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  • Phone : +33 3 68 85 37 27
  • Location : Toulouse, France
Last update 2022-09-18 15:21:57.853

Gaëtan LIGAT Associate Professor of Virology (Maître de Conférences)

Course and current status

Associate Professor of Virology (Maître de Conférences) at Toulouse III - Paul Sabatier University.

He coordinates the Young Microbiologists section of the French Microbiology Society (SFM) and he was Expert Young Doctor for the High Council for Evaluation of Research and Higher Education (HCERES). 

He is Review Editor for Frontiers in Microbiology, Frontiers in Virology and member of the reviewer board of Vaccines (MDPI); Guest Editor for the Research Topic “Human Cytomegalovirus: Recent Advances, Novel Targets and Vaccines” for Vaccines (MDPI).

He received two postdoctoral fellowships (ANRS 2018, 2020) and one research grant (2021) in his own name from the European Society for Clinical Microbiology and Infectious 

Scientific summary

PhD position

Human cytomegalovirus (HCMV) is responsible for life-threatening infections in immunocompromised individuals and can cause serious congenital malformations. Current antiviral inhibitors all target the viral DNA polymerase. They have adverse effects and prolonged treatment can select for drug resistance mutations either in the viral polymerase pUL54, the kinase pUL97 or both of them. Thus, we need new drugs targeting others stages of replication. 

Our research focused on the terminase complex (pUL56-pUL89-pUL51), involved in viral DNA packaging as it is highly specific for HCMV and has no counterpart in the cell. It represents a target of choice for new antivirals, confirmed by the recent development of letermovir in the transplant setting. However, its mechanism of action is still unknown. Elucidating its mechanism of action and identifying new patterns as potential targets within the complex could improve the terminase inhibitors family.

 

Postdoctoral position

Chronic hepatitis B (CHB), caused by hepatitis B virus (HBV), is a leading cause of liver cirrhosis, liver failure and hepatocellular carcinoma (HCC) worldwide. An estimated 250 million people are chronically infected by the virus. Current therapeutic strategies can control viral infection, but viral cure is rarely observed. HBV replication is characterized by the synthesis of a specific replication intermediate, the covalently closed circular (ccc) DNA, a minichromosome serving as a template for the transcription of viral RNA and which is not targeted by the current treatments. A few cccDNA copies per liver can reactivate full virus production upon therapy withdrawal, or loss of immunological control of the low-level replication going on even under therapy. Consequently, any cure of CHB will require elimination of this virus persistence reservoir. To date, little is known about cccDNA formation from the HBV genomic relaxed circular (rc) DNA. Notably, the involvement of hepatocyte host factors remains largely unknow, although it is likely that DNA repair factors play a key role in this process. The identification of novel host factors involved in cccDNA formation or regulation would provide new targets for viral cure.

The aim of the project is to identify and characterize cccDNA host factors and understand their mechanism of action using state-of-the-art cell culture system. 

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