Our group studies the host biological functions involved in the replication and pathogenesis of human viruses and in the response to these infections.
In particular, we are exploring the relationship between HIV-1 (human immunodeficiency virus), the causative agent of AIDS, and the host cell in order to better understand the molecular mechanisms that control viral replication and spread, with the ultimate goal of identifying potential strategies to control or eradicate the virus.
- The laboratory deciphers the mechanisms of HIV-1 latency that lead to the persistence of cells harboring replication-competent but transcriptionally silent viruses. These reservoirs are established early in the course of infection and can persist for an extended period of time. If treatment is interrupted, viral rebound occurs rapidly.
- We are also exploring the molecular basis of HIV-1 expression at both transcriptional and post-transcriptional levels. The HIV-1 transcriptome is complex and must be finely regulated to allow the morphogenesis of infectious viral particles.
- In addition, the team is studying how HIV-1 counteracts the restriction factors, intrinsic barriers of the host to infection. Restriction factors are proteins with direct antiviral activity and are an important facet of the innate immune response controlling infection in a cell-intrinsic manner. HIV-1 has evolved countermeasures to evade these mechanisms. In particular, we are studying the restrictions that viruses face during the assembly and release of new virions.
The emergence of the highly pathogenic coronavirus SARS-CoV-2 and its rapid spread worldwide have recently led us to explore the host-virus interactions involved in the replication of this pathogen. Proteomic approaches are being developed to characterize the cellular factors essential for the morphogenesis of infectious SARS-Cov2 virions.
To reach these objectives, we use genetic, cell biology, molecular biology, imaging and virology techniques.