Living fossil or evolving virus?

Tomonaga, Keizō

doi:10.1038/embor.2010.59

Cited by 3 publications

(2 citation statements)

References 8 publications

(6 reference statements)

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“…Importantly, these observations raise the possibility that non-retroviral RNA viruses act as mutagens [ 11 , 33 , 34 ]. The risk of somatic integration of RNA virus vectors should be evaluated, as for LCMV and BDV.…”

Section: Non-retroviral Integrationmentioning

confidence: 99%

Non-Retroviral Fossils in Vertebrate Genomes

Horie

Tomonaga

2011

Viruses

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Although no physical fossils of viruses have been found, retroviruses are known to leave their molecular fossils in the genomes of their hosts, the so-called endogenous retroviral elements. These have provided us with important information about retroviruses in the past and their co-evolution with their hosts. On the other hand, because non-retroviral viruses were considered not to leave such fossils, even the existence of prehistoric non-retroviral viruses has been enigmatic. Recently, we discovered that elements derived from ancient bornaviruses, non-segmented, negative strand RNA viruses, are found in the genomes of several mammalian species, including humans. In addition, at approximately the same time, several endogenous elements of RNA viruses, DNA viruses and reverse-transcribing DNA viruses have been independently reported, which revealed that non-retroviral viruses have played significant roles in the evolution of their hosts and provided novel insights into virology and cell biology. Here we review non-retroviral virus-like elements in vertebrate genomes, non-retroviral integration and the knowledge obtained from these endogenous non-retroviral virus-like elements.

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Section: Non-retroviral Integrationmentioning

confidence: 99%

Non-Retroviral Fossils in Vertebrate Genomes

Horie

Tomonaga

2011

Viruses

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“…Some of the primate EBLNs contain an intact open reading frame and are expressed as mRNAs; indeed, these elements have been suggested to code for gene products that might possess antiviral activity and protect cells from being infected by BDV (Belyi et al 2010). Although the presence of EBLNs indicates that an "ancient" BDV successfully infected humans in the past, it is unclear whether this might still be possible with the "current" BDV strains circulating in birds and animals (Tomonaga 2010).…”

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confidence: 98%

Viral interference with neuronal integrity: what can we learn from the Borna disease virus?

Schwemmle

Heimrich

2011

Cell Tissue Res

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The neurotropic Borna disease virus (BDV) is unusual in that it can persistently infect neurons of the central nervous system (CNS) without causing general cell death, reflecting its favourable adaptation to the brain. The activity-dependent enhancement of neuronal network activity is however disturbed after BDV infection, possibly by its effect on the protein kinase C signalling pathway. The best model for studying BDV, which has a non-cytolytic replication strategy in primary neurons, is the rat. Infection of adult rats results in a fatal immune-mediated disease, whereas BDV establishes persistent infection of the brain in newborn rats resulting in progressive neuronal cell loss in defined regions of the CNS. Our recently developed system of BDV-infected hippocampal slice cultures has clearly shown that the onset of granule cell loss begins after the formation of the mossy fibre projection. Quantitative analysis has revealed a significant increase in synaptic density on identified remaining granule cell dendrites at 6 weeks after infection, followed by a decline. Granule cells are the major target of entorhinal afferents. However, despite an almost complete loss of dentate granule cells during BDV infection, entorhinal axons persist in their correct layer, both in vivo and in slice cultures, possibly exploiting rewiring capabilities and thereby allowing new synapse formation with available targets. These morphological observations, together with electrophysiological and biochemical data, indicate that BDV is a suitable model virus for studying virus-induced morphological and functional changes of neurons and connectivity patterns.

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Bornaviruses

TOMONAGA¹

2012

Uirusu

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Bornaviridae is an enveloped animal virus carrying an 8.9 kb non-segmented, negative-strand RNA genome. The genus bornavirus contains two members infecting vertebrates, Borna disease virus (BDV) and avian bornavirus (ABV), which could preferably infect the nervous systems. BDV causes classical Borna disease, a progressive meningoencephalomyelitis, in horses and sheep, and ABV is known to induce proventricular dilatation disease, a fatal disease characterized by a lymphocytic, plasmacytic inflammation of central and peripheral nervous tissues, in multiple avian species. Recent evidences have demonstrated that bornavirus is unique among RNA viruses as they not only establish a long-lasting, persistent infection in the nucleus, but also integrate their own DNA genome copy into the host chromosome. In this review, I outline the recent knowledge about the unique virological characteristics of bornaviruses, as well as the diseases caused by the infection of BDV and ABV.

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Living fossil or evolving virus?

Cited by 3 publications

References 8 publications

Non-Retroviral Fossils in Vertebrate Genomes

Non-Retroviral Fossils in Vertebrate Genomes

Viral interference with neuronal integrity: what can we learn from the Borna disease virus?

Bornaviruses

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