Several virus-encoded products have been associated with transforming and/or oncomodulatory activities [4] , and with the ability to induce chromosome damage, abnormal mitosis and genetic instability when expressed in cell cultures (Table 2) [18,[36][37][38] . Recent findings point to viral proteins interfering with the epigenetic milieu of the infected cells, leading to the transcriptional repression of tumor suppressor genes, and interference with cell cycling control [39] (Table 3). However in vivo these activities must be particularly inefficient if one considers that the majority of the human population carries a number of resident viruses, but only a minority among infected individuals will develop tumors that can be correlated with persistent viral infections, and generally after very long latency periods (years to decades) [4,35] .…”

Section: A Mechanism For Tumor Initiation In Viral Persistencementioning

confidence: 99%

“…Several virus products are able to induce genetic damage (Table 2), and examples of encapsidated DNA nicking activities with a potential role in chromosomal damage have been reported [49,50] . Other viral proteins can interfere with the cellular DNA repair machinery (see [51] for a detailed review) or introduce transcriptional-silencing marks [39] . All these activities could in this context generate primary damage events, leaving the cell with permanent genetic and epigenetic damage before entering into latency.…”

Section: A Mechanism For Tumor Initiation In Viral Persistencementioning

confidence: 99%

How virus persistence can initiate the tumorigenesis process

Avanzi

Alvisi²,

Ripalti³

2013

WJV

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Human oncogenic viruses are defined as necessary but not sufficient to initiate cancer. Experimental evidence suggests that the oncogenic potential of a virus is effective in cells that have already accumulated a number of genetic mutations leading to cell cycle deregulation. Current models for viral driven oncogenesis cannot explain why tumor development in carriers of tumorigenic viruses is a very rare event, occurring decades after virus infection. Considering that viruses are mutagenic agents per se and human oncogenic viruses additionally establish latent and persistent infections, we attempt here to provide a general mechanism of tumor initiation both for RNA and DNA viruses, suggesting viruses could be both necessary and sufficient in triggering human tumorigenesis initiation. Upon reviewing emerging evidence on the ability of viruses to induce DNA damage while subverting the DNA damage response and inducing epigenetic disturbance in the infected cell, we hypothesize a general, albeit inefficient hit and rest mechanism by which viruses may produce a limited reservoir of cells harboring permanent damage that would be initiated when the virus first hits the cell, before latency is established. Cells surviving virus generated damage would consequently become more sensitive to further damage mediated by the otherwise insufficient transforming activity of virus products expressed in latency, or upon episodic reactivations (viral persistence). Cells with a combination of genetic and epigenetic damage leading to a cancerous phenotype would emerge very rarely, as the probability of such an occurrence would be dependent on severity and frequency of consecutive hit and rest cycles due to viral reinfections and reactivations

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Epigenetic reprogramming of host genes in viral and microbial pathogenesis

Cited by 203 publications

References 91 publications

Commensal microbiota-derived signals regulate host immune system through epigenetic modifications

Commensal microbiota-derived signals regulate host immune system through epigenetic modifications

Gene expression profiles in febrile children with defined viral and bacterial infection

How virus persistence can initiate the tumorigenesis process

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