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  • Phone : +33 3 68 85 37 27
  • Location : Strasbourg, France
Last update 2022-03-14 14:21:33.789

Gaëtan LIGAT PhD, Postdoctoral researcher - Molecular virologist

Course and current status

Dr Gaëtan LIGAT (born 13.03.1990) is postdoctoral researcher in virology at the University of Strasbourg. Member of the Inserm Institute for Viral and Liver Disease UMR_S1110.

He received his Ph.D (2017) in molecular virology from the University of Limoges (PhD supervisors: Profs. Sophie ALAIN and Sébastien HANTZ).

He has published 15 articles (h-index:8 and i10 score:7 according to Google Scholar) and was co-director of master students, and numerous students.

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

His is member of the reviewer board of Vaccines (MDPI) and 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 Diseases.

He obtained his qualification as University Lecturer in Section CNU 64, Section CNU 65 and Section CNU 87 (Teaching assistant at Faculty of Pharmacy in 2017. University of Limoges, France. Formal courses of virology. Practical courses of bacteriology and immunology - Teaching seminar at Faculty of Science and Technology for Master students in 2020. University of Limoges, France).

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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