Un nouveau cycle cellulaire des virus identifié

[Jean-Luc P]

Bonjour,

un article de EMBO reports : HSV, le virus de l'herpes détruit l'ADN mitochondrial de manière ciblée des cellules infectées.
Je crois bien que c'est la première fois qu'on identifie l'ADN mitochondrien comme cible de virus.

Abstract

Mitochondria have crucial roles in the life and death of mammalian cells, and help to orchestrate host antiviral defences. Here, we show that the ubiquitous human pathogen herpes simplex virus (HSV) induces rapid and complete degradation of host mitochondrial DNA during productive infection of cultured mammalian cells. The depletion of mitochondrial DNA requires the viral UL12 gene, which encodes a conserved nuclease with orthologues in all herpesviruses. We show that an amino-terminally truncated UL12 isoform—UL12.5—localizes to mitochondria and triggers mitochondrial DNA depletion in the absence of other HSV gene products. By contrast, full-length UL12, a nuclear protein, has little or no effect on mitochondrial DNA levels. Our data document that HSV inflicts massive genetic damage to a crucial host organelle and show a novel mechanism of virus-induced shutoff of host functions, which is likely to contribute to the cell death and tissue damage caused by this widespread human pathogen.

http://www.nature.com/embor/journal/...s/7400878.html
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[Jean-Luc P]

Qui a renommé ce fil ? Je pensais avoir écrit "une nouvelle cible cellualire" ?

Alzheimer quand tu nous guettes...

[JPL]

C'est moi. J'ai reconstitué les mots estropiés en fonction de ce qui paraissait le plus plausible (et ça continue : "une nouvelle cible cellualire" )

[sacharybalka]

Salut, j'ai une question.
Si le virus détruit les mitochondries, d'où la cellule tire l'énergie nécessaire à la multiplication dudit virus?

[A voir en vidéo sur Futura]

[Jean-Luc P]

En fait, comme le suggère

Our data document that HSV inflicts massive genetic damage to a crucial host organelle and show a novel mechanism of virus-induced shutoff of host functions, which is likely to contribute to the cell death and tissue damage caused by this widespread human pathogen

, ça se passe lors de la phase lytique de la pathologie locale associée à HSV et pas du tout lors de la phase de latence.

De toute façon les cellules vont mourir, mais ça permet probablement au virus de produire encore plus de particules virales en empêchant certains mécanismes de défenses antivirales de la cellule :

mitochondria have key roles in orchestrating cellular antiviral defences, including apoptosis and the type I interferon response, in addition to their crucial respiratory function. It is therefore tempting to speculate that HSV-induced depletion of mt DNA and/or mt mRNA neutralizes one or more host defence mechanisms. However, our studies have yet to provide any support for this hypothesis and further work is therefore needed to determine whether and how mt DNA depletion benefits HSV. In addition, it will be important to determine if other members of the herpesviridae also provoke mt DNA depletion.