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Identifier

000376375

Title

The role of extracellular-signal-regulated kinase (ERK)activation during herpessimplex virustype-1(HSV-1) lytic infection

Alternative Title

Ο ρόλος της ενεργοποίησης της ERK κινάσης κατά τη διάρκεια λυτικής λοίμωξεις από τον απλό ερπητοιό τύπου 1(HSV-1)

Author

Thiriou, Despoina

Author

Θήριου, Δέσποινα

Thesis advisor

Σουρβίνος, Γ.

Reviewer

Τσατσάνης, Χ.

Abstract

Viruses, alike other intracellular organisms, are ultimately dependent upon the host cell for their replication. To establish a successful infection, they need to overcome several host cell obstacles, such as virus binding-triggered apoptosis, induction of innate and inflammatory immune responses, cellular RNA interference, autophagy and restriction on virus gene transcription. Besides using their gene products, viruses have evolved better strategies to eliminate host cell defense. Manipulation of cellular preexisting signaling pathways is probably one of the best strategies used early during infection. Signaling pathways determine the cell’s ability to respond to external stimuli. Transduced signals can be interpreted as proliferative , mitogenic, differentiating or apoptotic, depending on the cell type and the quality and duration of the stimulus. Several DNA and RNA viruses have been documented to use various strategies to activate the Extracellular-signal- Regulated Kinase (ERK) signaling pathway. Conversely, Herpes Simplex Virus type 1(HSV-1), member of the Herpesviridae family of DNA viruses, is well-known to activate several other MAP kinase cascades, such as JNK and p38. To date, no data exist about a possible effect of HSV-1 on ERK pathway. This was the aim of the present study: to demonstrate the impact of HSV-1 infection on the cellular ERK signaling cascade, as well as to investigate the role of a functional ERK pathway on viral replication. For this purpose, briefly, we used cells receptive to infection from HSV-1 strain 17+ (wild-type). BHK cells were used for viral propagation and titration, while microscopy and biochemistry assays were performed in Vero cells. The latter were fixed or collected at different time points in the course of infection, in the presence or absence of a MEK-specific inhibitor, and immunostained or immunoblotted, respectively, for p-ERK and viral gene products. Our data demonstrate for the first time that ERK pathway is activated during ΗSV-1 infection, while this activation favors HSV-1 efficient replication.

Language

Greek

Subject

ERK

Extracellular-signal-regulated kinase

HSV-1

Herpes simplex virus type 1

Mapk pathway

Oncolytic viruses herpesviruses

Virology

Απλός ερπητοιός τύπου 1

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