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| Identifier |
000357843 |
| Title |
The effect of TGF-b grpwth factor on Herpes Simplex Virus type 1 (HSV-1) prageny viral yield during lytic infection |
| Alternative Title |
Η επίδραση του αυξητικού παράγοντα TGF-b στην παραγωγή ιικών σωματιδίων κατά την διάρκεια λυτικής λοίμωξης με τον ιό του απλού έρπητα τύπου 1 (HSV-1) |
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Author
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Σιακαλλής, Γεώργιος
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Thesis advisor
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Σουρβίνος, Γ.
Καρδάσης, Δ.
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| Abstract |
Alike many intracellular pathogens (viruses, bacteria, parasites), Herpes Simplex Virus type 1 (HSV-1) has evolutionary evolved throughout the course of its existence to employ cellular proteins and modulate cellular signalling cascades for its own purposes. Viral genome in general encodes for a limited number of proteins not sufficient to satisfy viral functions even for the largest DNA viruses. HSV-1 has adjusted to utilize cellular proteins to guaranty its replication, and manipulate several signalling pathways to modulate cellular functions such as immune response, apoptosis e.t.c.
The balance between host cells - virus interactions is achieved by complex mechanisms resulting in complete re-organization of the expression pattern of a great number of cellular genes. This pattern fundamentally changes when HSV-1 undergoes lytic infection compared to HSV-1 established latency in neuronal cells. DNA microarray studies have provided us with a useful tool for highthroughput analysis of the expression pattern of a wide variety of cellular genes upon diverse conditions. Using this technique, recent publications studied modulated gene expression upon HSV-1 productive infection. Among the many different signalling cascades shown to be altered, the TGF-β pathway was one of them. More specifically, HSV-1 lytic infection down regulated proteins implicated in TGF-β signaling cascade. However, until so far there has been no report of the actual effect of TGF-β stimulation on the release of progeny viruses during HSV-1 productive infection.
In this study we used in vitro cell cultures to examine the release of HSV-1 progeny viruses upon TGF-β stimulation. We used 2 different HSV-1 viral strains. HSV-1 17+ (laboratory wild-type strain) and its fluorescent counterpart VECFP-ICP4. Based on the data presented above, if our hypothesis is correct we expect to see abrogated virion release upon TGF-β stimulation.
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| Physical description |
45 σ. : πιν. ; 30 εκ. |
| Language |
Greek, English |
| Subject |
Herpesviridae |
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Herpesviridae Infections |
| Issue date |
2008-12-15 |
| Collection
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School/Department--School of Medicine--Department of Medicine--Post-graduate theses
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Type of Work--Post-graduate theses
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| Notes |
"Κυτταρική και γενετική αιτιολογία, διαγνωστική και θεραπευτική των ασθενειών του ανθρώπου |
| Views |
174 |
The effect of TGF-b grpwth factor on Herpes Simplex Virus type 1 (HSV-1) prageny viral yield during lytic infection
