Project Details
Description
KSHV is an oncogenic herpesvirus, responsible for disease in mostly immunocompromised patients mainly coinfected with HIV. The virus presents a lifelong persistent infection controlled by the latency associated nuclear antigen (LANA) and sporadic lytic reactivation.
During infection, the viral genome forms an episome, a circular and chromatinized DNA molecule, which persists in cell nucleus. Activating histone modifications such as H3K4me3 both in latency promoters and terminal repeats have been connected with LANA activity, through its interaction with the MLL1 COMPASS complex. This complex includes WDR5 which typically binds to MLL1 through the WIN motif. LANA has a WIN-like motif able to bind to WDR5, potentially competing with MLL1 and regulating its H3K4me3 deposition.
This projects aims to unravel how LANA is able to affect chromatin modifications and establish viral persistence and how this mechanism can be disrupted by drugs to create new therapies against latent KSHV.
During infection, the viral genome forms an episome, a circular and chromatinized DNA molecule, which persists in cell nucleus. Activating histone modifications such as H3K4me3 both in latency promoters and terminal repeats have been connected with LANA activity, through its interaction with the MLL1 COMPASS complex. This complex includes WDR5 which typically binds to MLL1 through the WIN motif. LANA has a WIN-like motif able to bind to WDR5, potentially competing with MLL1 and regulating its H3K4me3 deposition.
This projects aims to unravel how LANA is able to affect chromatin modifications and establish viral persistence and how this mechanism can be disrupted by drugs to create new therapies against latent KSHV.
Status | Active |
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Effective start/end date | 1/02/22 → 31/01/26 |
UN Sustainable Development Goals
In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This project contributes towards the following SDG(s):
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