CV Science

Henri Gruffat PhD

Course and current status

Current Position : INSERM Research Scientist (CRHC)  at "Centre International de Recherche en Infectiologie (CIRI)". INSERM U1111 CNRS UMR5308, ENS-Lyon, Université Lyon-I.

Principal Investigator (PI) Group "Oncogenic  Herpesviruses"

President Association HerPAs (Virus Herpes et Pathologie Associées) (http://assos-herpas.ens-lyon.fr/)

Member of the board of the french society of virology (SFV)

Education

2002- Habilitation à Diriger les recherches (HDR)

1991- PhD in Virology,

Training and Experience:

2013- ___: Team: "Oncogenic Herpesviruses"

2005-2012: Group "Molecular Biology of the γ-Herpesvirus". Co PI, INSERM U758

1993 – 1994: Post-doctoral fellow with Wolfgang Hammerschmidt. Institut für klinische Molekularbiologie und Tumorgenetik, GSF, Helmholtz Center Munich, Germany.

1988-1991 PhD training:Virology at the University Claude Bernard Lyon I, directed by Dr. Alain Sergeant.

Scientific summary

Molecular basis of Epstein-Barr virus lytic cycle activation: In our lab, we are studying the mechanisms by which Epstein-Barr virus (EBV) induces B cells immortalization and the regulation of the switch between latent persistence and virus replication. We focus our study on the biological role of some key viral genes that contribute to these processes at the genetic, molecular and cellular levels.

EBV is a ubiquitous human γ -herpesvirus which is associated with several human malignancies. After primo-infection, the virus persists under a latent state all the life of the infected individuals with intermittent viral production in the oropharynx. These phases of viral reactivation, associated with de novo infections, have been suggested to be a risk factor for the emergence of EBV-associated malignancies.
I focus on the study of different key EBV proteins that cooperate for efficient viral reactivation and virus production: The two immediate-early proteins EB1 (also called ZEBRA, or BZLF1) and R (also called BRLF1), two transcriptional activators responsible for the switch from latent to productive cycle and EB2, (also called BMLF1) a postranscriptional activator required for efficient export and translation of viral mRNAs. The two immediate-early proteins EB1 and R, are transcriptional activators that together induce the entire complement of early and late lytic EBV genes. This makes EB1 and R ideal drug targets for blocking induction of the lytic cycle at an early stage. Recently, I have characterized a viral transcription Pre-Initiation Complex (vPIC) formed by six viral proteins (BcRF1-TBP-like protein-, BFRF2, BGLF3, BVLF1, BDLF4 and BDLF3.5) required for expression of the viral late genes.

The overall goals of this project are i) to better understand how the EBV lytic cycle is activated; ii) to determine how the host cell regulates this process.